an experimental study of the pathology of cardiac dropsy, and its relation to that of local venous...

AN EXPERIMENTAL STUDY OF THE PATHOLOGY OF CARDIAC DROPSY, AND ITS RELATION TO THAT OF LOCAL VENOUS OBSTRUCTIONql

By CHARLES ROLTON, M.D., I).Sc., F.E.C.P., Director of the Research Laboratories, University College Hospital Medical School, Assistant Physician to University College Hospital, London.

From the Research Labvratmiea, University College Hospital Medical School.

INTRODUCTION. WORKERS on the pathology of passive mdema have during the last few years largely studied this problem by investigating the different conditions which modify the flow of lymph from lymphatic vessels, believing that the processes underlying lymph formation are, to a large extent, the same as those concerned in the production of adema. This involves the use of the “acute method ” of experimenting, in which a normal animal is placed under an anmthetic and the lympli flow estimated under different conditions, the animal being killed a t t h e end of the experiment. From the point of view of the physiology of lymph formation this method has yielded valuable results, especially in the hands of Starling (1894), who was able to show that Heidenhain’s (1891) experiments, by means of which he sought to egtablish his theory of lymph secretion, were not incompatible with Ludwig’s (1 8 5 0) filtration theory, and who a t the same time emphasised the importance of the permeability of the capillary wall, already laid stress upon by Cohnheim (1877). Heidenhain’s theory, although not proved, still receives considerable support from Hamburger (1 893) and other observers. Lazarus-Rarlow’s (1 8 94) experiments on lymph formation and edema led him to believe that the process was not one of filtration, but that the state of nutrition of the tissues themselves was of paramount importance. More recently, Asher (1897) has shown the importance of tissue metabolism in lymph formation, and his experiments have been repeated and extended by Bainbridge (1 9 0 0) and others.

A t the present day, then, physiologists incline to the view that the “ physical ” theory is not altogether adequate for the complete explana-

Received February 16, 1909.

4-JL. OF PATE.-VOL. XIV.

50 CHARLES BOLTON.

tion of lymph formation. From the p o i h of view of crdma, however, the value of this method is more questionable, and, holding the view that our knowledge of the diseased processes occurring in cardiac dropsy would advance no further towards a satisfactory solution until they were studied in an animal suffering from that malady, I endeavoured to produce this condition experimentally. Cohnheim ( 1 88 2) and Starling (1896) were the only two observers who had attempted to study the changes in the circulation in uncompensated heart disease, their method being the " acute ') one of the introduction of oil into the pericardium.

The method which I first employed is described in the Joumal of Pathology (1903). It was suggested by a certaiii form of adherent pericardiuru, in which cardiac dropsy results, aud consisted in con- stricting the pericardium by means of stitches so that the free diastolic expansion of the chambers of the heart was prevented. This method was successful, and dropsy resulted. The imiiiediate effects upon the circulation were the same as Cohnheini had found, but later when the animal was dropsical I found that the circulatory coiiditions were altered, and that the dropsy was produced whilst the yenous pressure was within normal limits. It was quite evident that certain adaptive changes had occurred, which were worthy of closer study. This method was, however, not a satisfactory one to employ for a large series of experiments, because so inany animals died from the operation, or recovered perfectly without developing dropsy. I had already concluded that the circulatory changes in uncoinpensated heart disensc differed from those of local venous obstructioii only because tho splanchnic circulation was involved in the former condition, and therefore considered that constriction of the inferior rena cam above the diaphragm should serve the purpose equally well. I therefore used this method alone and also combined with ligature or constriction of the superior vena cava, and at the same time compared the results with those obtained by constriction of the portal vein.

A preliminary communication on some of the earlier results has been published in the Proceedings of the Royal Xoeiety (1907). I n this way I was able : (1) To confirm my previous results by employing a different method. (2) To use a more easy method of obstructing the venous flow into the heart, and one which admitted of different ,degrees of obstruction, which could be accurately measured. (3) Tn bring the results of general venous obstruction into line with those of local venous obstruction.

The experiments fall into three groups: (1) Those relating t o the effects upon the production of dropsy. (2) Those relating to the immediate effects upon the circulation of the blood. (3) Those relating to the condition of the circulation in the dropsical animal.

STUDY OF THE PATHOLOGY OF CARDIAC DROPSY. 51

I. METHOD.

The animals used were in all cases cats. 1. In those experiments relating to the effects of the venous

obstruction upon the production of dropsy, the operations of con- stricting the veins were done under strict an tiseptic precautions, and the wounds dressed with cotton wool and collodion. The details of the operations are as follows :

Inferior vena cava.-The animal lying on its back, a skin incision is made on the right side of the chest parallel to the sternum and about an inch from it, beginning at the costal margin and extending forwards for about 3 in. The muscles are cut through and pulled aside with the skin by weighted retractors, exposing the costal cartilages and ribs. An incision an inch or more long is made in the seventh intercostal space, and the seventh and eighth ribs are ,drawn apart and fixed by weighted retractors. The lower lobe of the right lung is drawn aside by a copper spatula, exposing the inferior vena cava, with the phrenic nerve running along it. The inferior cava between the heart and the diaphragm is about an inch long. It lies in the free border of. a mesentery .attached behind to the'diaphrap, in front to the pericardium, and below to the sternum. Between this mesentery and the division between the right and left pleural cavities is a small space immediately behind the heart. This small space contains a fourth lobe of the right lung. The mesentery together with the phrenic nerve is dissected off the vein with two pairs of forceps. The vein is then either ligatured or n piece of Jilcyue's rubber catheter, of the .appropriate dianieter and aboit 4 in. in length, cut open longitudinally and having a piece of silk attached to each cut margin, is passed round the vein with curved forceps and tied on. The lungs are well blown up and the seventh and eighth ribs brought together with three or four silk sutures. The muscles and skin are then stitched up separately. No difficulty is experi- (enced with regard to pneumothorax, and the animals after a brief period of .apncea begin to brcathe naturally. During the operation cther is administered by artificial respiration through a bent piece of glass tubing, which is passed into the larynx and prevented from slipping out by a small piece of rubber tubing which eiicitses the glass for a quarter of an inch at its end and catches .in the larynx. The mouth is opened by n gag, and if the tongue be drawn out by tongue forceps, a light being cast into the throat from a head mirror, the glottis is brought into view. The operation takes from ten to fifteen minutes, and when the animal has recovered from the anzesthetic it can walk about like a normal animal, unless the vein has been completely occluded.

The diameters of the tubes used to constrict the vein were l1 ,2 , 24, 3, and 4 inm. The diaiiietcr of the inferior vena cavn was found to be about 5 mm. I t natnrally varies n. little in individual animals, but i t does not necessarily follow that because R cat is small it has a siiiall inferior vcua cava. The diameter of the vein was measured in three cats by washing the blood out .after death, and introducing warm gelatin a t the normal venous pressure through the femoral vein. The gelatin was allowed to cool and solidify. 'The inferior vena cava mas then cut out and its diameter measured.

Superior vena cava.-The skin incision in this case extends from the .clavicle backwards for about 3 in. The chest is opened in the third intercostal space on the right side and the anterior margin of the right lung retracted, It is ithen either ligatured with silk or constricted in the same way as the infesor

After a little practice it is quite easy to intubate a cat.

The vein is cleared and the phrenic nerve dissected off it.

82 CHARLES BOLTON;

vena cava. The diameter of the superior vena cava is like that of the inferior, about 6 mm. or possibly a trifle smaller, and the same sizes of tubing were used for producing the constrictions.

Portal vein.-The skin incision commences just below the ensiform cartilage in the middle line, and is about 3 in. long. The abdomen is opened by a similar incision, and the liver held upwards by a copper retractor. The duodenum is pulled down and the portal vein brought into view. The peritoneum is incised and the common bile duct and hepatic artery dissected off the vein. L t is then either ligatured or constricted by rubber tubing. The diameter of the portal vein in two cases was found to be just over 4 nim. by the gelatin method. I n all the above operations it is necessary to cast a good light into the wound by means of a head mirror. A post-mortem bacteriological examination was made in most of the cases in order to make quite certain that the dropsy was of mechanical and not toxic origin.

2. I n the experiments relating to the immediate effects upon the circulation of the blood, artificial respiration was maintained through a tracheotomy tube, the air being blown through an ether bottle fitted with a two-way apparatus, so that either pure air, ether-saturated air, or definite mixtures of the two, could be used at will for pulmonary ventilation. Morphia was also administered. The chest was opened by incisions similar to those described above, and the veins were constricted in the same way.

I n the experiments, which were done in order to determine, by a gradually increasing constriction, at what point the venous and arterial pressures were first altered, a fine wire was passed round the vena cava and the free ends of this wire, pushed through a piece of glass tubing, drawn out to a point so as to form a snare. The loop so formed was gradually tightened until an effect was observed upon the blood pressures ; the vein was then cut through and the wire loop removed and its diameter measured. The venous pressures were taken in the inferior vena cava, the cannula being introduced into the external iliac vein ; at the lower end of the femoral vein, where it divides into two branches a t the ankle, the cannula being inserted into one of the branches and pushed on until its point was flush with the opening into the femoral vein; in the portal vein, the cannula being introduced into a branch of the splenic vein, the spleen being then replaced in the abdomen ; at the upper end of the external jugular vein, the cannula being inserted into the posterior auricular vein and pushed down until its point was flush with the opening into the jugular vein. In this way an idea was obtained of the alterations in pressure in all parts of the systemic venous system. The venous pressure mas registered on a kymograph by means of an air tambour connected with the top of the venous manometer by means of rubber tubing. This simply denionstrates whether a rise or fall of venous pressure occurs : it is no indication of the exact amount of such rise or full. Tracings of the pressures are not shown in the protocols, because i t mas thought tliat it would be much moro valuable to state the actiial pressures registered. The pressure mas read off on a millimetre scale, and at the end of the experiment the exact height of the vein marked on the scale, and the actual venous pressure calculated by suh- tracting the number corresponding to the latter from the former. The fluid in the manometer was an aqueous solution of MgSO, (sp. gr. 1046) stained with methylene-blue. The arterial pressure was registered by means of a mercurial manometer, the cannula being placed in either the carotid or femoral artery ; the pressure curve 'was traced 011 the Irymogaph below the tracing of the venous pressure. The time was marked in seconds helow the arterial

STUDY OP THE PATHOLOGY OF CARDIAC DROPSY. 53

In each case the experiment was kept going for an hour or preasure curve. more in order to follow the alterations in pressure which occurred.

3. In tbe experiments relating to the condition of the circulation in the dropsical animals, the pressures in most of the cases were taken before the operation, and subsequently at various periods up to twenty-four hours after. A dropsical animal may be in,one of three conditions : the dropsy may be commencing and increasing, it may be stationary, or i t may be disappearing. During the first twenty-four hours the dropsy is being produced, and it is with this period that this third group of experiments is especially concerned.

I n all cases the animals were under identical conditions in regard to position and anaesthesia. In comparing the venous pressure on two occasions it is absolutely necessary to have the animal in exactly the same position at each time, to have the limbs and neck in the same degree of relaxation, and the head at the same height above the operating table. If the head be raised the pressure in the jugular vein falls; if it be lowered the pressure rises. If the fore limb be tightly tied down the circulation in the neck will be impeded.

If the least pressure be applied to the abdomen the venous pressures in all parts of the body will be altered. The animals were placed in the supine position, and the limbs loosely tied to particular holes in the operating table which mere marked. Marks were made on the vertical and horizontal bars of the head clamp, so as to ensure the position of the head being the same on each occasion. The bladder, if it were distended, was emptied before the pressures were taken.

On all occasions the anaesthetic used was ether, the animal breathing naturally. Ether probably causes a slight rise in the arterial blood pressure at the beginning, and it is only after prolonged anaesthesia that the pressure falls. Registering these pressures takes only a few minutes, and therefore the animals were in all cases in mi early stage of ether anaesthesia. Though varying to a certain extent in different aiiimals, the pressures in the same animal on two occasions are remarkably conetant under these conditions. (Experiments 50 and 51.)

There is no constant venous pressure which can be called the normal; all one can say is that under the above circumstances a venous pressure within certain maximum and minimum limits must be regarded as normal. A pressure of 40 mm. MgSOI solution corresponds to that of 3 mm. Hg, so that a few millimetres above or below a certain point cannot be of great importance. The amount of distension of a vein is no measnre of the height of the pressure within it.

Out of a large number of animals the normal venous pressures were found to be as follows :-

‘Average . . 97 nm. MgSO, solution. (Highest . . 125 mm. (on on0 occasion only; only

(lower end) ’ 1 Lowest . . 65 mm. (on one occasion only ; only down reached 120 in 2 out of 50 cases).

to 70 in 1 out of 50 cases).

Infmior uena cam I

\

54 CHARLES BOLTON

Average . . 79 mm. MgdO, solution. [Hghest . , 125 mm. (on one occasion only; very

rarely above 110). Lowest . . 40 mm. (on one occasion only; rarely

below 50).

External jugular vein . .

Average . , 104 nim. MgSO, (usually a few millimetres above that at the lower end of the inferior vena cava).

vein ' Highest . . 120 rum. MgSO, solution. Lowest . . 60 mm. (only on one occasion; usually

Average . , 160 mm. MgSO, solution.

Lowest . . 120 mm. MgSO, solution. Vein of .foot . Highest . . 200 mm. MgSO, solution.

The effect of artificial respiration upon the height of the venous pressure If the lungs be forcibly distended thc pressure rises a few

The arterial pressure in the cat is usually higb, and not uncommonly

not below 95). I {

is very slight, millimetres.

reaches 180 to 200 mm. Hg.

11. THE EFFECTS OF THE VEXOUS OBSTRUCTION UPON THE PRODUCTIOX OF DROPSY.

(A) Obstruction of Inferior Vena C'ava (Expe~i?iicnts 1 to 10 and 6 2 to 66).

Obstruction of the inferior vena cava above the diaphragm leads to engorgement of the abdominal organs with blood. This is especially marked in the case of the liver, which is swollen and dark in colour ; the edge is somewhat rounded, and it bleeds freely on section. More or less asc.ites is present,-in the higher degrees of obstruction a little blood stained, in the lesser degrees light yellow in colour, and depositing a slight coagulum on withdrawal from the body. The fluid on boiling becomes solid. CEclerna of the retroperitoneal tissues is likely to be found, and occasionally of the mediastinum round the inferior vena cava. Sometimes there is a little fluid in each pleural cavity. In the other parts of the body there is no cedema, the tissues being particularly dry and free from lymph.

The nrine is diminished in amount, and so far as I have investi- gated the point seems to vary in proportion to the amount of fluid consumed by the animal. I have noticed that those animals whose tissues are initially dry and free from lymph do not so easily become dropsical ns other animals.

The above pathological changes occur within the first twenty-four hours after obstruction of the veua cava. They niay appear as early as two hours or not till an hour or two later. Whether the dropsy disappears later, owing to the establishment of anastomoses, I have not yet ascertained. In one case (Experiment 9), after four months, complete anastomoses were established and ascites was absent, but

STUDY OF THE PATHOLOGY OF'CAHDIAC DROPSY 55

it waB not proved that in this particular case ascites had ever been present.

Conaptete occlusion of the inferior vena cava above the diaphragm leads to death in a few hours.

There is regularly to be found 15 C.C. or more blood-stained fluid in the peritoneal cavity. This is not always the case, for in Experiment 61 there w.~ 20 C.C. fluid quite free from blood in the abdomen two hours after ligature. This is quite exceptional.

Richard Lower (1728) obtained a similar result by ligatura of the inferior vena cava in the chest, although it is usually miquotedin the text-books, which state that he obtained edema of the hind legs. His idea was that the ascites resulted from the high pressure in the capillaries, which he concluded that the venous obstruction caused. Antiseptics were not used in his day, and, so far as I am aware, he left the lung collapsed. I n fact, it was precisely this collapse of the lung which induced Ranvier (1869) to ligature the vein in the abdomen, thinking that if dropsy were to be produced by venous obstruction he should obtain it by this means ; however, in this case the anastomoses are too readily established,' and Ranvier fell into error in thinking that he had disproved Lower's statement.

Incomplete occlusion. - Constriction to a diameter of 1.5 mm. (fiperi- ment 2) practically renders tlie vein impervious, and the animal dies as if the vein were ligatured.

Constriction to a diameter of 2 or 2.5 mm. (Experiments 3 and 4) may lead to death, but on the other hand the animal usually survives (Experiments 52, 66, 60), 15 to 20 C.C. ascites is found within the first twenty-four hours, but in one case no ascites developed, probably owing to the dryness of the - - tissues of the animal.

58, 59, 62, 63, 64, 65, 66) does not lead to death. Constriction to a diameter of 3 mm. (Experiments 5, 6, 7, 53,54, 55, 57,

The animal recovera perfcctly, and develops .from 2 t o 45 C.C. ascites within twenty-four hours. I have not kept tho nninial longer than thirteen days (Experiment 8), except in one case (Experiment 9) in which the animal was kept for four months. During this time i t gained weight, and at the autopsy the anastomoses were complete and no ascites wns found.

The permanence or disappearance of the fluid will form the subject of future investigations. Constriction to a diameter of 4 mm. (Experiment 10) does not prodrice nscites, nor lead to any apparent plethora of the abdominal viscera.

Whether fluid had been prrsent in the abdomen I cannot state.

The general statements may be made that when the diameter of tlie inferior vena cam in the chest is constricted to three-fifths of its normal size ascites develops, bnt if the constriction amounts to four- fifths of the normal size the anastornoses are too readily established to allow of the appearance of dropsy. It is probable that in the case of the lesser degsees of constriction the ascites suhequently disappears, owing to the gradual completion of the anastomoses. If the vein be constricted below two-fifths of its diameter, or if i t be completely ligatured, death will result in a few hours, and more or less ascitic fluid will be found in the peritoneal cavity. These statements apply to suddenly produced constrictions.

In all these cases more or less cedema at the seat of the wound was found in the subcutaneous and muscular tissues, bnt this is

56 CNARLBS BOLTON.

dependent upon mechanical laceration of the tissues and not upon the venous obstruction.

(B). Obstruction of Superior Vena Cava (Expmiments 11 to 23 and 67 to 7 3 ) .

Obstruction of the superior vena cava leads to edema of the mediastinum and root of the neck, and bilateral hydrothorax. There may be edema of the retroperitoneal tissue, but no ascites.

The same general remarks with regard to the character of the fluid and the state of the rest of the tissues which were made in the case of the inferior vena cava apply here also. The edema appears in a few hours, and is well marked by the next day. It is quite certain that the dropsy may completely disappear a t a later date, or may gradually increase till death is brought about.

(a) Complete occlusion.-The vein was obstructed both above and below the entrance of the azygos vein ( i e . between the entrances of the internal mammary and azygos veins, and between the azygos vein and the right auricle).

Obstruction below the a z y p vein.-In each case deiith resulted on the 1st (Experiment ll), 5th (Experiment 12), and 6th days (Experiment 13). The whole of the cellular tissue of the mediastinurn extending from the neck to the diaphragm was distended with clear serous fluid, which in one case reached to the retroperitoneal tissue. Iiilateral hydrothorax and a little hydro- pericardium were also present.

I n the two cases with the most extensive edema, the azygos vein was ligatured a t the same time as the superior cava, but it is probable that ligature of the azygos vein is not of much moment, because in other experiments where the superior cava was ligatured above the azygos, which was left free, even more extensive dropsy was liable to be found. The aninial refuses food, and wastes, and the urine is diminished in amount, probably to II large exteiit because the animal drinks very little.

Ohstruetion above the nzygos vein.-The animal may completely survive this operation (Experiment 18). The anastonioses are established by tlie azygos and intercostals, the comes nervi phrenici, internal mammary and diaphragmatic veins, and no dropsy is to be found. Before these anastomoses are completed, however, edema of the niediastinum and hydrothorax are regularly produced arid apparently may lead directly to the death of the animal (Experiment 17), in which the right pleural cavity contained 145 C.C. fluid and the left 125 c.c., or disappear as in the former case. The dropsy appears within the first twenty-four hours. The urine is diminished in amount.

(b) Inconiplete occlusion.-Constriction to a diameter of 1 .B rnm. (Experi- ment 19) causes complete obstruction of the vein, with the same amount and distribution of the dropsy.

Constriction to a diameter of 2 mm. (Experiment 20) likewise produces the same edema, and fluid flows slowly through the constriction post-mortem.

Constriction to a diameter of 3 mm. (Experiments 21 and 70) leads to cedema of the mediastinurn and a trace of fluid in the pleural cavities,

Constriction to a diameter of 4 mm. (Experiment 22) does not give rise to edema. There is slight haemorrhage and oedema in the subcutaneous tissues a t the seat of the wound, but this, as in all the other cases, is the direct result of the injury to the tissues.

The general statements may therefore be made that when the diameter of the superior vena caw is constricted to three-fifths of its

There was no ascites or cedema elsewhere.

Ascites has never been present.

STUDY OF THE PATHOLOGY OF CARDIAC DROPSK 57

normal size, cedema of the mediastinum and hydrothorax begin to appear, and that it is possible, but not usual, for an animal to absorb the fluid and recover completely when the superior vena cava is absolutely obliterated. These statements apply to constrictions which are suddenly produced.

( C ) Obstruction of the Superior, togethey with the Inferior, Venn Cam (Experiments 2 3 to 2 6 and-74 to 76).

In the jrs t class the inferior vena cava was constricted, and after fourteen to twenty-three days, the anastomoses being more or less established, the superior vena cava was constricted, or vice versa. I n the second class both veins were constricted at the same time.

In these cases the constriction of one vein tends to neutralise the effects of constriction of the other by limiting the amount of blood in either congested area, and dropsy is likely to be found in one congested area only ; or if in both it is not so extensive as if the vein draining each area were alone constricted. This is shown very strikingly in Experiment 26, in which the constriction was unequal, the superior vena cava being completely ligatured whilst the inferior was merely constricted. The dropsy was limited to the distribution of the superior vena cava, the liver and other abdominal organs hardly showing any venous plethora.

There are two classes of cases included in this group.

(D) Obstruction of the Portal Vein (Experiments 27 to 3 3 and 77). I have found that obstruction of the portal vein, in spite of

assertions to the contrary (190311), gives rise t o ascites. On the other hand, ligature of the superior mesenteric vein (Experiment 27) causes hemorrhagic infarction of the intestine and death within 2 4 hours. This of course occurs olinically in cases of thrombosis of the superior mesenteric vein.

The different result occurring in these two cases is probably explained by the circumstance that the veins of the stomach and spleen are included in the ligature in the case of the portal vein, and therefore a certain amount of venous anastomosis can become established and the spleen itself can act a8 a reservoir, but the anastomoses are not sufficient to prevent the occurrence of dropsy, although infarction of the intestine does not occur.

Conzplele ligature of portal vein.-Ligature of the vein where it enters the liver brings about death in a few hours (Experiment 28), and there is regularly found from 6 to 10 C.C. slightly blood-stained fluid in the peritoneal cavity, and small hsemorrhages may occasionally be seen in the mesentery.

Incomplete occlusion.-Constriction to a diameter of 1 *5 mm. (Experiment 29 and SO) does not in most cases completely occlude the vein ; the animal lives, and if killed on the next day 10 to 20 C.C. ascites is .found. This fluid may be perfectly free from blood, and straw-coloured. Constriction to a diameter of 3 mm. (Experiment 31) likewise produces ascites, about 10 C.C. clear straw-coloured fluid being present. In these cases the liver appears to

63 CHARLES BOLTOA?

contain less blood than normal. Constriction to a diameter of 4 mm. (Experiment 32) produces no effect,-as a fact, it hardly produces any narrow- ing of the vein at all. Experiment 33 shows that when the portal vein is constricted, and the mesentery is attached to the anterior abdominal mall by :~~Iliesions, perfect anastomoses are established with the superior epigastric and internal manitiiary veins. This operation is occasionally done in the human subject in cases of portal obstruction.

Speaking broadly, it may be stated that constriction of the portal vein to about three-fourths of its normal diameter will gi7.e rise to dropsy of the peritoneum. Complete ligature will only produce a small :mount of ascites and small occasional hamorrhages into the mesentery.

111. THE IMMEDIATE .EFFECTS OF THE VENOUS OBSTRUCTION UPON THE CIRCULATION OF THE BLOOD.

1. Obstruction of Inferior Vena Caoa in the Chest.

A ,y~ndztnll,tj increasing constriction of the inferior vena cava (Experiment 4 1 ) in the chest is perfectly compensated for, so that no alteration whatever occurs in the circulation of the blood until a diameter of 3 mm. is reached. At this poiut the arterial pressure falls 20 mm. Hg or more, whilst the venous pressure behind the obstruction simultaneously rises about 40 or '7 0 mm. MgSO, solution. The exact amount of alteration in the pressures varies in different experiments a little even with the same amount of constriction, probably owing to diff'erences in vasomotor tone. Constrictions greater than 3 mu. produce proportionately greater depressions in the arterial pressure curve and greater rises in the venous.

Complete ligature of the inferior veua cava (Experiment 34) c:iuses the arterial pressure to sink to 30 or 5 0 mm. Hg above zero, and the venous pressure beliincl the obstruction to rise 100 mm. MgSO, solution or more above its former level. It has for many years been known that ligature of either the inferior vena cava or the portal vein causes n great fall in the arterial pressure owing to accumulation of blood in the splauchnic area. This observation agrees with what has been mentioned above, so that it may be definitely stated that, in order to produce any effect upon the circulation of the blood such as will give iise to dropsy, the inferior vena cava must be constricted to three-fifths of its normal diameter.

On examining the condition of the venous circulation in other parts of the body i t was fonnd that the venous pressure not only went up in the inferior vena cava itself, but in all the venous territories which i t drains. Experiments 37 and 38 show that the pressure in the portal vein rises, and Experiment 39 that the vcnous pressure in the foot also rises. Experiment 40 is introduced to demonstrate that, whether the obstruction be within the pericardium (rise of pressure due to introduction of oil) or outside this structure, the


venous pressure rises in all the venoue territories drained by the inferior vena cava This experiment was made because Starling (1 89 7), using the plethysniograph, found that the. foot contracted, and therefore concluded that the venous pressure in the foot fell.

On the other hand, when the inferior vena cava is obstrllcted the venous pressure in all those vascular territories not drained by this vessel falls. Experiment 36 shows 8 fall of pressure in the head when the inferior cava is obstructed.

These alterations in the circulation indicate, therefore, that there has been a re-distribution of the blood ; by its accumulation in the territoiy of the inferior vena caw i t has been abstracted from all the other parts of the body (arterial system, territory of superior vena cava, and lungs).

So far I have dealt with the effects of the venous obstruction which occur nt once. The venous pressures in the varions parts of the body behind the obstrnctiou do uot, however, remain for long a t the high levels they have assumed. If the animals be kept under observation for au hour or more it will be found that the venous pressures in the inferior vena cnva (Experiinents 34 and 35), the portal veil1 (Experiments 37 aud 38), and the foot (Experiment 39) commence falling, and eveutnally reach the norlrisl level, or B point very near it. The venous pressure in the head, however, a t the end of this time, still remains a t the low level it had imniediately assumed (Experiment 36). The arterial pressure in all cases remains also a t the low level to which it had fallen on the occurrence of the obstruction, or it may be lower still, and perhaps the latter event is the commoner. The pressure in the inferior vena cava falls more quickly and to a greater relative extent when that vein is conipletely obstructed, than when i t is merely constricted.

2. Obstruction of Xupekw Venn Cura.

A grndzinlly increasing constriction of the superior vens cava (Es- periment 44) produces no effect whatever upon the pressure in the external jugular vein until it is narrowed to a diameter of 2fr to 3 mm. At this point the jugular pressure rises 20 or 40 mm. MgSO, solution above what. i t was before the constriction was commenced.

The exact amount of alteration in the pressure varies somewhat in different experiments with the same amount of constriction. The arterial pressure is unaffected.

Complete ligature of the superior vena cava (Experiment 42) causes a rise of 130 mm. MgSO, solution or more in the Jugular pressure, but the arterial prefisure is unaffected, or in some cases it may drop a few millimetres only. Cohnheim (1882) recognised the fact that on ligature of the superior vena cnva the pressure in the carotid artery is unaltered. In order, therefore, to produce an effect upon the circulatioii such as will give rise to dropsy, the superior

60 CHARLES BOLTON.

vena cava must be constricted to a half or three-fifths of its normal diameter. The venous pressure in the remaining parts of the body (Experiments 45 and 46) falls.

This indicates what has already been referred to in the case of constriction of the inferior vena cava, namely, that the blood has accumulated in the territory of the superior vena cam, and has therefore been abstracted from the remaining parts of the body. This fall of pressure is not always seen in the portal vein (Experiment 46), because the portal area is so large in comparison with the territory of the superior vena caw.

The high pressure in the jugular vein is not iriairitnined for long, and almost at once the pressure commences to fall, and within an hour has again become norinal or thereabouts. The pressure in the remaining parts of the venous system, however, still remains below normal.

The arterial pressure at the end of this period of time is usually lower than it was at the beginning.

3. Production of Hydrmmie Plethora (Experiment 47).

This experinlent was undertaken in ordey to determine whether, by the gradual absorption of fluid, an animal with constricted inferior vena cava would be able by this means to maintain a high venous pressure behind the constriction, because it is well known that in the normal auimal the venous pressure, which is temporarily raised by the injection of salt solution, soon falls to the normal level.

It was found that if small quantities of normal saline solution were slowly injected into the veins a large quantity (130 c.c.) could be injected in one and a half hour without inaterially altering the venous pressure behind the constriction.

From matching the experiment it was obvious that on intravenous injection of a large quantity of saline a t one time a greater relative rise of venous pressure in the obstructed vena cava could be produced than in the normal animal, and that this pressure could be betber maintained, and also that less effect could be produced on the arterial pressure than in the normal animal. Absorption, of course, occurs slowly, and therefore, from this experiment it is obvious that, although such absorption would tend to raise the venoiis pressure behind the obstruction more than in other parts of the vascular system, i t would not be sufficient to maintain a high venous pressure unless assisted by an increase of vasomotor tone, which could not occur in an animal under prolonged anesthesia. In spite of the venous pressure behind the obstruction not being appreciably raised, cedema was produced in the experiment. Such caderna is not produced by a similar procedure in an aniinnl with unobstructed cava. I t mill be noticed that the arterial pressure had fallen considerably during the experiment, and therefore the capillary pressure must have been below normal.

4. Obstruction of Inferior and Superior Vena Cawa together (Eqeriment 48).

It is seen from this experiment that the same result upon the arterial and venous pressures is obtaiued when both veins are obstructed simultmeously as when they are obstructed singly, constriction of each

STUDY OF THE PATHOLOGY OF CARDIAC DROPSY: 61

vein tending to prevent the rise of pressure in the other. The pressure behind the obstructed superior vena cava falls in the same way whether the inferior be obstructed or not. This shows that the fall of venous pressure is not due to the dilatation of snastomotic channels, and it agrees with my results given in a former paper, which showed that when the pericardium was constricted (and hence all the venous channels into the right ventricle obstructed) after a preliminary rise of venous pressure, the latter fell again approximately to normal (1 9 0 3). So t liat obstruction of the superior and inferior vena c a m together produces the same effects upon the circulation of the blood as does constriction of the pericardium or uncompensated valvular disease of the heart.

5. Obstruction of the Portal Vein (Experiment 49). The arterial pressure falls as a result of obstruction of the portal

vein for the same reason that it does on obstruction of the inferior vena cava, namely, from the accumulation of blood in the roomy splanchnic territory. The venous pressnre in the portal vein rises enormously when that vein is completely obstructed. As in the case of the other veins, the venous pressure falls again within an hour. The vessels of the alimentary canal and spleen, therefore, are as distensible as are those of the liver. The gradually increasing accumulation of blood in the portal area leads to a gradual fall of arterial pressure. It is worthy of note that a t the end of this experiment the intestinal vessels were distended with dark coloured blood, and that a few small hemorrhages were present, and yet there was no edema.

IV. THE CONDITION OF THE CIRCULATION IN THE DROPSICAL ANIMAL Experiments 5 0 and 5 1 are introduced to show that the method

which I have employed is reliable. In the early stage of ether ttnsesthesia the venous and arterial pressures in the normal animal on two separate occasions are quite comparable, and found to be the same.

1. Constriction of 1nfeel.ioel. Vcnu Caca (Experiments 52 to 66). Venous pressure in dropsical area (Inferior vena caaa and prtcd vein).-

The venous pressures in the inferior vena cava and portal vein may be within normal limits, or they may be above normal.

I n Experiments 52, 53, 54, 55, 56, 57, and 65 the pressures are within normal liniits ; in Experiments 54 and 57 the portal pressure is a trifle raised. Kxperiments 61, 62, 63, 64, and 66 show a definite rise of pressure above tlie normal. On comparing the amounts of ascitic fluid in the two series of cases it is sem that no definito relation exists between the amount of the fluid anti the height of the'venous pressure, although in Experiment 61 the pressure was high, and 45 C.C. ascites present.

In Experiments 58, 59, and 60 high venous pressures resulted from the constriction, and yet there mas lio dropsy.

I n those cases in which the venous pressure is high, this high venoiis pressure does not exist from the moment when the vein is constricted, but occurs subsequently.

62 CHARLES BOL TO&

The experiments in Group 11. have shown thrit the immediate alterations in the yenous and arterial pressures are no indication of what these pressures will be nfter a period of time. Without laying too much stress on the experiments in Group 11. in which tho animals are under anssthesia for a considerable time, and in which the prolonged anasthesia must have aflected the pressures, we may take it as certain, from a consideration of these experiments, that the venous pressure falls to varyiug extents from its initial height, and that it takes a considerable time for the circulation to adjust itself to the altered conditions imposed upon it.

To make quite certain upon this point, the pressures were taken, after the animal had been allowed to recover, at various periods of time from one and a half hours upwards after the operation, which was done ns speedily as possible. Experiments 56 and 57 show that, after the initial rise, the pressure may fall axid permanently remain within normal limits. Experiment 63 shows that after the initial rise the pressure falls as usual, and after some period of time longer than one and a half hours it may rise again and remain permanently high. Experiments 60 and 61 indicate that this subseyueiit rise of pressure probably occurs some time between one and a half and four hours after the vein isconstricted. Exyerixnent 61 does not quite come iiito the same category, as the vein was conipletely ligatured in this experiment; here the venous pressure was only 46 mm. MgSO,, or about 34 mm. Hg above its former height nfter the period of 2 hours. It may be stated, therefore, that after constriction of the inferior vena cava the venous pressure at once rises a d then commences to fall, that the circulation becomes readjusted after a few hours, that dropsy commences at this time, and that the venous pressure behind the constriction may remain within normal limits or may rise above these liinits. The maximum amount of elevation that I have recorded at this period is 84 mm. Hg.

Venous pressure in other parts qf the body (Head and .feet).--In a previous section it was shown that when the inferior vena cava was constricted the venous pressure in the foot went up as it did in the inferior vena cava itself, and also that the venous pressure in the jugular vein fell. It was also shown that the pressure in the foot began to fall a t once, and soon returned to its normal level, whilst the pressure in the jngular vein still remained subnormal. Experiments 64, 65, and 66 show what these pressures are in the dropsical animal. The venous pressure in the foot has never been found above normal i n the dropsical animal.

It is either normal or slightly subnorind in those cases where the venous pressure is raised in the trunk, and it is much below the normal (Experi- iiient 65) in those cases where the venous pressure in the trunk is within riorinal limits. There is therefore a relalive alteration in these two pressures. The pressure in the trunk is always wlatively raised, and that in the foot relativehy lowered. The venous pressure in the head is always considerably beZoow what it was before the constriction was applied (Experiments 64 and 66).

These alterations in the venous pressures are of the greatest importance iu that they indicate an abstraction of blood from the feet and head, and its accumulation in the trunk. There is in all cases, whether the pressure in the trunk is raised or not, a permanent alteration in the aniounts of blood in these different territories, and a consequent alteration in the pressure levels.

As is seen from these experiments, the arterial pressure may be below its normal level, as it was immediately after the vein was constricted, or it may have completely regained its normal level. Of course, all intermediate stages are seen, as in the case of the venous pressure in the trunk, which may be within normal lirnits or more or less raised above these limits. A glance at the protocols will at once show that when the venous pressure in the trunk is raised nhove normal the arterial pressure has regained its normal level more

Arterial pressure (Experiments 5 2 to 57 and 59, 60, and 62).


or less completely, and that when the venous pressure in the trunk is t i t h in normal limits the arterial pressure remains at its low level. The arterial pressure therefore variea directly with the venous pressure in the trunk ; when the former is raised so is the latter, when the former is low so is the latter. The venous pressures in the head and feet, on the contrary, do not vary in the same direction as the arterial pressure does.

It follows from this that whether the venous pressure in the trunk is raised or not depends upon the vasomotor recovery of the particular animal. The only other thing which could raise both arterial and venous pressures in this way would be general plethora, but if plethora were the cause, then the veiious pre.ssure in the head and feet would be also raised, but they are not. If the high venous pressure in the trunk were the result of a depletion of tlie rest of the system only, then the arterial pressure would be invariably low, and it is well known that there is not sufficient blood in the body to keep up a high venous pressure in the portal system in the absence of vasomotor constriction. These points are more fully discussed later.

2. Obstruction of Superior Vena Calja (Experiments 6 7 to 7 3).

Venous pressure in jugular vein.-The pressure in the jugular vein way be within normal limits (Experiments 67 to 70 and 72), or it may be definitely raised (Experiments 71 and 73). I n those cases where the pressure is mithiii normal limits it is usually above the average, and often slightly above what it was in the animal before constriction. Of course in these experiments the superior cam was completely obstructed except in one experiment (Experi- ment 70). It is interesting to note to what a slight extent the pressure is permanently raised after complete obliteration. The greatest amount by which the pressure was raised after complete obliteration was 7 mm. Hc. The extent of the dropsy does not appear to vary in proportion to the height of the venous pressure, except in Esperiment 71.

Venouspressure in the rest of the bod9 (Experiments 71 to 73).-The pressures in the inferior cava and in the portal vein remain slightly below the normal, but of course ligature of the superior vena cava does not lead to so much depletion of the rest of the vascular system as when the splanchnic area is involved by constriction of the inferior cava.

Arterial pressure.-The arterial pressure undergoes n o change on l ig~turc of the superior cava, or only a trifling fall may take place. A considernble quantity of blood must he cut otf by this procedure, but an inimediate vasomotor constriction is sufficient to compensate for this.

3. Obstruction of Superior and Inferior Yen, Cam? (Expei-iments 74 to 76).

If the idea be correct that on obstruction of the inferior vena cava the portal system is plethoric at the expense of the rest of the circulatory system, simultaneous ligature of the superior vena cava should mitigate the congested condition of the portal system by confining a certain amount of blood in the liead and chest.

Experiment 74 shows that the prcssure in the inferior veiia cava is lower than when the superior vena cava is not ligatured, showing that the plethora of the abdomen has been relieved. This is confirmed by the presence of dropsy in the territory of the superior vena cava and its absence in that of the inferior vena cava.

Experiment 75 shows that a constriction of the superior vena cava only is insufficient to prevent ascites, although the pressure in the inferior vena cava is fairly low.

Such has been found to be actually the case.

64 CHARLES BOLTON.

On the other hand, there is no cedema in the region of the superior cena cava.

Experiment 76 confirms Experiment 74. It malies no differecce which vein be obstructed first.

When both veins, therefore, are obstructed together, the effect of such a procedure is less felt in each territory than if either vein alone were constricted.

4. Obstruction of Portal JTeiein.

Experiment 77 illustrates the effect of obstruction of the portal vein. The blood is abstracted from other parts of the body and confined in the portal territory. The vasomotor activity in this case has been sufficient to raise the arterial pressure practically to the normal, and at the same time the portal pressure has been considerably raised.\ This rise in portal pressure corresponds to about 74 mm. Hg; in spite of this rise of pressure there was only a very small amount of ascites present.

Less blood is of course required to distend the portal system when the portal vein is obstructed than when the inferior vena cara is obstructed, because the liver, which is a very distensible organ, is left out in the former case.

V. CONCLUSIONS.

(A) Inferior Vena Cava.

Alterations in the circulation of the blood.-When the inferior vena cava is obstructed in the chest there is a rise of pressure in all the vascular territories (portal system, hind part of trunk, and limbs) which it drains. The changes in the capillary circulation which occur on obstructing a vein can easily be seen in the frog's tongue. Under noriiial circumstances the capillaries are not all filled with blood, some of them keep filling out whilst others are emptied; the velocity of the blood flow in them is slower than in the artery or vein, whilst occasional acceleration in that velocity can be seen as the arteries alter in size. If arterial dilatation occur, more capillaries fill out and become visible, and the rapidity of their blood flow is increased. If arterial constriction occur, the capillaries in great number appear to have vanished, and the velocity of their blood flow is diminished. If the efferent vein be obstructed, the veins and visible capillaries dilate, and the empty capillaries become filled out and also dilate, the velocity of the blood flow is diminished and the blood stagnates. The cause of this dilatation and filling out of t,hc capillaries is the rise of pressure, which occurs owing to the increased volume of blood in the part.

In the case of the obstructed vena cam this course of events will be somewhat modified, because the capillaries will take a considerable time to fill, and the vein drains such a large territory that the blood abstracted from other parts of the body to fill it causes marked fall in the Senera1 arterial blood pressure, and also in the

STUDY OF THE PATHOLOGY OF CARDIAC DROPSJ? 63

remaining veins of the body. The stagnation in the capillaries of the plethoric area must therefore be more marked, and there must be a limited height to which the pressure can rise. The venous pressure in all parts of the plethoric area soon begins to fall, and comes down to within the normal limits. This fall of pressure may to a very small extent be due to anastomoses rapidly forming with the branches of the superior vena cava, but, as the dropsy shows, these anastomoses are far from effecting compensation ; the increased flow of lymph which commences at once may also be responsible for a part of the fall; but the chief cause is the filling out of the capillaries, which must have a very extensive area in the portal system, and the dilatation of the capillaries and veins. The swelling of the liver is a visible proof of this. In those experiments described in Group II., in which the animal is kept for an hour or more in a condition of anmthesia, general vasomotor relaxation due to the ancesthetic must also assist, but onIy slightly, as the pressure is found to have fallen in animals who have not been in a condition of prolonged anzsthesia. It is therefore the distensibility of the abdominal organs, especially of the liver, which is responsible for the fall of pressure.

How much this distensibility is due to a nutritional loss of tone i t is impossible to say.

These organs, so to speak, abstract blood from the other parts of the body until they are fully distended.

The muscular tension in the limbs will, a t the same time, aid in keeping the vessels of these parts relatively empty.

The course of events will be readily followed by reference to the diagram on the following page.

When a constriction is applied t o the inferior vena cava at A, less blood will flow from this vessel than flows in ; hence P,, p,, and p will be raised. P and pz will be lowered, because blood is abstracted from them. The amount of blood flowing int:, the area drained by the inferior vena cava in a unit of time depends on the difference between P and P,, and since P has been lowered and P, raised, smaller and smaller ainounts mill flow in until the amount flowing in is equal to the amount flowing out, when equilibrium mill be established.

The portal system is distensible, and dilates before the pressure, therefore p , p,, and I?, begin to fall. The result of this is that less blood will flow out of the territory of the inferior cava than is flowing in, hence I? and p, fall again. Smaller amounts of blood will now Row into the territory of the inferior vena cava, until the amount flowing in is equal to the amount flowing out, when equilibrium will be oiice more established. Each time, therefore, the portal system dilates there is a fall in each portion of the circulatory system.

So that finallyy is practically normal and the portal system is distended with blood, Pl is normal, and P is less than normal, so that less blood than normal flows into the portal system and less than normal flows out, and therefore the velocity of the blood stream is diminished, the velocity, of course, depending upon the difference between P and I?,, and varying inversely as the diameter of the

This goes on till p falls to within the normal limits.

5 4 L OI PATE.-VOL. XW.

66 CHARLES BOLTON.

tubes through which the fluid passes. p 3 is below the normal, and p , is normal or slightly below normal.

In the normal animal the arterial pressure is kept a t a constant level, in order that the capillaries may be supplied with an adequate flow of blood.

This is maintained by vasomotor action, which keeps the sum of the total peripheral resistances constant. If more blood is required

HEAD

AORTA P

P =Prassure in aorta. PI= , , inferior vena cava. pz= ,, veins of head. p = ,, portal vessels.

pl=Preasiire in veins of hind feet.

by an organ its arterioles dilate, and there is a diminution in the resistance in that area ; this fall in resistance is, however, compensated for by vasomotor constriction in other areas, and the arterial pressure remains constant.

The efforts of the animal with a constricted vena cava are therefore directed towards raising its arterial blood pressure to the normal.

STUDY OR TH& PATHOLOGY OF CARDIAC DROPSI.: 67

It might presumably accomplish this in two ways-( 1) By increasing the total volume of its blood ; (2) by vasomotor constriction.

1. Absorption occurs in the regions that are depleted of blood, and cedema occurs in the congested area. It is probable that the one balances the other, and although individual differences may occur, it is unlikely that absorption predominates in any case to such an extent as to cause a general plethora, for the following reasons :-

(u) It has been shown above that, although the pressure in the congested area can be temporarily raised by injection of fluid, it soon falls again, as in the normal animal. The animal has certainly not sufficient available lymph in its tissues to maintain a high venous pressure on absorption, and the more available lymph it has to absorb, the more dropsy it forms.

The cats invariably refuse to drink or eat for some time after the operation, so no fluid enters the body. It is possible that less urine is excreted, although the above experiments point to the conclusion that the amount of urine excreted corresponds to the intake of fluid.

(6) Ligature of the superior vena cava at the same time as the inferior vena cava is constricted prevents the usual plethora of the abdominal viscera occurring by confining a part of the blood in the chest, head, and upper limbs. In other words, the portal system is relieved into the upper part of the trunk and head. This is exactly comparable to what is seen clinically in uncompensated heart disease. If such a patient sit up in a chair, the face shrinks from absorption of lymph, the ascites begins t o be absorbed, and the legs smell out enormously with cedema. I n this case the portal system is relieved into the feet.

(c) If the rise of arterial pressure were due to general plethora, fhe pressure in the superior vena cava should also rise, but it does not.

If any rise does take place it cannot be over a few millimetres MgSO,, and nothing comparable to the amount by which the arterial pressure rises.

(d) The rise of arterial pressure is evidently due to some variable factor, since, although it often reaches the normal, in an equal number of animals it does not. It seems much more likely that this factor is vasomotor action than absorption of fluid, which should occur with greater regularity.

(e) The blood shows no signs of dilution. Thie subject is now under investigation, but I give here the

results of two experiments which certainly indicate that dilution has not taken place.

A small amount of dilution probably could not be detected, and whether it occurs or not is of no moment ; but a dilution sufficient to raise the arterial pressure to normal should certainly be detectable.

68 CHARLES BOLTON.

EXPERIMENT 1.- Cut (weight, 2730 grms.).

Blood Counts.

Red corpuscles. . 11,628,800 per cmm. . 100 uer cent. From ear (small vein) { Hb

‘Red corpuscles. . 12,432,000 per cmm. From leg (capillaries) {Hb. . 106 per cent.

Inferior vena cava constricted to 3 mm. diameter. On the next day abdominal section shored a large amount of ascites.

{ Ret,corpnscles . . 11,934,000 per cmrn. From e a r (small vein) . lOO.per cent.

Red corpuscles. . 12,716,000 per cmm. {Hb. . 100 per cent. Fyonz Zen (capillaries)

Died four days later. Post-mortem showed 35 C.C. ascites.

EXPERIMEW 2.-Cat (weight, 3210 grms.).

B l o o d Counts.

corpuscles. . 10,404,000 per cmni.

Red corpuscles . . 11,084,000 per cmm. . 110 per cent.

{Hb . . 120 per cent.

From ear (small vein) {Ed. From leg (capillaries)

Inferior venlt cava constricted to 3 mm. diameter. On the next day abdominal section showed a large amount of ascites.

{ gbd corpuscles , . 12,269,000 per cinm.

Red corpuscles . . 12,188,000 per cum. . 130 per cent.

. 120 pcr cent.

From ear (small vein)

Froin leg (capillaries) { IIb

Died two days later. Post-mortem showed 20 C.C. ascites.

From these experiments it seems as if the blood might become concentrated in the depleted areas.

2. It is therefore by vasomotor constriction, which automatically occurs by stimulation of the vasomotor centre as the result of anzmia of the medulla, that the arterial pressure is raised more or less to the normal level in those cases in which such an event occurs. Two effects result from vasomotor constriction-( 1) The total peripheral resistance is increased ; and (2) the total capacity of the vascular system is diminished. The increased peripheyal resistance is the important factor in raising the arterial pressure ; the diminution in the capacity of the vascular system should raise the pressure in all parts. As a fact, in the norinal animal the pressure in the inferior vena cava, as pointed out by Bayliss and Starling (1 8 94), rises slightly on excitation of the splanchnics. This rise is only slight, because the veins are not normally filled to distension, according to Hill (1900).

In the animal with constricted inferior vena cava, that vessel and the portal system are overfilled and their walls thrown into

STUDY OI; TBE PATHOLOGY OF CARDIAC DROPSK 69

tension, whereas the veins of the feet and head contain less than the normal amount of blood. Vaso-constriction should therefore produce a greater rise than normal in the veins of the plethoric area, but should have relatively little effect in the depleted areas. This is precisely what occum ; a rise of arterial pressure being associated with a rise of venous pressure in the congested area, aa pointed out above.

It may be stated, therefore, that the subsequent heights of the arterial pressure, and the venous pressure in the congested area, depend entirely upon the extent to which the whole vascular system is able to recover its tone. Whether the venous pressure be high or low, dropsy is produced in the congested area in which the blood flows with a diminished velocity.

Capillary pressure in the congested area.-I. Parietal peritoneum- In those cases in which the venous pressure is within normal limits and the arterial pressure considerably below normal, the capillary pressure in the congested area must be below normal.

In those cases where the venous pressure is above normid and the arterial pressure at the normal level, it would seem at first sight that the capillary pressure should be above normal, but this by no mean8 follows. The reason is that the increased peripheral resistance which is responsible for raising the arterial pressure admits less blood than before through to tho capillaries; this would lower the capillary pressure still further, and it must remain a matter for speculation whether the obstacle interposed by the raised venous pressure sufficient to bring the capillary pressure up even to the normal level. It is now recognised by many physiologists that anatomoses exist in places between the arteries and the veins, so that the veins may be distended with blood whilst the capillaries are relatiVely empty. If the capillary pressure varied absolutely with the venous pressure it never could be much above the normal, as the following results show.

In Experiment 63 the pressure in the inferior vena cava went up from 75 mm. MgSO, to 186mm. MgSO,. This represents a rise of 110 mm. IQSO,, or about 84 mm. Hg. The normal capillary praasure would probably not be below 30 mm. Hg, and hence, after the vena cava was constricted, it would stand at 384 mm. Hg.

In Experiment 62 the rise in vena cava pressure was from 100 to 160 mm. MgSO,.

The rise in capillary pressure would therefore be 60 mm. NgSO,, or 4) mm. Hg.

2. Intestines and Ziuer.-The pressure in the portal vein in animals with constricted inferior vena cava has always been foiind to be higher than the pressure in the cava itself by about the same amount as normal, whether the venous pressures were within the normal limits or raised.

The liver therefore appears to act in these cams passively, as if &be vaso-constrictor fibres to the hepatic branches of the portal vein

70 CH;QRLBS BOLTON.

were of little moment,any rise of pressure in the inferior cava extending right through the liver and causing a corresponding rise of pressure in the portal vein.

The pressure in the hepatic capillaries, therefore, must follow the pressures in the inferior vena cava and portal vein. In those cases where the venous pressures are within normal limits the pressure in the hepatic capillaries will be within normal limits, and in those cases of raised venous pressure the pressure in the liver will be correspond- ingly raised.

What is the pressure in the intestinal capillaries is less obvious, because, as pointed out by Bayliss and Starling (1894), the pressure in these vessels may be normal, or even subnormal, whilst the portal and arterial pressures are raised. When the arterial pressure is subnormal and the portal pressure about normal, the pressure in the intestinal capillaries will be below normal.

(B) S?qerior Vena Cava. The alterations in the circulation of the blood produced by

obstruction of the superior vena cava differ from those just described only in the fact that the portal system is not involved, and therefore the congested area is not so large; neither is it so distensible, and therefore on the whole the pressures are higher. Otherwise, the same general principles are observed, Blood is abstracted from other parts of the body and confined in the territory of the superior vena cava. The congested and dropsical area is the chest, and i t is noteworthy that the head also suffers to some extent. This corresponds to what occurs clinically. The venous pressure in the jugular vein a t the augle of the jaw follows that in the superior vena cava, and varies in the same direction.

The subsequent fall of venous pressure, after ligature of the superior cava, is due chiefly to filling out of the capillaries and dilatation of the veins of the chest. It is rather surprising that a higher pressure cannot be maintained behind the constriction, considering the relative sizes of the congested and depleted areas ; the greatest rise of pressure which has been obtained being 7 mm. Hg. Of course, the vasomotor system is not called into play so much as in obstruction of the inferior cava. The capillary pressure in the congested and dropsical area is either within normal limits or a little raised.

(C) Inferior together with Superior Vena Cava. When the superior vena cava is ligatured and the inferior vena

cava constricted, the balance is in favour of the superior vena cava, as there is such a disproportion between the amounts of constriction. When both veins are constricted to the same extent the effects are evenly distributed, and congestion of both areas results as described above. This effect is exactly comparable to uncompensated heart


disease, and precisely the same as was described in the case of constriction of the pericardiuni (1 90 3). The abdominal viscera and chest are congested, and blood is abstracted from the limbs and head, the head not being so much depleted as the limbs.

The dropsy is produced in the congested area, whilst absorption occurs pari passu in the depleted areas. The dropsy of heart disease is therefore a local phenomenon, and the alterations in the circulation of the blood in uncompensated heart disease only differ from those occurring in local venous obstruction, because in the former the splanchnic circulation is interfered with. In uncompensated heart disease in the human subject the liver swells, and it is probable that the dropsy begins in the peritoneum. This is difficult to prove, because ascites can only be detected, clinically, when a considerable amount of fluid is present. At all event8 in mitral stenosis, and also in most forms of heart disease in children, it is by no means uncommon for the dropsy to be limited to the peritoneal cavity, or for it to begin here.

I n patients who are not very ill, and who are able to walk about, the first visible dropsy begins in the feet and ascends up the legs. This is due merely to the effect of gravity relieving the portal system into the feet, in exactly the same may as the portal system can be relieved into the head by ligature of the superior vena cava.

The dropsy of the feet disappears, unless i t be very extensive, when the effect of gravity is counteracted by elevation of the feet. When the feet are put down to the ground the ascites is absorbed, the face shrinks from absorption of lymph, and the aedenia of the feet increases.

(D) Portal Vein.

When the portal vein is obstructed the same changes in the circulation of the blood occur as when the inferior cava is obstructed, except that the congested area is more restricted owing to the liver being left out. Probably the pressure is higher in the portal branches when this vein is obstructed than when the inferior cava is obstructed. In spite of this, ascites is not more easily produced by portal obstruction than by obstruction of the inferior cava. In hepatic cirrhosis in man the portal pressure dilates the vessels and leads to hemorrhage, frequently before there is any sigu of ascites.

(E) The Parts played hy the Various Factom concerned in the Production of the Dropsy of Venous Stagnation.

Diminished absorption of$uid by the veins of the congested area undoubtedly occurs, but it no doubt plays quite a subsidiary part, because when the inferior cava is obstructed there is less resistance to the outflow of lymph from the thoracic duct, as the pressure in the innominate vein is subnormal.

72 CUARLES BOLTOh?

The lymphatics are no doubt easily able to drain away any excess of fluid resulting from non-absorption by the veins.

It is therefore an increased output of fluid from the cayillaxies which gives rise to the cedema.

The inwemed venous pressure, which is the immediate result of venom obstruction, leads to dilatation of the vessels behind the obstruction and filling out of the capillaries, and is in this way an indirect factor. It is not, however, the direct cause of the cedema, because this occiirs when the pressure is within normal limits. When the dropsy is produced with a high capillary pressure, such pressure beconies an important contributing factor; but in these case8 the venous territory in which the obstruction is situated must not be too large in proportion to the rest of the vascular territories of the body, so that sufficient blood can be Epared to maintain a high venous and capillary pressure ; moreover, the anastomoses must not be too free, as in Cohnheirn’s plaster experiment (1882). A parallel instance is seen in the case of hsniorrhagic infarction. In this condition the escape of blood from the capillaries may occur when the capillary pressure is high, as in complete venous obstruction; but it may also occur when the capillary pressure is low, as in arterial blocking.

The dilatation of the vessels and the filling out of the capillaries are indications of the local plethora which exists.

Local plethora, although associated with a high capillary pressure in active arterial hyperaemia, does not give rise to cedema.

The only exception to this statement that has been met with is the well-known experiment of Ostroumoff, in which active hyperaemia is induced by stimulation of the lingual nerve, and the edema in this case is not of invariable occurrence.

In active hyperzemia the velocity of the blood stream is increased and the surrounding tissues are usually in a state of increased functional activity, whereas in the local plethora under consideration the velocity of the blood stream is diminished, the walls of the vessels are stretched, and the nutrition of the capillary wall and tissues of the part is interfered with. All the mechanical changes, therefore, in the circulation of the blood in passive hyperzemia conspire together to interfere with the normal nutrition of the capillary wall and tissues, and it is this nutritional change leading to increased permeability of the capillary wall which is the immediate cause of the dropsy. It is more likely that the capillary wall is primarily at fault than the tissues of the part, because, although increased tissue metabolism gives rise to an increase in the lymph flow, there is no evidence that tissue metabolism is increased in passive hyperamia ; probably the reverse is the m e . There are many experiments which show the importance of damage done to the capillary wall, notably those of Wooldridge (1889) and Cohnheim (1877). If this structuye be damaged, excess

STUDY OF TXLE PATHOLOGY OF CARDIAC DKOPSY; 53

of fluid will pass through it whether the intracapillary pressure be normal, subnormal, or above normal.

These experiments therefore lend support to the “vital” as opposed to the ‘‘ physical” theory of cedema formation.

The exponents of the “physical” theory admit that in passive cedema the capillary wall is damaged, and therefore more permeable than normal ; but they insist that in addition to this a high capillary pressure is necessary, the high pressure resulting from the venous obstruction, as Cohnheim taught, or from hydrzmic plethora, as Starling holds. According to my results, a high pressure is unnecessary, and in this respect I differ from the ‘I physical ” theorists. On the other hand, I differ from those exponents of the ‘‘ vital ” theory who believe that the tissues of the part are primarily at fault, and agree with those who lay the stress upon the capillary wall, although I do not believe that the process ie one of perverted secretion (1 8 9 3) ; because, if the venous obstruction be complete enough, blood corpuscles will escape as well as fluid, and these are certainly not secreted.

If the factors concerned in the production of edema are the same aa those concerned in normal lymph formation, my experiments are in favour of Heidenhain’s secretory the0 ry, because they establish the fact, which Heidenhain endeavoured to prove, that an excess of fluid can pass through the capillary wall whilst the intracapillary pressure is normal ; a t the same time, they are in conformity with the established fact that the tissues themselves are also concerned in lymph formation.

On the other hand, if the two sets of factors are distinct, the method of venous obstruction is inapplicable to the study of normal lymph formation ; but even in this case these experiments show that the vital activity of the capillary endothelium is a necessary factor in normal lymph formation, because at all events it certainly regulates the output of fluid, 80 that, when its nutrition is interfered with, it reacts somewhat like a dead membrane.

I incline to the latter view, because it is impossible to produce venous obstruction without interfering with the vitality of the capillary wall and tissues, and a new factor is thus introduced.

In the normal condition it seems unlikely that such a membrane as the capillary wall should be absolutely independent of physical laws ; and, on the other hand, it appears that, being a living and actively metabolic tissue, it does not allow susbtances to pass through it as through a dead membrane, I n the diseased condition of venous obstruction, therefore, the normal activity of the capillary endothelium is overshadowed by a passive transudation through the damaged membrane.

This hypothesis is, I think, as justifiable as any one which can be framed from the small number of facts which we have at present at hand concerning this ditficult problem ; whether it will be proved or not must remain for future experiments to decide.

74 CHARLES BOLTON;

VI. PROTOCOLS OF EXPERIMENTS.

Group 1 EXPERIMEXT 1 .-Cut (weight, 3000 grms.). Ether and artificial respiration. DCC. 16,

190B.-Inferior vena cava ligatured above the diaphragm. Never recovered consciousness, and died in about six hours. Post-mo~tc~n.-l5 c.e. slightly blood-stained fluid in peritoneal cavity.

May 16, lgOl.-Inferior vena cava constricted to a diameter of 1'5 mm. above the diaphragm. Died in six hours. Post-~1iortem.-20 C.C. slight blood-stained fluid in peritoneal cavity. Liver=160*4 grms. The vein is rendered practically impervious by a tube of this diameter.

H a y 21, 19Ol.-Inferior vena cava constricted to a diameter of 2 mm. above the diaphragm. Died in seven hours. Post-mw&m.-20 C.C. slightly blood-stained fluid in peritoneal cavity. Liver= 106 grms.

EXPERIMENT 4.-Cat (weight, 2859 grms.). Dec. 30, 19Ol.-Inferior vena cava constricted to a diameter of 2.5 nini. ahove the diaphragm. DCC. 31, 19OL-Died in about thirty-six hours. Post-?)~ortfm.-15 C.C. slightly blood- stained fluid in the peritoncal cavity and 1 C.C. in each pleural cavity.

EXPERIMEST 5. -Cat (weight, 2840 grms.). Ether and artificial respiration. Juw I, 1906.-Inferior veiia cava constricted to a diameter of 3 mm. above the diaphragm. June 2. -Killed twenty-four hours later. Po8t-mortcm.-36 C.C. clear straw-coloured fluid in perkma1 cavity. (Edema of retro-peritoneal tissue, spreading slightly up the inferior vena cava above the diaphragm. Liver swollen and bled freely on cutting.

EXPERIMENT 6.-Cat (weight, 2950 grms.). Ether, artificial respiration. Jum 5, 1906.--Inferior vena cava constricted t o a diameter of 3 mm. above the diaphragm. JWZC 6.-Killed twenty- four hours later. Post-morfem.-25 C.C. clear ascitic fluid in peritoneum, and slight cedema of the retro-peritoneal tissues. Liver swollen and dark in colour, bleeding freely on section.

Aug. 17, 1904.-Inferior vena cava constricted t o a diameter of 3 mm. above the diaphragm. Aug. lg.-Respirations, 24. Eats badly. Passes very little urine. Bug. 20.-Died. Post-morlem.-20 C.C. clear yellow ascitic fluid in peritoneum. No fluid elsewhere. Liver swollen and dark in colour.

EXPERIMENT 2.-Cat (weight, 2960 grms.). Ether and artificial rcspiration.

EXPERIMENT 3.-Cut (weight, 3340 grms.). Ether and artificial respiration.

Ether and artificial respiration.

A few drops of fluid in the right pleural cavity. The urine contained albumin.

A few drops of fluid in the right pleura,

EXPERIMENT 7.-Cat (weight, 2600 grms.). Ether and artificial respiration.

EXPERIMENT 8.-Cat (weight, 2370 grnis.). Ether and artificial respiration. Jj~m 16, 1906.-Inferior vena cava constristed t o a diameter of 3 mm. above the diaphragm. JuZy 28.-Killed. Post-mortem.-12 C.C. ascitic fluid in peritoneum, 10 C.C. fluid in left pleura, and 6 C.C. in the right pleura. Liver swollen. Little Edema of mediastinum. Urine coutained a cloud of albumin. Before the operation the animal drank all its milk, about 470 to 500 C.C. daily, and passed 300 to 450 C.C. urine daily. For three days after the operation it drank from 10 to 70 C.C. daily, and passed 40 t o 150 C.C. urine ; after this period till it was killed it drank 300 to 600 C.C. daily and passed the normal amount of urine.

June 3, 190l.-Inferior vena cava Constricted to a diameter of 3 mm. above the diaphragm. Jirne 4.-Quite recovered. Julie 17.-Weight 2270 grammes. Ocl. 6,19Ol.-Killed. Post-mortem.-The tubc in position and surrounded by white fibrous adhesions, to which the lung was qdherent. No fluid in peritoneal cavity, pleura, or elsewhere. The superficial and deep epigastric veins were dilated, and also the capsular veins, which joined the renal veins with the lowest intercostal veins. In the chest the internal mammary, comes neiri phrenici, and the nzygos veins were dilated. The veins of the diaphragm were larger than normal, as

EXPElcIbrENT 9.-Cat (weight, 2120 grms.). Ether and artificial respiration.

June 7.-Jumps on the table quite easily.

Anastomoses well marked.

STUDY OF TBE PATHOLOGY OF C A R D I A C DROPSY; 75

was also the lower end of the superior vena cava where the azjgos joins it. The portal vein and its branches were a little dilated.

Ether and artificial respiration. June 11, 1906.-Inferior vena cava constricted to a diameter of 4 mm. above the diaphragm. Jmke 12.-Killed. Post-niortem.-No asoites. Chest normal. No fluid.

EXPERIMENT lO.-C& (weight, 2110 pms.).

EXPERIMENT 11.-Cut (weight, 2500 grms.). Ether and artificial respiration. Sept. 22, 1904.-Superior vena cava ligatured below azygos vein. Azygos vein a180 ligatured. S@. 23.-Died during the night. Post-mwtem.--ti C.C. blood-stained fluid in each pleural cavity. Much edema of the whole of the mediastinurn, extending for a short distance up the root of the neck. (Edema of the cellular tissue round each kidney and the adjoining retro-peritoneal tissue. Superior vena c a n thrombosed from tho ligature to the terminations of tho two innominate veins.

Oct. 27, 1904.--Superior vena cava ligaturerl below azygos vein. Oct. PB.-Recoveied. Nou. 1.- Died. No fluid in the pericardium. Oidema of the mediastinum round the azygos vein, aorta, and supcrior vena cava spreading 1111 the trachea to root of the neck and out into the axillw. No cedema round inferior vtiia cava nor in retro-peritoneal tissue. Small clot a t bottom of superior vena cava, adherent to the wall of vein a id , above this, black clot extending to innominate veins.

Ether and artificial respiration. Sept. 15, 1904.--Superior vena cava ligatured below azygos vein. Azygos also ligatured. Sept. 16. -Recovered. Sept. 19. --Taking food badly-losing , flesh. Sept. 21.-Died. Post- mortem.-Whole mediastiuum distended with clear serous fluid extending up to jugular veins and down inferior vena cava to diaphragm. 25 C.C. fluid in each pleural cavity. The fluid is clear and straw coloured. Lungs collapsed in places, but blow out normally. Superior vena cava thrombosed, the thrombus extending into the right subclavian vein.

&fay 24, 1906.-Superior vena cava ligatured above azygos vein, Killed. Post-mwtem-The right pleural cavity contained 4 C.C. blood-stained fluid and the left 6 C.C. (Edema of the whole mediastinum, round the pericardium, internal mammary veins, and azygos. The cedema extended down into tho cellular tissue of the abdomen for about 2 in. below the diaphragm. Above it extended to the root of the neck and out into the axillre. The superior vena cava was not clotted, bnt contained a considerable amount of lymph from the thoracic duct.

May 17, 1906.-Snperior vena cava ligatured above the azygos vein. May 21.-Quite well. Killed (weight 2750 grins.). Post-morlem-10 C.C. blood-stained fluid in each pleural cavity. (Edema of the mediastinum, extending round the heart up to the root of the neck and down the inferior vena cava, esophagus, and aorta into the abdomen.

May 11, 1906.-Superior vena cava ligatured above the azygos vein. Muy 17.-Drinks milk a little, but will not eat. Before the operation the amount of urine passed in twenty-four hours was 210 c.c., afterthe operation the daily amount varied from 30 to 90 c.c., and during this period the animal only drank from 10 to 60 C.C. daily. Before the operation it drank 200 C.C. May 19.-Killed (weight, 1800 grms.). Post-nwrtem.-75 C.C. blood-stained fluid in the left pleural cavity, and 60 C.C. in the right. A trace of fluid in the pericardium. The whole of the mediastinum distended with clear serous fluid, extending into the retro- peritoneal tissue for an inch below the diaphragm. The cedema extended up to the root of the neck and along the axillary vessels under the pectoral muscles. A small clot in the superior vena cava.

EXPEXIXENT 17.-Cat (weight, 2500 grms.). Ether and artificial respiration. May 24, 1906.--Superior vena cava ligatured above azygos vein. Has taken 30 C.C. milk during the night. June 1.-The animal is wasting, and has inspiratory

A trace of fluid in the pericardium.

EXPERIMENT IP.--Cnt (aeiglit, 2470 grms.). Ether and artificial respiration.

Post-mwte~t~.-5 C.C. fluid in each pleural cavity.

EYPERIMEKT 13.-C& (weight, 2430 grms.).

Little fluid in the pericardium.

Abdomen normal.

EXPsRIbIEsT 14.--Cat (weight, 2800 grms.). Ether and artificial respiration. May 25.-Quite well.

EXPERIMENT 15.-Cat (weight, 3100 grins.). Ether and artificial respiration.

A trace of fluid in the pericardium.

EXPERIMEST 16.-C& (weight, 2330 grms.). Ether and artificial respiration.

May 25.-Recovered.

76 CHARLES BOLTON;

dyspnea. Jum 11.-Since tlie operation it has passed from 20 to 100 C.C. urine daily, and drunk similar amounts of milk. It was lifted up to take out of the cage, when it got an attack of dyspucen and died (weight, 1600 grms.). h~t-mortem.-145 C.C. blood-shilled fluid in the right pleural cavity and 125 in the left. Edema of the mediastinum extending up to the root of the neck and down almost to the pelvis; no ascites. Both lungs completely collapsed except a t the extreme bases. Upper part of superior vena cava thrombosed.

Dec. 13, 190l.-Superior vena cava ligatured above azygos vein. Dee. 19. --Quite well (weight, 1860 grms.). Dec. 24.-Mreight, 1770. Seems quite well. JBN. 5, 1902.-Killed. Post- mortem.-No cedema whatever it1 any part of the body. The superior vena cava was quite obliterated, and tlie lipper part contained a thrombus, The following veins were very much distended and apparently acted as anastomotic channels,-azygos and intercostals as they entered it : comes nervi phrenici, internal maiumary, slid diaphragmatic veins.

Ether and artiticial respiration. MU^ 26, 1906.-Superior vena cava conbtricted to a diameter of 1.5 nm. above azygos. Nay 28. -Killed. Post-?nortem.-15 C.C. blood-stained fluid in left pleural cavity, and 7 C.C. in the right. The superior vena cava was opened and a cannula inserted, but fluid would not flow through the aonstricted portion of the vein, the latter ballooning out above the coustriction.

EXPERIMENT 18.-Cat (weight, I970 grms.). Ether and artificial respiration.

EXPERIMENT 19.-Cat (weight, 2260 grms.).

&dema of whole of mediastinum.

The vein was inipervions.

EXPERIMEST 20.-Cat (weight, 3100 grms.). Ether and artificial respiration. diay 26, 1906.-Superior vena cava constricted to a diameter of 2 Inm. above azygos. May 28.- Killed. 11 C.C. blood- stained fluid in right pleura, and 9 C.C. in left. Fluid flowed through the constriction

Nay 26, May 28.-

Po.qtost-morten~.-2 C.C. blood-stained fluid in right pleural cavity, and 1 C.C. in the

May 31, 1906.--Siiperior vena cava constricted t o a diameter of 4 mm. above azygos. Juiu 1.- Killed. Post-moi*tenz.-No cedema anywhere.

Xov. 18, 190l.-Infcrior vena cava constricted to a diameter of 3 mm. above the diaphragm. Dee. 10.-Has gradually lost weight (weight, 1870 grms.). Dee. 11.-Superior vena CBVD constricted to a diameter of 3 mm., and azygos vein ligatured. Dec. 16.-Death. Post-morte?n. -11 C.C. clear straw-coloored fluid in the right pleura, 6 C.C. in tlie left, and slight cedema of the mediastinum. 5 C.C. ascites.

ExPERfMrNT 24.-Cat (weight, 2460 grms.). Ether and artificial respiiration. Nov. 25, 1901.-Superior vena cava constricted to a diameter of 3 mni. Dec. 9.-Has lost w igh t (weight, 2070 grms.). Dee. IO.-Inferior vena cava constricted to a diameter of 3 mm. above the diaphragm. Dcc. 16.-Death. Post-nwrtem.--l C.C. stran,-coloured fluid in the peritoneal cavity. No hydrothorax.

Feh. 27, 1907.-Inferior vena cava constricted to a diameter of 3 mm. above the diaphragm. Superior vena cava also constricted to a diameter of 3 mni. Feb. 28.-Klled. Post- ntortom.-2 C.C. ascites. No hydrothorax or mediastinal edema.

Ether and artificial respiration. MUT. 11, 1907.-Inferior vena cava constricted to a diameter of 3 nim. above the diaphragm. Superior vena cava ligatured between the azygos and internal mammary veins. MUT. 12.-The animal is apprently all right. Killed. Post-mortem-Edema of mediastinum, 5 C.C. clear fluid in the right pleural cavity, and 4 C.C. in the left. No ascites.

EXPERIMENT 27.-CuA (weight, 3760 grms.). Ether. Sept. 16, 1901.-Superior niesenteric vein ligatured. Recovered and walked about. Sept. 17.-Died about eight

Post-mrtem.-(Edema of mediastinuni as in all yrevioiis cats.

slowly.

EXPERIMEST 21.-Cut (weight, 3000 grms.). Ether and artificial respiration. 1906.-Superior vena cava constricted to a diameter of 3 mm. above azygos. Killed. left. Edema of mediastiunni. Fluid flowed readily through the constriction.

EXPEWMEST 22.-Cat (weight, 2530 grms,). Ether and artificial respiration.

EXPERIMENT 23.-Cad (weight, 2140 gms.). Ether and artificial respiration.

EXPERIMEXT 25.-Cut (weight, 2950 gnus.). Ether and artificial iespiration.

EXPERIMENT 26.-Cat (weight, 2400 grms.).


honra after the operation. Post-,mortcm.-Stomach and 2 in. of duodenum, great omentum, rnd spleen normal. Sniall intestine and colon t o a point ahout 4 in. above the rectum illtensely congested. On section the wall of the intestine was thick and dark coloured, with hemorrhages into the mucous membrane. The lower part of the mesentery was in places srollen and cedematow. A few drops of blood-stained fluid were found in the peritoneal cavity. The remaining organs were normal.

EXPERIMENT 28.-Cat (weight, 1650 p i s . ) . Ether. Sept. 30, 1901.-Portal vein ligatrired m it enters the liver. Death in about three hours. Post-mortcm.-5 C.C. blood- stained fluid in the peritoneal cavity. Spleen almost black and soft (weight, 13.4 grnis.). Liver very pale and free from blood.

Ether. June 23, 1906.-Portal vein oonstricted to a diameter of 1'5 mu. Post-v~ortem.-lO O.C. slightly blood-stained fluid in the peritoneal cavity. (Edema round the portal vein and pancreas in the loose cellular tissue. A cannula was introduced into the vein and fluid found to flow through the constriction.

EXPERIMENT 30.-Cat (aeiglit, 2160 grms.). Ether. June 25, 1906.-Portal vein coiistricted to a diameter of 1.5 nini. June 23.-Killed. Post-nwlenl.-2O C.C. clear stlaw-coloured fluid in the peritoneal carity : chest normal.

EYI~EILIYENT 31.-Cat (aeiglit, 2970 grms.). Ether. June 25, 1906.-Portal vein constricted to a diameter of 3 mm. Jzim 26.-Killed. Post-martem.-lO C.C. clear straw- coloured fluid in the peritoneal cavity. Chest normal.

EXPERrhfEXT 32.-Cd (weight, 2000 grms.). Ether. Aug. 10, 1906.-Portal vein constricted t o a diameter of 4 mm. Awg. 11.-Killed. Post-inortern.-No fluid. All organs normal. Gelatin was run into the portal vein, the diameter of which w-as found t o be just over 4 mm.

EXPEHIMEN~ 33.-Cd (weight, 3060 grms.). Ether. 01%. 11, 1901.-Portal vein coiistricted to a diameter of 3 mm. An umbilical hernia was present and a radical cure n-as done. Nov. %-Died. Post-morteiit.-No ascites. The omentum had prolapsed into the hernia, which had reappeared. The onientum was adherent to the abdominal mall, and contained enormous veins which anastoniosed with the superior epigastric and internal mammary veins.

Vessels of stomach and mesentery distended. No infarction of intestine.

EXPERIMENT 29. -Cd (weight, 2250 grms.). J m e 24.-Killed.

No albumin in the urine.

EXPERIMIEKT 34.-Obstrz~ction of iilferior veika caoa. Presswe in inferiurvena cavn.-Cat (11 oight, 3130 grniu.). Morphia, & g. Ether and artificial respiration. (Sept. P, 1905.)

1 ~~~ ___ __

Fressuies. ' Carotid Artery. , Inferior Vena Cars. I -- ...

Before obstructioii . After complete ol)strnction 2 minutes later . . 2 ,, '2 9 ,

2 I ,

'2 9 ,

2 ,, 2 9 ,

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. . .

. . * I

100 nim. H 50 ,,

...

...

...

...

...

...

...

...

... . . . . 36 , I I 1 ,,

I Obstructioii removed . . . 1 40-50 ,, . . . . i 2minuteslater . I

. . . . ... 2 9 ,

I 1 ,, I Obstructioii removed . . . . 40-50 ,, I 2minuteslater . . . . . I

. . . . ...

. . . . * I ::: , Animal killed . . . . . j ...

2 ,$ . . . . . 2 1 )

95 mm. IlgSO, 229 ,, 22.5 ,, 180 ,.

...

solution. I ,

1 2

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9 ,

3 ,

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78

Pressures. _-

Before obstruction . . . . Obstruction to 2 n~w. . . . . 5 minutes later . . . . . 5 ,, 5 ,, 5 I ,

5 9,

5 I ,

5 9 , . . , , . 5 ,I

5 , I

5 I ,

5 , I

5 9 ,

5 I ,

5 ,, 5 9 ,

. . . . . . . . . . . . . . . . . . . . . . . . .

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. . . . . . . . . . I I 5 . . . . . . . . . . . . . . .

. . . . . 5 I , . . . . . I Abstruczon removed . . . . . . . . . . 2 niinutea later

. . . . . . . . . . Animal%lled l 2 .~ -_____._

CHARLES BOLTON.

- Carotid Artery. Inferior Vena Cava.

130 mm. Hg. 86 .. 165 ,, I , ... I58 ,, I ,

108 .. 155 ,t I 9 ... 154 9 9 ... 150 ,, ... 150 ,* 115 .. 148 ,, 108 ,, 145 ,, * I

108 .. 144 ,, 3 ,

140 ,, 1.

137 I ,

133 I ,

132 ,, 1,

78 .. 125 ,, 9 , ... 125 ,, 1 1

122 ,, 9 ,

74 120 , I 3 ,

86 .. 8 3 ,, 9 1

89 9 , 9 , I

82 ,, t *

115 111111. bIgSO, solution.

, I

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...

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$ 3 i ...

... .. ... 119 I , .. 74 1 115 I , 3 , I

... ... I ... ... i I

~ _. -- ~ . ~-

EXPERIMENT 36.-Obstn~ctwn of inferior venn cnva. Presswe in external jugular voi?b. -Cut (seight, 2750 gnns.). Morphia, 3. gr. Ether and artificial respiration. (Oct. 18, 1906.) ......

I

___ - - -

Pressures. Carotid Artery. External Jugular Vein.

-I - ._ - .- ! Before obstructiou Obstruction to 2 mm. 5 minutes later .

1 ; ”

1 ; ,, ”

I ; :: , I

15 I ,

I 5 ”

I ii I ,

, 9

Obstruction removed 1 Animal killed . I

74 mm. Hg. 46 , I

55 , I

65 ,,

...

STUDY OF THE PATHOLOGY OF CARDIAC DROPSK i 9

EXPERIMENT 37.-Obslrnict&?n of inferior wiua eava. Pressure in portal vein.-Cnt (weight, 3800 grins.). Morphia, -+ 6. Ether and artificial respiration. (Oct. 13, 1906.)

-

Pressures. Carotid Artery. Portal Yein. I ~- ..... .

I

Before obstruction . . . . I 60 mm. Hg. 120 mm. MgSO, solution. ~ . . . ” I 5 minutes later : ! 50 ), 183 ,, 1)

Obstruction to 2 mm. 1 35 9 , 160 ,, 5 ,* : 50 ), 186 9 , I

I 5 t s 170 ,, 5 ,, . . . . . , 50 ,, 166 ,, I ,

162 ,, ,, 163

5 I , . i 5 , I * I 9 9

5 I , 155 I , 1 1 I j 52 ,, 149 ,, 9 ,

144 #,

5 I ,

. . . . . ... , 136 ,, 5 I , I

5 I 9 1

, I

5 I ) . , . . . I 4 4 ) ) ~ 130 ,, , I

5 ,) , 4 0 ,, 1 123 ,, ,* 1 . . . . . 4 0 ,, 120 ,, 3 ,

:; j Obstruc&n reniowd , 56 , , 105 ,, 2 minuteslater . . . . . ’ ... i 90 ,, a ~ 46 ,, I 89 I , ) t I

Animcal<illed * I I

. . . . . . . . . . . . . . ... ,*

. . . . ... . . . . ... . . . . . ... . . . . . . . . . ... * : t )

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. . . . . . . . . . . . . ... ...

EXPERIMENT 38.-Obslruetion of inferior veiia eava. Pressure in portal oein.-Cut (weight, 2535 g r m s . ) . Morphia, 3 gr. Ether and artificial respiration. (Oct. 1, 1906.)

~

Pressures. I

Before obstruction . . . . After complete obstruction . . . 2 minutes later . . . . . 2 I , 1 . . . . . 1 minute later . . . . .

. . . . . ] ObstrucGonremoved . . . .

. . . . . 1 , I t I #

Complete obstruction, second time . 2 minutes later . . , . I

2 ,, 1 9 9

Obstruction removed . *

2 minutes later . . . . . 1 . . . . .

1 Anirnel’killed . . , . . I

. . . . .

. . . . . . . . . . . .

Carotid Artery.

44 3 , ...

Splenic Vein.

... ... ___ .

80 CHARLES BOLTON:

.

Pressrires. Carotid Artery. I Vein of Foot.

. . . . . . . 204 , I ,, 120 I . 9 ,

160 ,, * I

. . . . . . . . . $ 9 . . . . . . . . . ... i 195 ,, . . . . .

-

Before obstrnctiori After complete obstructioii : 46 ,, Obstruction remorerl 104 ,, 2 miiiutes later 110 ,, I 135 ,, Obutrnction to 2 m i l l . 64 ,, 5 niinntes later 5 11 96 ,, 5 3 ,

5 I ,

,* , I

9 ,

9 1

. . . . . ... ‘ 5 . . . . . ...

, . . . . ... . . . . . ... i 5 ,, ,) . . . . . ... . . . . . ... . . . . . i0 ,,

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. . . . , i 4 ,, 3 minutes later ’ 80 ,,

. . . . . ...

. . . . .

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. . . . . ... * !

. . . . .

. . . . . .. . 1 hiiiiiial killed

EXVERINENT IO.--llise of Ctra-prieardial pressure. (The pressure was raised by Prcssicre ill foot.-Ca‘at (weight, allowiiig oil to run into the pericardium by gravity.)

3050 grms.). Morphia, $ gr. Ether and artificial respiration. (Nov. 24, 1906.) ~ - - - ..- ___ -~ --

172 ,,

164 ,, I t

158 , I ,, 152 ., 143 ~, 123 ,, 120 ,‘

165 .: :: j

” I ... I

1’i.rssiircs. .... . .

, Before introduction of oil . .

~ During injection . i Half-minnte intervals \ * .

Oil allowecl to run out . . .

. I

I Injection stopperl . . .

i I’ressnrcs at Iinlf-minute intervals

! oil introduced, seconil time. . Pressures at half-minutc intervals

I Carotid Artery.

I I

...

I . 90 ,, I

I 8-1 t ,

... I

...

1 32 ._ ,, Oil allowed t o run out . . . . I ...

Pressures at half-minute intervals ... . I g o ... ,, ’ Animal killed . . . . .

Veiu of Foot. -.

STUDY OF THE PATHOLOGY OF CARDIAC UROPSX 81

Femoral Artery. Pressures. -1 ___ ____

EXPEBIYEKT 41.--Oradzlally inereashy o b ~ t ~ ~ c t i o i ~ of iwferior veiia mva. PrmwTe in inferior vcna caz.a.-Cat (weight, 2830 grms.). Morphia, + gr. Ether and artificial rwpiration. Initial pressures-inferior vena cava = 110 mm. MgSO, solution. Carotid artery= 66 mm. Hg. A fine wire was passed round the inferior vena cava just below the heart, and tlie free ends of this wire pushed through a piece of glass tubing so as to form a snore. The loop so formed waB gradually tightened until the first efiect was observed upon the circulation. The venous presanre rose to 180 mm. XgSO, solution, aud the arterial pressure simultaneously sank to 48 mm. Hg. The vein wwa then cut through and the wire loop removed. This killed the animal. The diameter of the loop mas found to be 3 mni. (Sept. 13, 1906.)

External Jugular Vein. ~

I i

EXPERIXENT 4 2 . - O b a t W h of w p r i o ~ v e m cava. h c r e in externnl j W 2 n . r cein.--Cat (weight, 2500 grnis.). Morphia, + gr. Ether and artificial respiration. (Oct. 6, 1906.)

. .

I Femoral Artery. I

Pressures.

66 54

Before obstruction Complete obstruction 1 minute later . 5 minutes later . 5 I *

5 ). 5 1,

5 , 9

5 , 9

5 I >

5 Obstruciion removed Animal killed .

1 I ,

.-

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ...

60 mni. Hg. . : i 60 ,, ... . TO ,, ... ... ... : 1 ... ... ... ... . j 50 ,, . 60 , I ...

Ex terna! Jugular Vein.

- I 60 mm. MgSO,

205 ..

... I _.

, Before obstruction Obstruction to 2 nim. 1 minute later .

I 1 ,,

5 ,t l 5 Animal " k l l ed :

60 60

1 1 : i 60

mm. Hg. ,% ...

... ,, 1 1 ...

...

... ... ...

...

...

...

100 mm. 111 112 112 113 206 i 221 206 185 174 170 130 110

I Io5

641.. OF PA~IL-TOL. XIV.

83 CHARLES BOLTOA?

EXPBHlMEXT 44.-Gradually iiicrcusing obstmcclim of superior rena cara. Prcssztre i?b

external juyzrlar vein.-Cat (weight, 2200 grnis.). Morphia, + gr. Ether and artificial rebyiration. A fine Tire was passed round the superior vena csvajust above the azygos vein, and tho free ends of this wire pushed through a piece of glass tubing so as to form a snare. The loop so formed was gradually tightened until the first effect was observed upon the circulation. The veuons pressure rose a t once, but the arterial pressure W R S unaffected. The vein was cut through after the pressure had fallen, and the wire loop removed. The alterations in the venous pressure were as follows :-

(Oct. 11, 1906.)

The diameter of the loop was found to be 24 nim.

- ._ . _ __ ~ - .~

Pressures. Carotid Artery. External Jngular Vein.

1 Before obstruction . . . . 50 mni. Hg. 75 iuni. MgSO, solution. Obstruction to 24 mni. . . . 50 ,, 100 3 ,

2 minutes litter . , . . ... 108 ,, I . . . . . ... 115 ,, 2 $ 9 , 2 ,, 112 ,, 2 9 , . . . . . 108 >, . . . . . ... 108 ,, 5 2 ,

5 ,, . . . . . . 95 , I

. . . . . 50 .. 70 ,, 1

._ -. . . - .- [

1 ; I , . . . . . 96 , I I ,

. ” I . . . . . I Animal’klled i - - __

- -.. - - . ~- I

Pressures. I Carotid Artery. 1 Portal Vein. I I - _ ~. - - _ _ _ ______~ __ ~ _ _

EXPERIMENT 45.-0bstmc2ion of superior vena eaua. Pressure im inferior vera CUNL.-

Cat (weight, 3350 grms.). Morphia, 4 gr. Ether and artificial respiration. (Oct. 17, 1906.)

_.._ ~- _ _ - ~ - __ Pressures. Carotid Artery. Inferior Vens Cava. I

I _ _ -__ - 1 I

Before obstruction . . . . 110 mm. Hg. I 116 nun. bIgS0, solutioii.

5 minutes later I 95 I , I ,

I 5 ,. 100 ,, ,,

1 5 ,, 96 108 9 ,

’ 5 . I . . . . . . 96 .. I 108 .. I ,

. . . . . I 78 .. 1 109 ..

. . . . .. .. Complete obstruction 106 I 100 I , 1 6 $ 9 i 108 ,, ,

1 :: . . . . . . I 76 .. I 108 ..

. . . . .

. . . . . .. ” 1 I 5 ,. 86 ~ 87 ,, . . . . . ... . . . . .

. . . . . .. 5 , t . . . . . 86 .. I 111 ..

15 76 106 9 , . . . . . .. ’ ” I Animalxilled . . . . .

_ _ . -~ I

STUDY OF THE PATHOLOGY OF CARDIAC DROPSY 83

EXPERIMENT 47. - Hydrarnic plethora. Obslrzletivn of inferior wna cava. - Cat (weight, 3150 grms.). Morphia, b gr. Ether and artificial respiration. (Nov. 5, 1906.)

... I , 5 ,,

...

I Pressures.

Before obstriiction , Obstruction t o 2 mm. 1 minute later . . 5 minutes later. . 5 3 9

5 I ,

5 I 2

6 ,, . . 5 I ,

5 , I

5 8 ,

5 I ,

3 :, 1 3 ,

1 9 , . . 1 ,, 1 I ,

. . . . . .

. .

. . . . . . . . . .

. .

. .

. . 1 3

,, ,, I ,

, I . . , . .

. . . . . .

. . 2 I , . . 1 , I . . a 9 , . . . .

I , . . 2 . . , . .

, I . . . . ,, . . 9 , . . 9 :

I ,

. .

. .

11 1 2

6

. . ,, . . , I . . . .

. . :* I ,

,* I .

. . . . . . 1. . - 1

. . ( 9 : . .

. . . . I , . . . . 9 ,

1,

,* ,, ,, , I

, I

>>

. . . . . . . . . . . . . .

I Saline (slowly ! Carotid Artery. i Inferior Vena Cava. into External

I Jugular Vein).

104 mni. Hg. 73 I ,

72 I ,

...

...

... 72 9,

...

... 48 7:

... ... 46 ,, 44 I , ...

...

...

...

...

...

...

...

...

...

...

...

... 40 I ,

...

...

...

...

...

... 40 ,,

...

...

...

...

...

...

...

...

...

...

...

...

...

... 30 I.

110 mm. MgSO,

195 1 ,

158 ,, 156 ..

-. - 1 ... j

... i

...

...

...

... I j . .

...

...

...

... Saline 5 C.C.

... * 9 5 ) I

...

... 1 7

$ 8 i >, 5 I , I ...

... 9 9 5 *, 3 , 5 9 , ... I ... 9 , 5 I , 1

...

I ... I , 5 , I

,, 5 I ,

. I 5 I ,

,> 5 I 7

I , 5 I, I

...

...

...

... 1 ,, 3 *,

... i I , 5 I , ... ,, 5 I, 1

... ( I 5 I , ' , I 5 ,, ~

5 I t 1 ... ...

... I 9. 5 I ,

, I 5 I ,

I , 5 , I

...

...

...

84 CHARLES BOLTON.

1 minute later . . 3 minutes later. . 3 $ 9

2 ,, 3 ,, . .

. . . .

Asphyxia

_- - -- EXPERIMENT 47 (conth?ked)- I

... 113 mm. MgSO, solution. Saline 5 C.C.

... 115 ,, ...

... 112 ,, I , 1 ) 5 ,f ... 114 ., ... ... ..

50 mm. Hg. 98 ,, . . . . . , . Total. . M i n e 130 C.C.

Saline (slowly into External

Jugular Vein). Carotid Artery. Inferior Vena Cava. I I Pressures.

Pressures. Caiotid 81 tery. _ _ - - - _ _ __- -~

Initial pressure . . . . . 110 mm. Hg. Obstruction to 3 mm. (inferior vena cava) 90 ,,

5 minutes later . . . . . 100 .. 5 , I 100

. . . . . 90 .. 6 ,,

. . . . . 86 .. 5 I ,

5 7, 80

5 I , 78 ,, 5 , 9 81

5 I , 78 1 ,

5 , I

Complete obstruction (superior vena cava) 90 , ,

. . . . . ..

. . . . . ..

. . . . .

. . . . . ..

. . . . .

. . . . . ...

External Jugular Vein.

60 mm. MgSO, solution.

44 ,,

192 ,, 182 I ,

167 ,, 170 , 170 ), I ,

140 I ,

131 ,) I 3

128 9 ,

118 I , 7 ,

- __

360 ,, I ,

9

I I Poshnmtem -10 C.C. ascites. Solid on boiling.

(Nov. 19, 1906.)

. . . . . 5 9 9

5 I ,

5 1,

5 ,, 5 9 ,

5 I ?

5 > I

5 , I

5 I ,

. . . . .

. . . . .

. . . . .

. . . . .

. . . . .

. . . . .

. . . . .

. . . . .

. . . . . G

2 1 ,

Animal killed . . . . . . . . . .

... I 111 .. I 102 ,) 75 ,,

G6 .. ... 92 ,, 89 I ,

84 9 , t

83 1 ,

GO 1 83 ,, 79 ,, 75 t ,

60 ,, 68 ,, 63 ., I ,

...

... ..

I

.. 60

... ...

STUDY OF THE PATHOLOGY OF CARDIAC DROPSY; 85

EXPEBIMEHT 4Y.--Obstmetim~ of portal vein. Pressure in portal vein.-Cat (weight, 3600 grms.). Morphia, + gr. Ether and artificial respiration. (Oct. 27, 1906.)

Pressures.

Initial pressures . . Complete obstruction . 3 minutes later . . 3 9 ,

3 I ,

3 I ,

3 I t

3 I ,

3 5 ,

3 3,

3 9 ,

3 I ,

3 , 9

3 3 ,

3 ,, 3 , I

3 I ,

4* . . Animal kllerl . .

. .

. .

. . . .

. . . .

. .

. .

. .

. .

. .

. . . .

. .

* . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Carotid Artery. Splenic Vein. - .-

54 min. Hg. 34 ,,

I . .

34 I ,

34 I ,

34 I,

...

... 30 I , ...

... ...

...

I 94 mm. MgSO, 275 ,, 339 I ,

332 9 ,

320 ..

... ... I I At the end of this time all the veins of the abdopien were distended with dark-coloured

blood, and there mere a few small haemorrhages into the mesentery. The heart was beating all right, bnt weakly.

Group 111. EXHJBIMEN’T 5O.-Cat (weight, 2840 gnns.). Ether and normal respiration. June 11,

1908.-Fressure in inferior vena cavsr=85 to 90 mrn. MgSO, solution. Pressure in femoral artery= 140 to 160 mm. Hg. June lZ.-Prcssures taken in opposite femoral artery and iliac vein. Femoral artery=150 t o 160 Hg. Animal killed.

EXPERIMENT 51.-Cat (weight, 3200 grms.). Ether and normal respiration. Aug. 12, 1908.-Pressure in inferior vens cava=90 to 100 mill. MgSO, solution. Pressure in femoral artery=l40, falling to 120 mm. Hg. Awg. 13.-Pressures taken in opposite femoral artery and iliac vein. Femord artery=l20 mm. Hg. Animal killed.

1906.-Infwior vena cava constricted t o 2 nim. above the diaphragm. carotid aitery=70 mm. Hg. Pout-morlem.-lO C.C. clear straw.coloured ascites.

Inferior vena cava-90 mm. MgS04 solution.

Inferior vena cava=90 mni. MgSO, solution.

Ether and artificial respiration. EXPERIMENT 52.-Cat (weight, 3750 p is . ) . Oct. 29, Oct. 30.-Pressiire in

Pressure iu portal veiu=l05 to 115 mm. MgSO, solution. No hydrothorax or other cedema.

EXPERIMENT 53.-cat (weight, 3160 grms.). Ether and artificialrespiration. Arm. 30, Dec. 1.-Inferior vena cava constricted

Pressure 1906.-Pressure in carotid artery= 180 ULN. Hg. t o 3 mni. above the diaphragm. in portal vein = 98.

Ether and artificial respiration. 1907.-Pressure in carotid artery=170 mni. Hg., rising to 210 and falling again. vena cava constricted to 3 mm. above the diaphragm. =72 to 80 mm. Hg. Pressure in portal vein=130 mm. MgSO, solution. to 55 min. MgSO, solution. on taking portal pressure, so exact amount not determined.

th.-Pressure iii inferior vena cava=82 to 92 mm. MgSO, solution.

Dec. 2.-Pressure carotid artery=llO mm. Hg. Post-mortem.-lO C.C. ascites, straw-coloured and free from blood.

EXPEEIMENT 64.-Cat (weight, 3535 grms.). Feb. 8, Inferior

Feb. 9.-Pressure in carotid artery Pressure in inferior vena cava=100 to 105 mm. MgS0,solution.

Pressure iii external jugular vein=50 Post-morlcnt.-Considerable amount of ascites, some escaped

EXPERIMENT 55.-Cat (weight, 3450 grms.). Ether. Jan. 24, 1908.-hroima2 re@ra- Artifcia2 req~irativri.

86 CHARLES BOLTON.

--Inferior vena wva constricted to 3 mm. above the diaphragm. Norma2 respiratior.-Pressure in inferior vena cava = 100 nim. MgSO, soliitiou. in portal vein=115 nim. MgS04 solution. Killed.

Three hours Zutcr- Pressure

Pressure in femoral artery=gO to 100 mm. Hg. Post-mwtem.-Z C.C. ascites-slightly blood stained. Liver eiilarged = 120 grms.

EXPERIMENT 56.-Cat (weight, 3600 grms.). Ether. Jan. 25, 1908.-~OrmaL rcsi,iration.-Pressiire in infekior vena cava = 90 mm. MgSO, solution. Pressure in femoral artery=l4O mm. Hg. Artijkid respirdio,a.-In~erior vena cava constricted to 2 mm. above tlie diaphragm. Thrce hours Znter-NormnZ reqirutio,l.-Pressure in inferior vena cava= 115 mm. hIgSO1 solution. Considerable amount of ascites present. Twenty-one hours late?.-iVormul respirakioli.-Pressnre in inferior vena cava=90 inm. MgSO, solution. Pressure in femoral artery= 80 to 90 mni. Hg. Liver enlarged anJ dark in colour = 107 grms.

EXPERIMENT 57.-Cnt (weight, 3720 grms.). Ether. Mar. 27, 1908.-NwmaZ rcspiratkm.-Pressure in inferior vena cava = 120 to 115 mm. MgSO, solution. Pressure in femoral artery= 120 to 140 mm. Hg. Artijcia2 respirdimt.-Inferior vena cava constricted to 3 mm. above the diaphragm, Three hoicrs Inter-Norm2 [email protected] Pressure in inferior vena cava=115 to 130 (during expiration) mm. MgSO, solution. Pressure in femoral artery=110 to 120 mm. Hg. Small amount of ascites present. Twentyfour hours Eater-Normal rcqiiratim~-Pressure in inferior vena cava= 105 to 115 mni. MgSO, solution. Pressure in femoral ai-tery=90 to 110 nini. Hg.

respiration.-Pressure in inferior vena cava=7O to 75 mm. NgSO, solution. respiratioii.-Iiiferior vena cava constricted to 3 mm. above the diaphragm. N o m Z raspiration.-Pressure in inferior vena cava= 145 mm. NgSO, solution. in portal vein= 160 mm. MgSO, solution.

EXPERIMENT 59.-Cat (weight 2450 grms.). Ether. Fcb. 26, 1907.--Artifi~aZ respiratim.-Pressure in carotid artery =140 mm. Hg. Inferior vena cava constricted to 3 mm. above the diaphragm. Yeh. 27.-ArtijciaZ respi~atim.-Pressure in carotid artery = 140 mni. Hg. Pressure in portal vein=180 nim. MgSO, solution. Pressure in jugular vein=65 mm. MgSO, solution, Post-mortem.-No ascites. Animal pregnant, and all veins of abdomen enormously dixtended.

EXPERIMEST 60.-Cnt (weight, 2940 grms.). Ether. May 29, 1908.-Nwmal Pressure in inferior vena cava

Artiwal rcs~ratioa.-Inferior vena cava constricted to Four hours later-iYonnaZ 1,espiratioit.-Pressure in femoral

Post-

Pressure in femoral artery=100 mni. Hg.

Post-niortem.-25 c. c. straw-coloured ascites.

Pressure in portal vein=125 to 130 mm. MgSO, solution. Port-ntortem.--d C.C. ascitcs present.

EX~~ERINEBT 58.-Cat (weight, 2480 grnis.). Ether. Nou. 21, 1907.-Normal Artifiial

Nov. 26.- Pressure

Post-mortem-No free fluid in abdomen.

Pressure in inferior vena cava=160 mm. MgSO, solution.

respiratio~i.-Press~~re in femoral artery =140 mm. Hg. = 70 mm. 3IgS0, solntion. 2 mm. above the diaphragm. artery= 140 mm. Hg. mortem.-No free fluid in abdomen.

EXPERKMEKT 61.--C‘cct (weight, 2860 grnis.). Ether. Aug. 14, 1908.-Normd respiralivn.-Pressure in infciior vena cava = 95 mm. MgSO, solution. Pressure in femoral artery= 120 t o Id0 mm. Hg. Artijcial r~si-’iratima.-Infrior vena cavit ligatured above the diaphragm. Two hozlrs later-Normal rcspiratios.-Pressure in inferior vena cava=l4O mm. MgSO, solution. Post-mwtcm. -20 C.C. clear watery ascites.

E-XPERIIENT 62.--Cat (weight, 4220 grnis.). Ether. Feb. 7, 1908.-iVornuzl respiratio~a.-Pressure in inferior vena cava =go to 100 nim. MgSO, solution. Pressure in femoral artery= 150 to 160 mm. Hg. ArtihiuJ 1’esi’ircc.timi.-IiiIferior vena cava constricted to 3 mm. above the diaphragm. Six Itours Zuter-Nonnn2 rcs~iration.-Pressure in inferior vena cava=150 to 160 mm. MgSO, solution. Pressure in femoral artery= 120 to 150 mm. Hg.

EXPERIMENT 63.-Cat (weight, 3150 grms.). Ether. Jan. 21, 1908.--Normal respiration. - Pressure in inferior vena cava=75 mm. MgSO, solution. Artijdal respiratimc.-Infenor vma cava constricted to 3 mm. above the diaphragm. One and u hrf hours Inter-Normab respiration. -Pressure in inferior vena rava = 95 mm. hfgS0,

Pressure in inferior vena cava=l4O iiini. MgSO, solution.

Pressure in femoral artery= 50 mm. Hg. Liver=100 grms.

Post-mortem.-l C.C. ascites-clear and straw coloured.

STUDY OF THE PATHOLOGY OF CARDIAC DROPSY: 8 i

solution. Jan. 22, 1908.-h'ormaZ v~irntioa.-Pressiire in inferior vena cava=185 mni. MgSO, ~olution. Pressure in portal wiu= 190 mni. hIgS0, solution. Post-mortem- 45 G.C. ascites present.

EXPEnIYENT 64.-Cat (weight, 31E0 grms.). Ether. Jan. 10, 1908.-Nmal respirnlion.-Pressure in vein of foot=2OO mm. MgSO, solution. Pressure in inferior vena cava=95 mm. MgSO, solution. Pressure in external jugular vein=125 mm. MgS0, solution. AvtijciaZ reupiratiola.-Infcrior vena cava constricted t o 3 rum. above the diaphragm. Jan. I l . --Noml respiratio~a.-Pressire in veiu of foot= 170 mm. MgSO, solution. . Pressure in inferior vena eava=133 mm. MgSO, solution. Pressure in external jugular vcin = 20 mni. MgSO, solution. Post-mortcm.--5 c.e. slightly blood-staiiied :rucites. Liver enlarged=115 grms. Rest of tissues very dry.

EsPmmfmT 65.--Cat (weight, 3300 grms.). Ether. Jan. 6, 1908.--NomaZ respiratioii.--Pressure in inferior vena cava=95 nim. bIgS0, solution. Pressure in vein of foot= 170 mm. MgSO, solution. Artijcial rqJivatimt.- Inferior vena eava constricted to 3 mni. above the diaphragm. Jua. i.--Norii~al rcsyiratim.-Pressure in inferior vena cava=78 mm. MgSO, solution. Pressure in vein of foot=llO mm. MgSO, solution. Pressure in portal vein=90 nim. MgSO, a solution. Post-inor&em.-15 C.C. ascites present.

EXPERIMEST titi.-Cat (weight, 3150 p i s . ) . Ether. Jam. 13, 1 9 0 8 . - N ~ a l rcspirnlim- Pressure in inferior vena cava= 82 mm. MgSO, solution. Pressnre in veiu of foot=195 mm. hIgS0, solution. Pressure in external jugular vein=80 mni. MgSO, solution. Artificial respiratioia.-Infei.ior vena cava constricted to 3 mm. above the diaphragm. J ~ q t . 14.--,Vormat reupirdiola.-Pressnre in inferior vena cava= 167 mm. MgSO, solution. Pressure in external jugular vein=48 mm. YgSO, solution. Pressure in portal vein=183 mm. MgSO, solution. Post-moTtcm-lO C.C. straw-colonred ascites. Liver enlarged =125 grms. Rest of tissues very dry.

EXPERIMEST 67.-Cat (weight, 2500 grnis.). Ether and artificial respiration. Oct. 31, 1906.4uperior vena cava ligatured above arygos. Nor. 1.-Pressure in external jugular vein a t thiee elevations : 73 nim. MgSO, solution ; 100 mm. MgSO, solution ; 110 mni. MgSO, solution. Post-ntorce~n.-(Edema of the mediastinuni.

Liver=100 grms.

Pressure in vein of foot=198 MgSO, solution.

Pressure in carotid artery= 110 mm. Hg. 5 C.C. slightly blood-stained fluid in each pleural cavity.

ESPERIXIENT ti8.-Cut (weight, 2000 -1s.). Ether. NOIJ. 5, 1906. - Nonmd res3iirntion.-Pressure in left external jugular vein = 105 mm. MgSO, solution. Pressure in carotid artery = 150 mm. Hg. Arlijciul respiration.-Superior vena cava ligatured. h'ov. 6.--No~vkal respiratim.-Pressure in right external jugular vein=100 to 110 mni. MgSO, solution. Pressure in carotid artery= 150 mm. Hg. Killed. Post-nwrtem,- Gdema of mcdiastiuum extending down through diaphragm into abdomen. 5 C.C. blood- stained fluid in each pleural cavity. A little urine in the bladder containing pliosphatcs, but no albuniin.

EXPERIMEST 69.-Cat (weight, 2470 gms.). Ether. Nov. 4, 1907.--NormaZ respiratim.-Pressure in left external jugular vein =45 mm. MgSO, solution. Arta3ciaZ vcspiration. -Superior vena wva ligatured. Noo. 5.--NorinaZ rcs~iiratiol~.-Pressure in right external juo@ar vein =70 mm. MgSO, eolution. Killed. Post-mortem.-(Edema of nicdiastinum.

EXPEHIMENT 7O.-Cat (weight, 3200 grms.). Ether. NOU. 18, 1907.-Normd ?as~iration.-Pressure in left external jugular vein=50 to 60 mm. MgSO, solution. Artificial respiratio?t.-Superior vena cava constricted to a diameter of 3 mm. Nov. 19.- Nomzal respiratioR.--Pressiire in right external jugular vein = 76 mm. YgSO, solution. Killed. Trace of fluid in each pleural cavity.

ESPERIXEXT 7l.-Cat (weight, 2550 gmu.). Ether. Jan. 2, 1908.-NonnaZ re- spiratima.-Presuure in left external jugular vein=i5 mm. MgSO, solution. Pressure in inferior vena cava= 85 mm. MgSO, solution. Arti~%M rcspil'alimt.-Supenor vena cava ligatured, azygos vein ligatured. Jan. 3.-h70r?nal respiration.-Pressure in right external jugular veinz155 mm. MgSO, solution. Pressure in inferior vena cava='iO mm. bfgS0,

No ascites.

34 C.C. fluid in right pleura. 54 e.c. fluid in left pleura.

Pmt-mortem.-Very slight cedema of mediastinum.

88 CHARLES BOLTON.

solution. Killed, Post-mortem.--(Edema of niediastinum, extending up neck to chin. 7 C.C. blood-stained fluid in right pleura.

spiratim.-Pressure in left external jugular vein = 105 to 109 miti. MgSO, solution. Pressure in inferior vena cava= 75 mni. Hg. Arti&AnI res~irutioiz.-Superior vena cava ligatured above azygos. Dec. 17.-NormuZ res~il’ution.-Pressure in right external jugular vein=112 mni. MgSO, solution. Pressure in inferior vena c u a = 64 mni. MgSO, solution. Pressure in portal vein=95 mni. MgSO, solution. Killed. Post-mortem. -Marked edema of mediastinum extending into axillw.

EXPEIUMENT 73.-Cat (weight, 1980 grms.). Ether. Dec. 6, 1907.--iVoonnaZ rospira- tion.-Pressure in left external jugnlar vein= 40 mnl. MgSO, solution, Pressure in inferior vena cava= 105 mm. MgSO, solution. Arti&iuZ respirutio7b.- Superior vena cava ligatured above azygos. Dec. 7.-hrom~mZ rc.yimtim.-Presssure in right esternal jugular vein=135 mm. MgSO, solution. Pressure in inferior vena cava=84 mni. MgSO, solution. Killed. Post-mcrrtern.--(Edema of mediastinurn. 2 C.C. blood-stained fluid in right pleural cavity.

EXPERIMENT 74.-Cat (weight, 3000 grms.). Ether. ilfiar. 1, 19Oi.--drtijciuZ re- spiratioa.-Superior vena cava ligntured. Inferior vena cava constricted to 3 nim. above tho diaphragm. Four h o w s Inter.-Pressure in external jugular vein=95 t o 98 nun. MgSO, solution. Pressure in inferior vena cava=75 to 80 mm. MgSO, solution. Pressure iri portal vein= 95 to 100 mm. MgSO, solution. Yost-mortcm.-G3dema of mediastin~iiii extending t o root of neck and along axillary vesels. Little fluid in pericardium. 1 C.C. fluid ill each pleural cavity. No ascites. Liver not enlnrged.

EXPERIMENT f5.-Cat (weight, 2950 grms.). Ether. Fcb, 2 i , 190i.-Adt+fciul respirntion. -Inferior vena cava constricted to 3 mm. above the diaphragm. Superior vena cavacmstricted to 3 mm. Fcb. 28.-Pressure in inferior vena cava=’iO mm. MgSO, solution. Pressure in poi.tal veiii = lo3 to 105 miti. MgSO, solution. Pressure in external jugular vein=65 t o 70 mm. MgSO, solution. Pressure in carotid artery=84 mm. Hg. Post-mortem. -2 C.C. ascites. No 11 ydrcthorax. No mediastinal cedema.

EXPELLIMEST 76.-Cut (weight, 2400 grms.). Ether. Mar. 11, 190i.-A&ficiuZ l’es~irntio,i.-Inferior vena cava constricted to 3 mni. above the diaphragm. Superior vena cava ligaturetl. Mar. 12.-Animal quite recovered. ArtijcinI respirutiox. Pressure in external jugular vein=95 to 100 mni. MzSO, solution. Pressllre in carotid artery=122 to 150 mm. Hg. ~ost -morte in . -5 C.C. flnid ill the right pleural cavity. 4 C.C. fluid in the left pleural cavity. &dema of niediastinum. No ascites. Liver not apparently swollen.

EXPERIMENT 77.-Cat (weight, 2550 grms.). Ether. S ~ p t . 23, 1908.--Yressure in femoral artery= 150 mm. Hg. Pressure in inferior veils caw= 120 mm. MgSO, solution. Pressure in external jugular vein=40 mni. blgS0, solution. Portal vcin constricted to 2 mm. diameter. Sept. 25 (41 hours after constriction).-Pressure in fcmoral artery= 130 to 140 mm. Hg. Pressure in external jugular vein=30 mm. MgSO, solution. Pressure in portal rein=200 mm. ?rIgSO1 solution.

4 C.C. blood-stained fluid in left plenra.

ESPERIMENT 72.-C~t (Weight, 2400 grms.). Ether. DPC. 16, 1907.-~OrmaZ 1%-

1 C.C. fluid in each pleural cavity.

Few drops stained fluid in left pleural cavity.

Jugular veins distended.

Pressure in inferior vena cava=92 nim. MgSO, solution,

Post-mortem.+ C.C. free fluid in peritoneal cavity.

REFERENCES.

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STUDY OF THE PATHOLOGY OF CAKDIAC DROPSY; S9

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an experimental study of the pathology of cardiac dropsy, and its relation to that of local venous...

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