annurev.ph.21.030159

HEAT AND COLD1

BY HERBERT HENSELDepartment of Physiology, University of Marburg, Marburg (Lahn), GermanyTemperature is one of the most important factors that determine life

on earth. Among numerous means developed by living organisms to existunder various thermal conditions, "thermodynamic freedom" (61) of homeo-therms is without doubt the most ingenious achievement. According to thereviewers interests, this review is devoted mainly to temperature regula-tion, its limits, and its slow changes. Despite a wealth of valuable experi-mental results, the fundamental processes of thermoregulation are far fromunderstood, especially the nature of central thermal sensitivity and theintegrating mechanisms. As to the basic problems of acclimatization,physiology has hardly left the era of mere description.

The practical importance of some aspects of thermophysiology, such ashypothermia, has led to an enormous increase of literature during theperiod covered by this review. In view of space limitation, an arbitrary selec-tion of papers has been necessary. General problems of heat and cold in manand animals have been reviewed in recent years by Burton & Edholm (61),Burton (60), Precht, Christophersen & Hensel (254), Lee (208, 209), Levitt (213); reviews on special topics will be mentioned in the respectivesections.

HEAT EXC~AN6ESMethods.reNew climatic chambers have been described (130, 241). The

type constructed by Mfiller & Wenzel (241) allows differences of 100C.between air and radiant temperature without convection on the radiatingsurfaces. Brtick & Hensel (55) designed a climatized respiration chamber forstudying temperature regulation in newborn infants. Benzinger et al. (37)have further improved their gradient calorimeter. Basic work on heat trans-fer of living skin is being continued. Model experiments revealed consider-able errors of surface temperature measurements by thermocouples as com-pared with radiometric methods (300); however, whether such comparisonsmay be properly applied to living human skin remains to be clarified, as thepossibility of radiation sources below the skin surface cannot be excluded(247, 248). In order to calculate "thermal inertia" (product of heat conduc-tivity and heat capacity) of living skin, Hendler et at. (153) recorded skintemperature radiometrically during infrared irradiation, whereas Vendrik &Vos (316) used skin temperature changes on contact with glass plates known thermal properties. Values of 8.6 to 14X 10-4 cal. 2 cm.-4 see. -x C.-~have been obtained (79, 147, 153,316). A description of a microthermoneedleis given by Vere (317).

~ The survey of literature pertaining to thi$ review was concluded May 31, 1958.91

www.annualreviews.org/aronlineAnnual Reviews

Ann

u. R

ev. P

hysio

l. 19

59.2

1:91

-116

. Dow

nloa

ded

from

arjou

rnals.

annu

alrev

iews.o

rgby

Uni

vers

idad

Nac

iona

l de

Colo

mbi

a-se

de M

edel

lin o

n 10

/20/

06. F

or p

erso

nal u

se o

nly.

92 HENSEL

Heat transfer.--The insulating effect of vasoconstriction in the humanhead and face is relatively small (108, 312). Froese & Burton (108) pointout the importance of head protection in the cold, since 50 per cent of totalheat loss may be given off from the head. Thermal comfort obtained fromheated ceilings was studied by Wenzel & Miiller (323). The irradiated bodysurface being relatively small, a raise in radiation temperature by 10C.was necessary to compensate the physiological effect of an air temperaturedrop of IC. The human respiratory tract is demonstrated to have a con-siderable importance as a heat exchanger preventing heat losses to cold sur-roundlngs (319). Countercurrent heat exchange systems between arteriesand veins allow nutritive blood flow to the extremities without transporta-tion of heat to the surroundings. In whales and seals, countercurrent systemsare found in the tail fluke and in the flippers (24, 175, 186). The most elab-orate heat exchangers are the vascular bundles in the extremities of sloths,in which Scholander & Krog (282) have measured temperature gradientsalong the flow of lC./cm., which is 30 times steeper than in the human arm.

Miller & Blyth (238) find no difference in heat transport to the bodysurface between fat and lean subjects during heat exposure. They concludethat the insulating effect of fat is negligible under these circumstances be-cause practically all heat is transferred by convection. The diminished heattolerance of fat people might be caused by factors other than fat insulation.In the seal, however, fat is a serious hindrance to heat loss during activityon shore (24). The high thermal insulation of fur from arctic animals has beendemonstrated once more, but even the poorest fur from an opossum hasproved superior to any pile fabric made to simulate fur. Replacing the air byfreon led to a fourfold increase of thermal insulation (138). In U. S. Air Forceprotective clothing, humidity and hydrostatic compression in water reducethe insulation by 60 to 80 per cent (137).

The puzzling story of dry and damp cold has been studied by Burtonet al. (62). When skin temperatures and heat losses were the same, dry coldcaused a higher metabolic rate and a more pronounced cold sensation thandid damp cold. This effect is discussed in connection with Bazetts gradienttheory of thermoreceptor excitation; this concept is disproved, however, byrecent investigations on cold receptor discharge (56, 161, 242). A series measurements was made on spectral reflectance and distribution of radiantenergy in the skin of man (8, 79, 146, 179, 180) and laboratory animals(8, 80, 147). According to Hardy et al. (146) and former investigators (80,179), there is no influence of different pigmentation at wavelengths above1.2 ~z. In this region the spectral absorption is primarily that of water. Thecurrent belief that an arctic animal may derive some advantages frombeing white, because of less radiative heat loss, has been definitively dis-proved (139).

Internal body temperatures.--Further evidence is adduced that practicallyno heat exchange takes place at the alveolar level. Bligh (43) measured thetemperature difference between pulmonary artery and bicarotid trunk in thecalf during thermal polypnoea. Despite considerable variations in air tem-.


Ann

u. R

ev. P

hysio

l. 19

59.2

1:91

-116

. Dow

nloa

ded

from

arjou

rnals.

annu

alrev

iews.o

rgby

Uni

vers

idad

Nac

iona

l de

Colo

mbi

a-se

de M

edel

lin o

n 10

/20/

06. F

or p

erso

nal u

se o

nly.

HEAT AND COLD 93

perature, the temperature difference never exceeded the measuring errorof 0.05C. The surprising finding of Good & Sellers (127) that the tempera-ture in the left atrium of dogs in severe cold is even 0.01 to 0.15C. higher thanin the pulmonary artery might be explained partially by thermodynamicsof gas exchanges.

In contrast to the current view that the highest temperature in the rest-ing body is that of the liver (131), Graf & Graf (129) found the liver perature in healthy resting subjects to be 0.18+0.03C. below rectal tem-perature. This is probably due to a cooling effect of blood passing the liver;increased liver flow caused a temperature drop, the rectum-liver gradientbeing increased, whereas reduced liver flow had the opposite effect. Inone single case, an increase of liver temperature above rectal temperaturewas seen after pyrogen injection.

HEAT PRODUCTION

In seals as bare-skinned animals, Irving & Hart (175) found criticaltemperatures in water from 20 to 0C., varying with body size and fat in-sulation. The skin temperature of only IC. raises problems concerningtemperature reception, because in homeotherms no cold impulses are de-tected below 10C. Are they completely abolished in the seal? What thencauses the metabolic increase?

Chemical thermogenesis.--Chemical thermogenesis (heat production with-out visible or invisible muscular activity) contributes to a considerabledegree to total heat production of rats in the cold. Donhoffer et al. (84, 85)found a periodic increase in oxygen consumption with a coincident drop inmuscle temperature and a rise in abdominal temperature. Davis & Mayer(77) estimated the chemical thermogenesis in the curarized rat to be about40 per cent of the metabolic increase in the cold. This partition could beabolished by "internal" microwave heating in the curarized as well as inthe normal animal in the cold, but no reduction of the remaining 60 percent of physical thermogenesis was achieved by microwave heating. Theadrenergic system plays an important role in stimulating chemical heatproduction (169, 170).

Shivering.--It has been suggested that shivering can be elicited fromcutaneous receptors alone. This conclusion is drawn from experiments withman and animals (127, 128, 168, 297) showing a rapid onset of shivering the cold without any drop, or even with a slight increase, in rectal or hearttemperature. As hypothalamlc temperature has not been recorded directly,these experiments are not conclusive as yet though it seems unlikely that adrop in hypothalamic temperature had occurred (195). Shivering is inhibitedby hypoxia (152), CO2, and intravenous epinephrine (128). The effectivenessof shivering to compensate heat loss depends largely on the mass of shiveringmuscles, as, e.g., in the pigeon, where the big pectoral muscles are importantheat sources in the cold (299). Horvath et al. (168) and Spurt et al. (297) havedetermined that in man shivering is about 11 per cent effective in protectingagainst total heat loss at --3C.


Ann

u. R

ev. P

hysio

l. 19

59.2

1:91

-116

. Dow

nloa

ded

from

arjou

rnals.

annu

alrev

iews.o

rgby

Uni

vers

idad

Nac

iona

l de

Colo

mbi

a-se

de M

edel

lin o

n 10

/20/

06. F

or p

erso

nal u

se o

nly.

94 HENSEL

VASCULAR REACTIONS

Cutaneous blood flow.--Further studies have been made on the influenceof cold on blood flow in the dogs limb (132) and the isolated ear of the rabbit(98). Blood pressure and tone of small veins in man increase considerablyin the cold (313, 318). Cold vasodilatation in the human finger does notchange after application of antihistaminic substances (326) but decreasesduring general chilling (192). Cooper & Kerslake (69) believe the increase heart frequency during skin heating to be reflex and not hemodynamic inorigin, because it starts before vasodilatation occurs.

Does heating increase human skin blood flow by release of sympatheticvasoconstrictor tone or by stimulation of vasodilator fibres? An answer tothis controversial question has been sought by plethysmographers usingnerve blockade. Direct heating increases hand blood flow to about 50 per centof the amount obtainable with a combination of direct and indirect heating

(272). During indirect heating, Gaskell (114) and Roddie et al. (275) foundno change in hand blood flow after nerve blocking. Thus, heat vasodilata-tion is brought about by release of constrictor tone alone. In the forearm,however, heat dilatation is abolished almost completely by nerve blockade,as Edholm et al. (89) have observed. Cholinergic mechanisms (274) and haps bradykinin formation from sweat gland stimulation (105, 106) mightbe involved in the active heat vasodilatation of the forearm skin..

Muscle blood flow.--Using a heated thermocouple introduced into themuscle, Barcroft et al. (22) noticed no change or a slight decrease of muscleblood flow in human limbs during indirect heating. This has been confirmedby Roddie et al. (271, 273, 276) and Edholm et at. (88) with different tech-niques, such as venous oxygen saturation and epinephrine eleetrophoresisof the skin. S6derberg (294) obtained similar results in the eat, in whichlocal hypothalamic heating caused a decrease of muscle flow by 30 per cent.Clarke et al. (63) found an increased muscle flow on local eoollng of the fore-arm. The increase was prevented by nerve blocking but no:t by sympathec-tomy. Determinations of muscular tone might decide whether this factor isinvolved in the increase in flow.

SWEATING AND EVAPORATION

Kunos competent book on human perspiration (i97) h~s appeared in new edition. Evidence as to regional sweating patterns is given by Randallet al. (256), using direct sympathetic stimulation in man, and by Hertzman(162). I~erslake (193) found a close relationship between deep skin tempera-ture and sweat rate. A series of measurements of Na, K, and urea concentra-tions in the sweat under various conditions has been carried out (58, 59,214, 219, 267, 285). In wet heat the sweat clearance of urea may amount tovalues comparable with those of a kidney (58, 219). Schwartz & Thaysen(285) and Bulmer & Forwell (59) found a reciprocal linear relationship tween Na concentration and sweat rate. At high rates, Na reaches a constantlevel equal to plasma concentration. The authors put forward the theory


Ann

u. R

ev. P

hysio

l. 19

59.2

1:91

-116

. Dow

nloa

ded

from

arjou

rnals.

annu

alrev

iews.o

rgby

Uni

vers

idad

Nac

iona

l de

Colo

mbi

a-se

de M

edel

lin o

n 10

/20/

06. F

or p

erso

nal u

se o

nly.

HEAT AND COLD 95

that an isosmotic sweat production from the blood takes place with followingreabsorption of Na limited to a maximum of about 50 m.eq./l.

Insensible perspiration.--Thls somewhat nebulous term includes diffusivewater transport through the skin and low threshold sweat secretion. In thehand, a very low water output at high external vapour pressures and an inputduring immersion in water were observed by Craig (74). The correlation insensible weight loss to vapor pressure gradient between skin and sur-roundings has aroused some discussion (48, 135, 188, 320). Kaufmann et al.(188) found a nonlinear relationship between vapor pressure gradient andtotal cutaneous weight loss in man below the so-called sweating threshold;water loss from low-rate sweating areas, such as palm and sole, was not takeninto account. This factor is of considerable importance, as shown by a 60per cent reduction of insensible perspiration from the hand after atropineinjection (74). Having covered the low threshold sweating areas by plastic,Brebner et al. (48) found that the relationship between water transfer andvapor pressure gradient becomes linear. The same holds true for water lossat high temperatures after sweat gland activity has been suppressed byatropine (320).

NERVOUS MECHANISMSCentral mechanisms.--The present evidence from which to construct an

engineers blueprint of the heat-regulating system in terms of cyberneticsand feedback mechanisms is far from adequate (3). Most physiologists agreethat central body temperature is the leading factor in homeothermy. Glaser& Newling (121), finding the rectal temperature in man to be not constant,suggest that the essential mechanisms of temperature regulation in man areconcerned with a constant thermal balance, not a constant deep body tem-perature. This theory cannot be considered conclusive, for certain types ofautomatic controllers (proportional action controllers) show an "offset" de-pendent on external disturbance; human temperature regulation probablyrepresents such a system (254). On the other hand, thermal balance per is not a feature with which to characterize homeothermy adequately. Evena physical heat source in the steady state has a "balance" of heat productionand heat loss at any external temperature. If thermal balance were the es-sential mechanism, spontaneous rewarmlng from hypothermia, for instance,would be impossible (34).

Thermoregulatory mechanisms are activated from external as well asfrom internal temperature stimulation (76, 293). What "internal" or "cen-tral" temperature means is not clear; usually it means rectal temperature.As long as the respective temperatures are not measured directly, sweepingdeductions should be avoided as to hypothalamic temperature changes andmysterious thermoreceptors somewhere in the body. Bligh (44) observed the calf an onset of thermal polypnoea before blood temperature in thebicarotid trunk changed. In the anesthetized dog, panting is brought aboutby external and carotid heating as well (215).


Ann

u. R

ev. P

hysio

l. 19

59.2

1:91

-116

. Dow

nloa

ded

from

arjou

rnals.

annu

alrev

iews.o

rgby

Uni

vers

idad

Nac

iona

l de

Colo

mbi

a-se

de M

edel

lin o

n 10

/20/

06. F

or p

erso

nal u

se o

nly.

96 HENSEL

There is no evidence in man for a spinal thermosensitive centre. Wynd-ham & Guttman (332), investigating a patient with a complete chronictransection lesion at C.6, noticed no sign of regulation against heat or cold,such as sweating, vasomotor reactions, and shivering, in the region in-nervated from the isolated spinal cord. Similar results were obtained by other~vorkers (67, 258).

Birzis & Hemingway described a fairly discrete "shivering pathway"from the posterior hypothalamus to the spinal cord. The pyramidal tract,rubrospinal tract, and periventricular hypothalamic efferents seemed notinvolved, but bilateral section of the white columns of the thoracic cordabolished the shivering response in the hindlimbs (39). Electric stimulationof the medial part of the tuberal hypothalamus and of the shivering pathwayin the midbraln elicited typical shivering (40). Impulse discharges were re-corded along the shivering pathway, the frequency of single units rangingfrom 6 to 26 per sec. (41). Local hypothalamic heating inhibits gamma fibreactivity, as found by yon Euler & S6derberg (95). The hypothalamic thermo-receptive structures influence the activating relay system of the midbrainthat controls wakefulness, and muscular tone as well. Vice versa, stimulationof the gamma motor system appears to set the body thermostat to a higherlevel, whereas inhibition of gamma motor activity lowers the level of tem-perature regulation (96).

ttypothalamlc stimulation in unanesthetlzed anlmals.--Electric stimulationin the goat of the "heat loss centre" between anterior commissure and opticchiasma causes polypnoea, cutaneous vasodilatation, and inhibition ofshivering (10). Andersson & Persson (11) were able to lower the rectal perature in the goat to 29.5C. by prolonged stimulation of the heat losscentre at room temperatures of --6C. Cold defense reactions, such asshivering, peripheral vasoconstriction, and inhibition of panting, could beelicited by electric stimulation of the septal area, medial and dorsal to theheat loss centre (9).

Kundt et al. (195) implanted thermoneedles 0.4 ram. in diameter into thehypothalamus of cats over a period of some months. Unlike Forster &Ferguson (104), they established a close relationship between thermoregu-latory vasomotor reactions and hypothalamic temperature fluctuations.Vasoconstriction produced in the ear by cooling the paws was followed by arapid rise in hypothalamic temperature amounting to 0.6C., the latencybeing only a few seconds, whereas warming caused vasodilatation and a sub-sequent temperature drop in the hypothalamus of 0.05 to 0.4C. Rectaltemperature changed in the same directions, but very slo~vly. Thus, undermoderate conditions of heat and cold, hypothalamic temperature changescounteract the effects from peripheral afferents.

Str/Sms (301,302) finding that hypothalamic cooling fails to producevasoconstriction or shivering could not be confirmed in the unanesthetizedcat by Kundt et al. (196) or by Hensel & Krtiger (160) by use of a thin cool-ing tube chronically implanted into the hypothalamic region. Cooling by


Ann

u. R

ev. P

hysio

l. 19

59.2

1:91

-116

. Dow

nloa

ded

from

arjou

rnals.

annu

alrev

iews.o

rgby

Uni

vers

idad

Nac

iona

l de

Colo

mbi

a-se

de M

edel

lin o

n 10

/20/

06. F

or p

erso

nal u

se o

nly.

HEAT AND COLD 971C. or even less caused a marked vasoconstriction in the ear, as recorded bya heated thermocouple, the amount of vasoconstriction being closely relatedto the degree of cooling; shivering and a rise in rectal temperature wereevoked too. Withdrawal of the cooling unit 5 ram. away from the hypo-thalamus extinguished these effects.

Thermoreceptors.--Most investigators of human temperature sense usewell defined external stimuli but do not measure intracutaneous temperaturepatterns. Therefore, a great many of their deductions cannot be consideredconclusive, e.g., some work on spatial summation (211) or the "thermopile"hypothesis (212). Concerning the latter, no specific refutation has been madeas yet of electrophysiological work giving evidence that spatial gradientsare not the adequate stimulus for thermoreceptors (56, 161, 242). In experi-ments with small thermal stimulators, a relationship between cross-sec-tional area of stimulus and thermal threshold may be a matter of physics,not of physiology (155).

Sinclair (290), discussing the anatomical basis for cutaneous sensationsrecently studied by the Oxford group led by Weddell, states that temperatureand other sensations in man are elicited from skin areas where no organizedendings of any kind can be found. The same holds true for the tongue of thecat; although mechanical and thermal impulse discharges are recorded fromthis area, Kantner (184) found nothing but a network of free nerve endings.As Sinclair admits, it remains possible that specific endings exist, but not inthe sense of v. Freys theory (107) of different organized endings. The differ-ence must be too subtle for our present investigative methods.

It is generally agreed now that the cold receptors in the tongue exhibit asteady discharge frequency that depends on absolute temperature. Rapidcooling elicits an overshoot in frequency, whereas rapid warming causes afalse start. The discharge is inhibited by hypoxia (156), increased CO2 con-centration (46, 81), and efferent stimulation of the lingual nerve (82), stimulation probably causing vasomotor changes. Landgren (201, 202) re-corded impulses from single cells in the cortical area of the tongue. About 4per cent of the total number of ceils reacted specifically to cold stimulation,whereas a higher percentage reacted to cold as well as to mechanical stimula-tion or even to a more complicated combination. The convergence of differentqualities is ascribed to central nervous processes.

Cold receptor discharges from the external skin in dogs, cats, and ratshave been reported (45,225,330). In the paw of the cat, Witt (330) found very few specific cold receptors reacting like those of the tongue. A consider-able number of nerve endings could be stimulated by cooling and pressureas well, but no warm receptor has been found as yet. Even in the trigeminalarea, which is very sensitive to warmth, as proved by behavioral experi-ments in the awake cat, Boman (45) has observed as yet nothing but a cessa-tion of cold impulses during warming. Iggo (173a) observed that single fibre preparations responded to noxious stimuli on the skin as well as to lighttouch and to temperature changes.


Ann

u. R

ev. P

hysio

l. 19

59.2

1:91

-116

. Dow

nloa

ded

from

arjou

rnals.

annu

alrev

iews.o

rgby

Uni

vers

idad

Nac

iona

l de

Colo

mbi

a-se

de M

edel

lin o

n 10

/20/

06. F

or p

erso

nal u

se o

nly.

98 HENSEL

Therrnorecet;tors in poikilotherms.--As any receptor discharge is influencedby temperature (155, 242, 243), the definition of a "thermoreceptor" ismerely a matter of quantitative sensitivity. The ampullae of Lorenzini in theray and dogfish, though reacting to mechanical stimulation (158, 24:4), areeven more sensitive to temperature than the thermoreceptors in home0-therms. Hensel (157) found that the isolated ampulla contains a uniformpopulation of "cold" receptors, with a steady discharge, between 3 and34C. and a maximum at about 20C. The reactions to cooling and warming,as well as to changes in O~ and CO~ pressure, are the same as those found inthe cold receptors of the tongue (159). Pure "warm" receptors are the nerveendings in the thin membrane of the facial pit in pit yipers. Bullock & Diecke(56), in an elaborate study, found an irregular steady discharge and an ex-ceedingly high overshoot sensitivity to warming, whereas cooling caused afalse start. The receptors are able to detect infrared radiation from warmblooded animals. Even in these organs, only flattened palmate nerve struc-tures with free endings could be seen by Bullock & Fox (57).

HEAT STRESS . An~mals.--Lee (207) discusses the practical importance of heat tolerance

in cattle. Heat tolerance of guinea plg~ varie~ inversely with body size, prob-ably an effect of surface-volume ratio (327). Donhoffer et al. (83) concludefrom experiments with hypothalamic lesions that the metabolic increase inthe hyperthermic rat is of central nervous origin and not a direct temperatureeffect on peripheral tissue metabolism. At high environmental temperaturesinorganic phosphate in plasma and urine of dogs decreases, possibly as a re-sult of polypnoelc alkalosis (183). A blood sugar drop of 16 to 22 pe~ centmight be caused by metabolic factors since no glucosuria occurred-(182).Acute hyperthermia of 42.5C. increases plasm~ levels of 17-hydroxy.cortico-steroids in the dog frorn 4 to 15 gg. per cent or even more (23). During heat-ing of animals to a rectal temperature of 44 or 45C., Richards & Egdahl(262) observed circulatory failure with a drop in liT-hydroxycorticosteroidexcretion. Hypophysectomy abolishes the increase of corticoids during heat-ing. On exposure to heat, water excretion of normal rats, but not that ofdiabetes insipidus rats, was markedly reduced (177).

Man.--The effective temperature scale has not proved satisfactory toassess the physiological severity of hot climates, for thermal comfort is notequal to physiological thermal stress. Lind & Hellon (216), defining physio-logical heat stress by "predicted 4-hr. sweat rate" (P4SR), found the P4SR-scale to be adequate under various hot conditions. Investigations on menworking in the heat have been continued (199, 217, 230, 251, 322). Ladell(199) found a lower sweat rate after replacing drinking water by saline.Sweating is independent of the amount of dehydration until wate~ deficitexceeds 2.5 1. Pearcy et al. (251) have demonstrated that dehydration reducessweat secretion even if thermoregulation fails and body temperature rises.Petrunj (252) found a cutaneous oxygen absorption of 193 ml. per hour


Ann

u. R

ev. P

hysio

l. 19

59.2

1:91

-116

. Dow

nloa

ded

from

arjou

rnals.

annu

alrev

iews.o

rgby

Uni

vers

idad

Nac

iona

l de

Colo

mbi

a-se

de M

edel

lin o

n 10

/20/

06. F

or p

erso

nal u

se o

nly.

HEAT AND COLD 99the resting subject; during work and heat, the absorption increased to 730ml. per hour.

Exposure to 41C. room temperature shifts the Na/K ratio in urine from1.5 to 0.4 (221); this might be in connection with a higher output of aldos-terone. Hellman el al. (149) observed an increased urinary excretion of aldos-terone during heat stress but no change in the excreted 17-hydroxycortico-steroids. No change, or, in some cases, a slight increase of plasma ACTHoccurs (136) whereas 17-ketosteroid excretion drops by 50 per cent duringwork in hot atmospheres (266).

COLD STRt~SS

Animals.--The mechanism of "restraint" or "emotional" hypothermia inrodents (27) remains a matter for conjecture. Bartlett et al. (26) found thete~nperature drop in restrained rats to be more pronounced at highermuscular activity. A warning to experimenters who use restrained animals atlow room temperatures comes from Wilber & Robinson (329), stressing thatin the cold every route of heat loss might become significant. Adjustment offood intake to cold has been studied in pigeons (298). Using 14 i ncorporationinto fatty acids, Masoro et aL (226, 228) found a high lipogenesis from carbo-hydrates in the cold even during weight loss of the animal.

Many problems remain to be solved concerning the role of endocrineglands in acute cold stress. The stimulation of adrenocortlcal function is ap-parently transient in nature and, moreover, varies widely with species (47).Egdahl & Richards (90), exposing dogs forsome hours to extreme cold with-out hypothermla, found that the increased steroid output from the lumbo-adrenal vein returned to normal values within 1 to 3 hr. despite continuedcold stress. This effect cannot be explained by adrenal exhaustion, sinceACTH injection evoked an immediate rise in steroid output.

Cold of 10C. increases I TM output from the thyroid gland of the rat, butat 2C. a depression of thyroid activity takes place (51). The increased thy-roid activity in the cold is depressed by posterior pituitary hormones (16).Bartlett (25) demonstrated that in restrained rats the TM uptake i n t he c oldis higher than in normal animals. Thyroxine administration was found toincrease basal metabolism in the rat at 29C. but not to stimulate the meta-bolic response to cold (12). Thyroidectomy shifts the critical temperatureof the rat from 29 to 33C. (210). Significant decreases of blood protein-bound iodine (187) and of the epinephrine-potentiating effect of thyroxine(309) have been observed in ttie cold.

Man.--Cold tolerance is an important factor in hazards to shipwreckedpersons as proved by a review of the cases during World War II. Themortality was from 20 to 30 per cent at water temperatures of 5C., and de-creased to 1 per cent at 20C. (233). Studies on human performance in thecold have shown that manual dexterity (310), tactile discrimination (239),and visual-motor performance (311) are seriously impaired. Ralli et el. (255)have tested effects of vitamin supplementation on the reaction to acute


Ann

u. R

ev. P

hysio

l. 19

59.2

1:91

-116

. Dow

nloa

ded

from

arjou

rnals.

annu

alrev

iews.o

rgby

Uni

vers

idad

Nac

iona

l de

Colo

mbi

a-se

de M

edel

lin o

n 10

/20/

06. F

or p

erso

nal u

se o

nly.

100 HENSEL

cold stress. Kreider & Buskirk (194) reported that thermal comfort of mensleeping in the cold is considerably improved by supplementary feeding.Six hundred or 1200 kcal. given before sleeping increased rectal and periph-eral temperatures as well as metabolic rate.

ACCLIMATIZATIONThe term "acclimatization" or "acclimation" is widely used by physiol-

oglsts, whereas "adaptation" is claimed by physiologists as well as by blol-ogists for at least three quite different processes. Hart (148) stresses the neces-sity for differentiating between natural and laboratory experience; for thelatter the terms "acclimation" or "conditioning" are suggested. In a com-parative study Adolph (2) finds more adaptations to be specific than non-specific to diverse stressors, such as cold, low oxygen pressure, etc., and ques-tions on the basis of these findings the concept of a general nonspecificadaptation syndrome. Adaptations are thought to be superimpositions ormodifications of more stable regulating mechanisms. The basic processes in-ducing acclimatization remain obscure. What is the role of thermal recep-tors? What is the nature of peripheral acclimatization? Which central nerv-ous mechanisms are involved? None of these questions can be answered atpresent, leaving a wide field for future research.

Some additional data on animals living in hot or cold climates are avail-able. Small mammals in the tropics have critical temperatures of about27C., whereas those of birds range between 24 and 20C. (93). Irving et al.(176) proved that the melting points of fat in arctic animals, being 10C. the distal and 40 to 50C. in the proximal parts of the extremities, are notdetermined by acclimatization. Even in man and in tropical animals a similarpattern is found. Camels are able to tolerate 17 days in the heat withoutwater supply. As demonstrated by Schmidt-Nielsen et al. (279), this achieved by a dehydration tolerance amounting to 30 per cent, low waterloss by urine and feces as well as by evaporation, and tolerance to high bodytemperatures.

Wilber (328) critically discusses Bergmanns and Allens rules and rejectsany causal role for the origin of human types (284). As he justly says, in manthe ecological forces supposed to be acting are not doing so: Esl~imos werenot cold, the skinny aboriginal Australians were. Behavioral and techno-logical as well as physiological adjustments are possible in man without grossmorphological changes.

Heat acclimatization.--Heat acclimatization in mice increases anoxicresistance (163). The melting point of body fat, but not of cutaneous fat,rises with high environmental temperature (336). Robinson & MacFarlane(265) found a doubling of antidiuretic substances in the heat acclimatizedrat. Histological changes in the posterior pituitary lobes and in hypothalamicnuclei were observed by Ueno (314) in rats exposed to heat and cold. In thechicken, heat adjustment of body temperature requires three to five days,whereas respiratory frequency is acclimatized after eight to ten days (164).


Ann

u. R

ev. P

hysio

l. 19

59.2

1:91

-116

. Dow

nloa

ded

from

arjou

rnals.

annu

alrev

iews.o

rgby

Uni

vers

idad

Nac

iona

l de

Colo

mbi

a-se

de M

edel

lin o

n 10

/20/

06. F

or p

erso

nal u

se o

nly.

HEAT AND COLD 101

ACclimatization to heat has been studied chiefly in man. Evidence is giventhat no essential difference in heat tolerance exists between Bushmen andacclimatized Europeans (334). Most of heat adjustment is achieved within few days, the process being delayed by atropine (75), whereas loss of acclima-tization occurs after six days (333). A reduction of 17-ketosterold output 23.7 per cent has been found by Robinson et al. (264) in the spring as com-pared with the summer. Hand blood flow apparently does not change duringrepeated heat exposure (325). The reduced salivation in the heat returns normal during heat acclimatization (291). Changes in blood volume are stilla matter of discussion. Bass et al. (28), in a reinvestigation under standardconditions, found plasma, blood, and circulating red cell volume not to bealtered by heat acclimatization for three weeksl The findings of increasedblood volumes in the summer and during sedentary living in hot climates(29) might be due to continuous living in the heat, not to the acclimatizationprocess per se.

Cold acclimatization in animals.--The climatic and temperature influenceson the energetics of homeotherms have been recently discussed by Hart (148)in an excellent review. Only a few additional remarks will be given here.Changes of metabolism and overall insulation are the predominant featuresof adjustment to cold in animals. Apparently not all changes induced byprolonged cold are beneficial, e.g., coronary lipide deposition in the rat (287).Cold acclimatization reduces rapid reactions to acute cold stress, e.g., oxlda-tion of C14-glucose (78) or incorporation of ps~ in the adrenals (246). Masoroet al. (227) have found that hepatic llpogenesis is depressed during prolongedcold exposure. According to Hannon (141, 142), respiration of liver tissuefrom rats kept in the cold for four weeks was increased; no increase was foundafter nine weeks of cold acclimatization. Anaerobic glycolysis, however, de-creased continuously during cold exposure. In the monkey, Dugal & Fortier(87) did not observe an effect of ascorbic acid on the respiratory quotientduring six months of mild cold exposure. Further studies are concerned withchanges in mast cells (206), blood clotting and electrophoretic properties plasma (308), and electrolyte metabolism (20) during prolonged cold. Covino& Beavers (70) found the incidence of ventricular fibrillation in hypothermiato drop from 96 to 9 per cent in dogs which had been kept previously for oneto four weeks in the cold; deaccllmatlzation is accomplished after five days.

Cold acclimatization in man.--Unlike the dramatic reactions in heatacclimatization, the physiological changes in man during prolonged cold ex-posure are rather small, being apparently more important for thermal com-fort than for regulation of body temperature against cold. Living in severecold is a matter of "cultivation", of behavioral and technical adjustmentsrather than of physiological acclimatization (268).

Several reports on caloric requirements of men living and working in theArctic have been published (181, 204, 229, 321), the optimum requirementranging between 3000 and 4200 kcal. a day. Living in a cold climate haslittle or no effect on the diurnal pattern of rectal temperature (173). Sea-


Ann

u. R

ev. P

hysio

l. 19

59.2

1:91

-116

. Dow

nloa

ded

from

arjou

rnals.

annu

alrev

iews.o

rgby

Uni

vers

idad

Nac

iona

l de

Colo

mbi

a-se

de M

edel

lin o

n 10

/20/

06. F

or p

erso

nal u

se o

nly.

102 HENSEL

sonal variations of basal metabolism and protein-bound iodine in Jap-anese subjects have been ascribed to changes of thyroid activity (249).Rodahl & Bang (269), however, using TM uptake, d id n ot f ind a ny s ign o f i n-creased thyroid activity in men exposed to cold.

The Eskimo, as well as the Lapp, lives in an almost tropical mlcrocli-mate. As Rodahl (268) points out, the cold adjustment of Eskimos merelyconsists in avoiding the cold. Scholander et al. (283) found the critical tem-peratures in Lapps to be the same as in man living in moderate climates (94).Physiological differences between Eskimos, white men, and Negroes mightbe caused by racial differences rather than acclimatization, perhaps with theexception of higher finger temperatures in the Eskimo during cold stress (1,235, 260). Adams & Covino (1) have confirmed that basal metabolic rates Eskimos are about 30 per cent higher than those of Caucasians and Negroes;the metabolic increase to a standard cold stress, however, is the same inEskimos and Caucasians whereas the response of the Negro group is less.According to the higher basal metabolism, the sweat rate of Eskimos in theheat is higher than in the control group (270). Differences in plasma volume(31) and blood levels of adenine nucleotides between Eskimos, Caucasians,and Negroes have been reported (140).

Prolonged severe cold stress is practically without influence on basalmetabolic rate (172, 281); in the cold, however, metabolism, as well ascutaneous blood flow, is significantly higher in cold acclimatized subjectsthan in controls (92, 281). Scholander et al. (281) found that foot tempera-ture of acclimatized white men resting in the cold was 32C., control valuesbeing as low as 18C. The reduced thermal insulation of acclimatized personsis compensated by a higher metabolic rate. A quite different mechanism ofcold adjustment, which is physiologically more effective, has been found byScholander et al. (280a) in the naked Australian aborigines. Their thermalinsulation in the cold is higher than that of unacclimatized whites. At airtemperatures frequently dropping to 0C., the natives sleep through thenight with normal resting heat production, with their foot temperaturedropping to 12C. Thus, cold acclimatization in man apparently aims toreduce thermal discomfort and peripheral cold injury, at the~ price of a wasteof heat. The results concerning rectal temperature changes during cold ac-climatization are not consistent (172, 203, 281) ; if existing at all, the changesare very small. The overshooting metabolic response to acute cold stressseems to be diminished by cold acclimatization. As LeBlanc (203) says, thebody acquires "more confidence in itself." In the reviewers opinion, psycho-logical factors should be taken into account, for acute cold stress is combinedwith nonspecific affective reactions causing per se peripheral vasoconstrictionand increased muscular tone (124). It remains uncertain whether similarfactors are involved in the changes of the cold pressor test found by LeBlanc& Rosenberg (205) during repeated local cold exposure. A decrease in latencyof cold vasodilatation, as observed in the same experiments, gives furtherevidence for local cold acclimatization. Glaser & Whittow (122) reportedthat cold pain was reduced and blood pressure and pulse rate rose less after


Ann

u. R

ev. P

hysio

l. 19

59.2

1:91

-116

. Dow

nloa

ded

from

arjou

rnals.

annu

alrev

iews.o

rgby

Uni

vers

idad

Nac

iona

l de

Colo

mbi

a-se

de M

edel

lin o

n 10

/20/

06. F

or p

erso

nal u

se o

nly.

HEAT AND COLD 103

repeated immerslon of the hand in water of 4C. This adaptation to localizedcooling persisted for one day in a warm environment and was confined tothe hand which had been repeatedly cooled. The authors explain their find-ings on the basis of central nervous processes.

HYPOTHERMIAThis subiect has been discussed at length in two conferences (64, 85) and

a recent review (292a). Hypothermia has now lost somewhat of its practicalinterest for cardiac surgery, since extracorporeal circulation is increasinglyused. The so-called "artificial hibernation" or moderate pharmacologicalhypothermia has not been included in this review, for this procedure does notsuppress thermoregulation in the dog (200), nor has it any "histoplegic"effect (315). Hibernators are treated only with respect to hypothermia. Con-cerning hibernal sleep, which is a normothermic regulation at a low level,Eisentrauts book (91) and the last review by Kayser (189) may e con-sulted.

1-Zeal exchctnges.--Behmann & Bontke (3~) developed a method for intra-vascular cooling with automatic control of rectal temperature within 0.1C.Even deep anesthesia does not abolish nervous thermoregulatlon completely(34, 36). Intravascular cooling of dogs under light anesthesia causes shiveringbelow an aortic temperature of 36.3C. without stimulation of peripheral coldreceptors (33). Internal temperature gradients have been measured in thedog (295) and in man (68, 303) during hypothermla. Werner al. (324) haveobserved spontaneous rewarming from a rectal temperature of 25C. in theunanesthetized curarized dog, thus demonstrating the importance of chem-ical thermogenesis. The critical body temperature at which spontaneous re-warming from hypothermia occurs is much lower in the hibernator than inthe homeotherm, as Adolph & Richmond (4) have demonstrated; rewarmingrates of hibernators are also much higher.

Respiration, circulation, body fluids.--Arterial-aiveolar O, and CO,gradients have been measured during hypothermia in the dog (7, 250, 288)and in man (288). Gas exchanges are reduced in hypdthermia but stillsufficient for the lower metabolism. Albers et al. (7) suggest the existence functional atelectases in the hypothermlc dog; the diffusion factor for O~turned out to be 0.44 at 38C. and 0.26 ml. min.-x kg.-1 mm. Hg-1 at 20C.Further evidence is given (6) that no hypoxia occurs during hypothermia;even arterial hypoxemia as low as 17 ram. Hg Po2 has no influence on thelethal temperature.

Brendel et al. (49, 50) have observed responses to carotid sinus stimula-tion, CO, inhalation, and stimulation of cutaneous cold receptors at rectaltemperatures of 20C. Covlno & Beavers (71) found an increased blood flowin the hind limb of the hypothermic dog; it is suggested that in moderate cool-ing the increased flow is due to cholinergic vasodilator fibres, whereas lowertemperatures act directly upon the blood vessels. During deep hypothermia,Lynch & Adolph (220) did not notice a change in diameter of small vessels;blood flow was reduced by increased viscosity.


Ann

u. R

ev. P

hysio

l. 19

59.2

1:91

-116

. Dow

nloa

ded

from

arjou

rnals.

annu

alrev

iews.o

rgby

Uni

vers

idad

Nac

iona

l de

Colo

mbi

a-se

de M

edel

lin o

n 10

/20/

06. F

or p

erso

nal u

se o

nly.

104 HENSEL

Acid-base balance during hypothermia is greatly dependent on anesthesiaand respiration (17, 120). Metabolic acidosis in man can be prevented hyperventilation, provided that no additional stress, e.g., shivering, occurs(154).

Heart.--Much research work has been focused on the hypothermic heart,the main problems still being ventricular fibrillation and cardiac efficiency.Angelakos (13) demonstrated statistically that the terminal temperatures dogs are independent of either ventricular fibrillation or asystole as theterminal events. Although considerable practical progress has been made incontrolling ventricular fibrillation during hypothermia (32, 66, 73, 198, 261,263), the basic cause of hypothermic cardiac arrhythmias is still unknown.Covino & Beavers (72) have found a fivefold decrease of ventricular fibrillarythreshold at 22C. but a constant basic ventricular threshold. Changesin re-fractoriness are obviously not the cause of fibrillation (15). Important factorsin inducing cardiac arrhythmias are acidosis (73), potassium loss from themyocardium (126, 232), hypersensitivity to sympathetic stimulation (113,289) and to calcium (14). Hannon & Covino (143) suggest that changes cellular metabolism of the myocardium might be the basic cause of fibrilla-tion, but no biochemical evidence for this has been found as yet (143, 178).

As has been confirmed by several investigators, the hypothermic heartdoes not undergo undue stress. In the heart-lung preparation the workingcapacity is higher than necessary for the hypothermic organism (19, 259).Badeer & Khachadurian (19) proved that the higher mechanical efficiency the heart during hypothermia results from cold per se and not from brady-cardia. Hansen et at. (144) could not observe any decrease of cardiac effi-ciency in the dog when rectal temperature was decreased from 38 to 23.5C.Coronary O2 utilization remained constant, whereas coronary blood flow, O2consumption of the left ventricle, and total O2 consumption dropped pro-portionally to temperature, reaching about 25 per cent of the initial value at23.5C. Fisher et al. (103) found the first signs of cardiac failure to occur after14 hr. at 23C. Gollan & Nelson (125), using extracorporeal circulation combination with general hypothermla of 20C. in the dog, achieved ananoxic tolerance of the resting heart of 1 hr.

Nervous system.--The spontaneous cortical activity in the rat stops at16 to 18~C., whereas evoked potentials are noticed even at 13~C. The depres-sion in nervous function is preceded by a transient stage of hyperexcitability(30). Oxygen consumption, blood flow, and occlusion tolerance of the brainhave been studied in monkeys at 25~C. ; a tolerance limit of 12 min. has beenfound (38, 234). Localized cerebral cooling in the dog by means of an extra-corporeal circulation has practically the same effects as has general hypo-thermia (331). Malmejac et al. (222) find that, in dogs and monkeys cooledto about 18C. for a short time, cortical recovery as studied by conditionedreflexes needs three to eight days, this time being decreased by epinephrineinfusion during hypothermia. Epileptiform activity (21) and effects of vagalstimulation (337) are diminished at low temperatures. During the phase hyperexcltability between 35 and 25C., a spreading of synaptlc transmission


Ann

u. R

ev. P

hysio

l. 19

59.2

1:91

-116

. Dow

nloa

ded

from

arjou

rnals.

annu

alrev

iews.o

rgby

Uni

vers

idad

Nac

iona

l de

Colo

mbi

a-se

de M

edel

lin o

n 10

/20/

06. F

or p

erso

nal u

se o

nly.

HEAT AND COLD 105

to the surrounding neurons takes place (304). In the hibernator rewarmingfrom hypothermia, the first electrical activity is seen in the mldbrain attemperatures of 6 to 8C. This holds also for the arousal from natural hiber-nation; however, other parts of the brain are active in hlbernal sleep atlower temperatures than in hypothermia (257).

Miscellaneous.--Whether hypothermia evokes a general stress responsedepends largely on anesthesia; barbiturates appear to inhibit stress (100,278). No evidence for tissue damage is found generally in hypothermia (101) however, necrotic loci in the heart have been described by Sarajas (277).Fructose metabolism (335), hepatic oxygen consumption (97, 102), and tein formation in the liver (18) have been investigated in man and animalsduring hypothermia. Intestinal absorption below 19C. appears to be afiltration independent of osmotic pressure and nature of substances absorbed(119). Further studies have been concer.ned with renal function. Renalcirculation and glomerular filtration rate are greatly reduced during hypo-thermia (42, 166, 240). Also a reduction of the reabsorptive and secretorytubular functions takes place (166, 286). The tubular maximum of p-amino-hlppurlc acid has been confirmed to decrease considerably at low tempera-tures (42, 240).

Deep hypothermia and suspended anlmation.--Cooling of homeotherms tobody temperatures of about 0C. with cardiac standstill may be followed byresuscitation, provided that rewarming starts within 1 to 2 hr. This wasconfirmed in further experiments, e.g., in the monkey, where Niazi & Lexvis(245) observed complete recovery after 2 hr. of cardiac asystole at rectaltemperatures of 4 to 9C. It is not known as yet why homeotherms cannotsurvive severe hypothermia for more than this short period. The limitingtime factor is apparently independent of temperature in the range below15oc. (5).

Reanimation of ice-cold rats is achieved by artificial respiration andsimple irradiation with a bench lamp (122a). In these experiments Goldzveig& Smith (123) found a severely reduced fertility fo~ eight weeks. Smith (292)succeeded in resuscitating golden hamsters from cooling to -5C. internalbody temperature; recovery is possible even if 50 per cent of the body waterhad been frozen (218).

Even at complete standstill of the hypothermic heart, the pacemakerfibres continue to discharge. The link between pacemaker and auricle, broken.by cooling, can be restored by acetylcholine (223, 224). No changes in mem-brane and action potentials occur in the dogs heart, when it has been keptpreviously at 1 to 3C. for 72 hr. (231). The changes in heart performancefollowing resuscitation from deep hypothermia of 15C. for 1 to 3 hr. havebeen studied by Giaja & Radulovi6 (116). In the posthypothermic state, theanoxic resistance of the heart shows a fourfold increase; also the workingcapacity is doubled (118). The profound posthypothermic changes are fur-ther demonstrated by an increased survival time of the isolated heart takenfrom rats in deep hypothermia (117). The temperature for cardiac standstillin hypothermia is different in hibernators and homeotherms. Kayser and co-


Ann

u. R

ev. P

hysio

l. 19

59.2

1:91

-116

. Dow

nloa

ded

from

arjou

rnals.

annu

alrev

iews.o

rgby

Uni

vers

idad

Nac

iona

l de

Colo

mbi

a-se

de M

edel

lin o

n 10

/20/

06. F

or p

erso

nal u

se o

nly.

106 HENSEL

workers (190, 191) found asystole to occur at 0C. in hibernators and 15C. in homeotherms. No differences, however, could be detected betweenthe two groups in the temperature coefficients of heart frequency or of diverseparts of the electrocardiogram.

COLD INJURY

This subject has been treated in the Fourth Macy Conference on cold in-jury (99) and in two reviews by Meryman (236, 237). Many factors might involved in local cold injury, such as vasoconstriction, thrombosis, nervelesions, ice formation, and dissociation of anabolic and catabolic processes atlow temperature (145). Present research is progressing mainly along twolines: vascular responses and tissue freezing.

Freezing of tissues.--The freezing point of living tissue has been foundby Pichotka et al. (253) to be "1.08_+0.04C., thus suggesting that intra-cellular fluid is not isotonic with blood plasma. The mechanism maintainingthe higher intracellular osmotic pressure is not known as yet; possibly it isan active metabolic water transport out of the cell. However, the freezingpoint of organized tissues is no suitable measure of osmotic pressure, as Kuhn(194a) has shown. Local cooling leads to an increased water uptake andswelling of the cells (5, 65). According to Scholander etal. (280) freezing arctic fishes is prevented either by supercooling and avoidance of ice seedingor by an increased osmotic pressure. In intertidal animals, however, 80 percent of body ~vater can freeze without damage of the organism (185).

The deleterious factor in tissue freezing is increase in concentration ofelectrolytes and other substances rather than mechanical damage by iceformation (236, 237). Clinical frostbite usually occurs at moderate rates cooling, leading to extracellular ice formation, whereas intracellular freezingis only seen during rapid cooling. In this respect, laboratory experiments inanimals have been criticized by Meryman (237) as being not comparable all with frostbite in man. Fuhrman (110) has shown that oxygen consump-tion and anaerobic glycolysis of isolated rat tissue are disturbed neitherafter prolonged cooling at --0.4C. without freezing, nor after st~percooling,but are greatly reduced after freezing. Rapid thawing in water of 42C. isconsidered the best treatment of frostbite, at least in animal experiments(111, 112, 237, 306). Brief freezing or burning preceding a standard frostbitereduces tissue loss (109).

Vascular reactions.--Vascular responses to cold injury in the cheek pouchof golden hamsters have been investigated by Sullivan and co-workers (305,306, 307). After thawing of the tissue, the blood flow is it/creased initially;later a gradual decline in rate of flow occurs, with arteriolar constriction,thrombosis, and stasis. Inositol causes a greater edema but reduces stasis andtissue loss. Imlg et al. (174) noticed an increase in blood flow above the initialvalue in the dogs hind llmb after thawing, whereas Hardenbergh & Barn-berg (145) found the flow after thawing to be slightly reduced or normal. long as freezing did not occur, reactions to epinephrine and acetylcholineremained unchanged during cooling.


Ann

u. R

ev. P

hysio

l. 19

59.2

1:91

-116

. Dow

nloa

ded

from

arjou

rnals.

annu

alrev

iews.o

rgby

Uni

vers

idad

Nac

iona

l de

Colo

mbi

a-se

de M

edel

lin o

n 10

/20/

06. F

or p

erso

nal u

se o

nly.

HEAT AND COLD 107

ONTOGENY O~ THERMOREGULATION

An important comparative survey on the ontogeny of physiologicalregulations in the rat is given by Adolph (3). Mo~e attention should be paidto the question whether postnatal changes of thermoregulation are congenitalpatterns or caused by external conditions, such as temperature or birth perse. The metabolic thermoregulation in piglets is very unsatisfactory withinthe first six days and becomes nearly perfect around the twentieth day afterbirth (165). A somewhat more developed thermogenesls has been reported Gelineo (115) as a result of experiments in newborn dogs. Even thoughtemperature regulation is still very imperfect, signs of homeothermic be-havior of metabolism can be seen one day after birth. Thyroldectomy inyoung rats has no influence on the development of thermoregulation within14 days after birth but depresses rectal temperature and metabolic rise inthe cold after 18 days (133, 134).

Development of thermoregulation in man.--It is surprising enough that,despite an immense amount of work in newborn animals and in adult man,very little is known about the ontogeny of thermoregulation in man. Brticket al. (52, 53, 54), using a small climatic chamber (55), have followed up meta-bolic and vasomotor thermoregulatory responses in premature and full-termnewborn infants from the very first hour until 14 days after birth. The mini-mal metabolic rate at a room temperature of 33C. is 1.4 to 1.6 kcal. kg.-~

- hr. -~ in premature as well as in full-term babies, and remains constant forthe whole period of time: In full-term infants the metabolic rise in responseto a standard cold stress of 23C. amounts to 100 per cent at birth and in-creases to about 170 per cent after eight days (52). At birth an almost maxi-mal cutaneous vasoconstriction is seen at a room temperature of 23C, nodilatation occurring on warming, whereas at the end of the first week a con-siderable dilatation takes place at 35C. (53).

Similar experiments have been carried out in premature newborn infantsof 1550 to 2050 gm. (52). They show the same postnatal pattern of develop-ment of vasomotor and metabolic responses, the latter being 30 to 50 per centsmaller than in full-term infants; but, for example, the metabolic rise on cool-ing of a premature infant two weeks after birth is even higher than that of afull-term infant at birth. From these facts it is possible to conclude that thepattern of postnatal development of human temperature regulation isgreatly dependent on birth per se and external conditions, or, in other words,is a matter of postnatal rather than of conceptional age. It seems necessaryto reconsider, on this basis, the material On the ontogeny of thermoregula-tlon in animals.

Aging.mExperiments in animals (171) and in man have shown a de-crease in thermoregulatory responses with age. Hellon & Lind (150) foundno significant difference in the number of active thermal sweat glands in theheat but a doubling of time for onset of sweating in the older men. In thelatter, forearm blood flow in the heat was higher (151). Horvatb et al. (167)compared the reactions to a cbld stress of 10C. in two age groups of menaveraging 25.5 and 64 years respectively. In the old men, no subjective dis-


Ann

u. R

ev. P

hysio

l. 19

59.2

1:91

-116

. Dow

nloa

ded

from

arjou

rnals.

annu

alrev

iews.o

rgby

Uni

vers

idad

Nac

iona

l de

Colo

mbi

a-se

de M

edel

lin o

n 10

/20/

06. F

or p

erso

nal u

se o

nly.

108 HENSEL

comfort, shivering, metabolic rise, or increased respiratory volume could beobserved; peripheral vasoconstriction was less marked than in the youngergroup, and rectal temperature dropped by 0.3C. The young men showed allsigns of cold defense, including subjective discomfort, and kept their rectaltemperature constant. A diminished cold vasodilation in old people has beennoticed by Spurr et al. (296).

LITERATURE CITED1. Adams, T., and Covlno, B. G., J. Appl. Physiol., 12, 9 (1958)2. Adolph, E. F., Am. J. Physiol., 184, 18 (1956)3. Adolph, E. F., Quart. Rev. Biol., 32, 89 (1957)4. Adolph, E. F., and Richmond, J., J. Appl. Physiol., 8, 48 (1955/56)5. Adolph, E. F., and Richmond, J., Am. J. Physiol., 187, 437 (1956)6. Albers, C., Brendel, W., Hardewig, A., and Usinger, W., Arch. ges. Physiol., 266~

373 (1958)7. Albers, C., Brendel, W., Hardewig, A., and Usinger, W., Arch. ges. Physiol., 266,

394 (1958)8. Alpen, E. L., Butler, C. P., Martin, S. B., and Davis, A. K., J. Appl. Physiol.,

8, 399 (1955/56)9. Andersson, B., Acta Physiol. Scand., 41, 90 (1957)

10. Andersson, B., Grant, R., and Larsson, S., Acta Physiol. Scand., 37, 261 (1956)11. Andersson, B., and Persson, N., Acta Physiol. Stand., 41, 277 (1957)12. Andik, I., Nagy, L., and T6th, I., Acta Physiol. Acad. Sci. Hung., 8~ 399 (1955)13. Angelakos, E. T., Proc. Soc. Exptl. Biol. Med., 97~ 107 (1958)14. Angelakos, E. T., Deutsch, S., and Williams, L., Circulation Research, 5~ 196

(1957)15. Angelakos, E. T., Laforet, E. G., and Hegnauer, A. H., Am. J. Physiol.,

591 (1957)16. Arimura, A., Takagi, Y., and Ueno, T., Japan. J. Physiol., 6~ 284 (1956)17. Axelrod, D. R., and Bass, D. E., Am. J. Physiol., 186, 31 (1956)18. Babskaya, Y. E., Dokl. Akad. Nauk S.S.S.R., 114~ 598 (1957)19. Badeer, H., and Khachadurlan, A., Am. J. Physiol., 192, 331 (1958)20. Baker, D. G., and Sellers, E. A., Can. J. Biochem., 8, 631 (1957)21. Baldwin, M., Frost, L. L., Wood, C. D., and Lewis, S. A., Science, 1:24, 931 (1956)22. Barcroft, H., Bock, K. D., Hensel, H., and Kitchin, A. H., Arch. ges. Physiol.,

261, 199 (1955)23. Barlow, G., Agersborg, H. P., Jr., and Keys, H. E., Proc. Soc. Exptl. Biol. Med.,

93, 280 (1956)24. Bartholomew, G. A., and Wilke, F., J. Mammal., 37, 327 (1956)25. Bartlett, R. G., Jr., Proc. Soc. Exptl. Biol. Med., 94, 654 (1957)26. Bartlett, R. G., Jr., Bohr, V. C., Foster, G. L., Miller, M. A., and Helmendach,

R. H., Proc. Soc. Exptl. Biol. Meal., 92~ 457 (1956)27. Bartlett, R. G., Jr., Bohr, V. C., hnd Helmendach, R. H., Physiol. Zo6l., 29,

256 (1956)28. Bass, D. E., Busklrk, E. R., Iampietro, P. F., and Mager, M., J. Appl. Physiol.,

1:2, 186 (1958)29. Bass, D. E., and Henschel, A., Physiol. Revs., 36, 128 (1956)30. Battista, A. F., Am. J. Physiol., 191, 209 (1957)


Ann

u. R

ev. P

hysio

l. 19

59.2

1:91

-116

. Dow

nloa

ded

from

arjou

rnals.

annu

alrev

iews.o

rgby

Uni

vers

idad

Nac

iona

l de

Colo

mbi

a-se

de M

edel

lin o

n 10

/20/

06. F

or p

erso

nal u

se o

nly.

HEAT AND COLD 10931. Baugh, C. W., Bird, G. $., Brown, G. M., Lennox, C. S., and Semple, R. E.,

J. Physiol. (London), 140, 347 (1958)32. Beavers, W. R., and Covino, B. G., Arch. Surg., 75, 776 (1957)33. Behmann, F. W., Arch. ges. Physiol., :~63, 166 (1956/57)34. Behmann, F. W., Arch. ges. Physiol., 206, 422 (1958)35. Behmann, F. W., and Bontke, E., Arch. ges. Physiol., 263, 145 (1956/57)36. Behmann, F. W., and Bontke, E., Arch. ges. Physiol., 266, 408 (1958)37. Benzinger, T. H., Huebscher, R. G., Minard, D., and Kitzinger, Ch., J. Appl.

Physiol., 12~ S 1 (1958)38. Bering, E. A., Jr., Taren, J. A., McMurrey, J. D., and Bernhard, W. F., Surg.,

Gynecol. Obstet., 102, 134 (1956)39. Birzis, L., and Hemingway, A., J. Neurophysiol., 19, 37 (1956)40. Birzis, L., and Hemlngway, A., J. Neurophyslol., 201 91 (1957)41. Birzis, L., and Hemingway, A., J. Neurophysiol., 201 156 (1957)42. Blattels, C. M., and Horvath, S. M., Am. J. Physiol., 192, 357 (1958)43. Bligh, J., J. Physiol. (London), 136, 404 (1957)44. Bligh, J., J. Physiol. (London), 1361 413 (1957)45. Boman, K., Acta Physiol. Scand., 441 Suppl. 149, 79 pp. (1958)46. Boman, K., Hensel, H., and Witt, I., Arck. ges. Physiol., 2641 107 (1957)47. Boulouard, R., Compt. rend. soc. biol., 151, 913 (1957)48. Brebner, D. F., Kerslake, D. McK., and Waddell, J. L., J. Physiol. (London),

132~ 225 (1956)49. Brer~del, W., Albers, C., and Uslnger, W., Arch. ges. Physiol., 266, 341 (1958)50. Brendel, W., Albers, C., and Usinger, W., Arch. ges. Physiol., 266, 357 (1958)51. Brown-Grant, K., J. Physiol. (London), 131, 52 (1956)52. Briick, K., Arch. ges. Physiol., 268, 7 (1958)53. Br~ick, K., Briicl~, M., and Lemtls, H., Arch. ges. Physiol., 266, 518 (1958)54. Brtick, K., Brtick, M., and Lemtis, H., Arch. ges. Physol., 267, 382 (1958)55. Briick, K., and Hensel, H., Arch. ges. Physiol., 266, 556 (1958)56. Bullock, T. H., and Diecke, F. P. J., J. Physiol. (London), 134, 47 (1956)57. Bullock, T. H., and Fox, W., Quart. J. Microscop. Sci., 98, 219 (1957)58. Bulmer, M. G., J. Physiol. (London), 137, 261 (1957)59. Bulmer, M. G., and Forwell, G. D., J. Physiol. (London), 132, 115 (1956)60. Burton, A. C., Rev. can. biol., 16, 293 (1957)61. Burton, A. C., and Edholm, O. G., Man in a Cold Environment (Edward Arnold,

Publishers, Ltd., London, Engl., 273 pp., 1955)62. Burton, A. C., Snyder, R. A., and Leach, W. G., J. Appl. Physiol., 8, 269

(1955/56)63. Clarke, R. S. J., Hellon, R. F., and Lind, A. R., Clin. Sci., 17, 165 (1958)64. Colloques Nationaux du Centre National de la Recherche Scientifique, Arch.

sci. physiol., 9, C 3 (1955)65. Conway, E. J., and Geoghegan, H., J. Physiol. (London), 130, 438 (1955)66. Cookson, B. A., and DiPalma, J. R., Am. J. Physiol., 188, 274 (1957)67. Cooper, K. E., Ferres, H. M., and Guttmann, L., J. Physiol. (London), 136,

547 (1957)68. Cooper, K. E., and Kenyon, J. R., Brit. J. Surg., 461 616 (1957)69. Cooper, K. E., and l~erslake, D. McK., Clin. Sci., 141 125 (1955)70. Covino, B. G., and Beavers, W. R., Am. J. Physiol., 191, 153 (1957)71. Covino, B. G., and Beavers, W. R., J. Appl. Physiol., 10, 146 (1957)72. Covino, B. G., and Beavers, W. R., Proc. Soc. Exptl. Biol. Med., 95, 631 (1957)


Ann

u. R

ev. P

hysio

l. 19

59.2

1:91

-116

. Dow

nloa

ded

from

arjou

rnals.

annu

alrev

iews.o

rgby

Uni

vers

idad

Nac

iona

l de

Colo

mbi

a-se

de M

edel

lin o

n 10

/20/

06. F

or p

erso

nal u

se o

nly.

110 HENSEL

73. Covlno, B. G., and Hegnauer, A. H., Surgery, 40, 475 (1956)74. Craig, F. N., J. Appl..physiol., 8, 473 (1955/56)75. Cullumbine, H., and Miles, S., Quart. J. Exptl. Physiol., 41, 162 (1956)76. Davis, T. R. A., and Mayer, J., Am. J. Physiol., 181, 669 (1955)77. Davis, T. R. A., and Mayer, J., Am. J..physiol., 181, 675 (1955)78. Depocas, F., Macleod, G. K., and Hart, J. S., Rev. can. biol., 16, 83 (1957)79. Derksen, W. L., Murtha, T. D., and Monahan, T. I., J. Appl. Physiol., 11, 205

(1957)80. Dimitroff, J. M., Kuppenhelm, H. F., Graham, I. C., and McKeehan, C. W.,

J. Appl. Physiol., 8, 532 (1955/56)81. Dodt, E., Arch. ges. Physiol., 263, 188 (1956/57)82. Dodt, E., and Walther, J. B., Arch. ges..physiol., 265, 355 (1957)83. Donhoffer, S., Mesty~n, G., Nagy, L., and Szegv~ri, G., Acta Neuroveget.

(Vienna), 16, 390 (1957)84. Donhoffer, S., Szegv~ri, G., Varga-Nagy, I., and J~rai, I., A.r6h. ges. Fhysiol.,

265, 97 (1957)85. Donhoffer, S., Szegv~ri, G., Varga-Nagy, I., and ]~rai, I., Arch. ges. Physiol.,

265, 104 (1957)86. Dripps, R. D., Ed., Natl. Aad. S6i.-Natl. Research Council, .publ. 451

(Washington, D. C., 447 pp., 1956)87. Dugal, L. P., and Fortier, G., Can. J. Biochem. and Physiol., 35, 169 (1957)88. ]~dholrn, O. G., Fox, R. H., and Macpherson, R. Fl., J..physiol., (London) 134,

612 (1956)89. Edholm, O. G., Fox, R. H., and Macpherson, R. K., J..physiol. (London), 139,

455 (1957)90. Egdahl, R. H., and Richards, J. B., Am. J..Physiol., 185, 239 (1956)91. Eisentraut, M., Der Wintersehlaf mit seinen ~kologischen und physiologisehen

Begleiterscheinungen (Gustav Fischer, Jena, Germany, 160 pp., 1956)92. Elsner, R. W., Alaskan Air Command, Arctic Aeromed. Lab., Ladd Air Force

Base, Proj. No. 8-7951, Report No. 1 (1955)93. Enger, P. S., Acta .physiol. Scand., 40, 162 (1957)94. Erikson, H., Krog, J., Lange Andersen, K., and Scholander, P. F., Acta Physiol.

Scand., 37, 35 (1956)95. yon Euler, C., and S~derberg, U., Electroencephal. and Clin. Neurophysiol., 9, 391

(1957)96. yon Euler, C., and S6derberg, U., Acta Physiol. Stand., 42, 112 (1958)97. Fedor, E. J., Levine, M., Russ, C., and Fisher, B., Surg. Forum, 6, 141 (1956)98. Ferguson, I. D., and Levinson, N., J..physiol. (London), 128, 608 (1955)99. Ferrer, M. I., Ed., Cold Injury. Trans. of the Fourth Conf. (Josiah Macy, Jr.,

Foundation, New York, N. Y., 371 pp., 1956)100. Fisher, E. R., Fedor, E. J., and Fisher, B., Am. J..physiol., 188, 470 (1957)101. Fisher, E. R., Fedor, E. J., and Fisher, B., Arch. Surg., 75, 817 (1957)102. Fisher, B., Fedor, E. J., Lee, S. H., Weitzel, W. K., Selker, R., and Russ, C.,

Surgery, 40, 862 (1956)103. Fisher, B., Russ, C., and Fedor, E. J., Am. J..physiol., 188~ 473 (1957)104. Forster, R. E., 2rid, and Ferguson, T. B., Federation .proc., 10, 44 (1951)105. Fox, R. H., and Hilton, S. M., d..physiol. (London), 133~ 68P (1956)106. Fox, R. H., and Hilton, S. M., d..physiol. (London), 137~ 43P (1957)107. v. Frey, M., 23~r. sachs. Ges. (Akad.) Wiss., 47, 166 (1895)


Ann

u. R

ev. P

hysio

l. 19

59.2

1:91

-116

. Dow

nloa

ded

from

arjou

rnals.

annu

alrev

iews.o

rgby

Uni

vers

idad

Nac

iona

l de

Colo

mbi

a-se

de M

edel

lin o

n 10

/20/

06. F

or p

erso

nal u

se o

nly.

HEAT AND COLD 111

108. Froese, G., and Burton, A. C., J. Appt. Physiol., 10, 235 (1957)109. Fuhrman, F. A., J. Appl. Physiol., I0, 139 (1957)110. Fuhrman, F. A., J. Appl. Physiol., 10, 224 (1957)111. Fuhrman, F. A., and Fuhrrnan, G. J., Medicine, 36, 465 (1957)112. Fuhrman, F. A., and Fuhrman, G. J., J. Appl. Physiol., 11, 45 (1957)113. Garb, S., and Penna, M., J. Appl. Physiol., 9, 431 (1956)114. Gaskell, P., J. Physiol. (London), 131, 647 (1956)115. Gellneo, S., Bull. aead. Serbe sci., 18, 97 (1957)116. Giaja, J., and Radulo~i~, J., Compt. ~end. 242, 2039 (1956)117. Giaja, J., and Radulovi6, J., Nature, 178, 1286 (1956)118. Giaja, J., Radulovi~, J., and Gavrilovi_ ~, Z., Compt. rend. 244, 27 (1957)119. Giaja, J., and Rajevski, V., Compt. rend. soc. biol., 149, 449 (1955)120. Giustina, G., and Meschia, G., Arch. fisiol., 56, 173 (1956)121. Glaser, E. M., and Newling, P. S. B., J. Pl*ysiol. (London), 137, 1 (1957)122. Glaser, E. M., and Whittow, G. C., Jr. Physiol. (London), 136, 98 (1957)122a. Goldzveig, S. A., and Smith, A. U., J. Physiol. (London), 132~ 406 (1956)123. Goldzveig, S. A., and Smith, A. U., J. Endocrinol., 14, 40 (1956)124. Golenhofen, K., Arch. ges. Physiol., 266, 665 (1958)125. Gollan, F., and Nelson, I. A., Proc. ~oc. Exptl. Biot. Med., 95~ 485 (1957)126. Gollan, F., Rudolph, G. G., and Olsen, N. S., Am. J. Physiol., 189, 277 (1957)127. Good, A. L., and Sellers, A. F, Am. J. Physiol., .188~ 447 (1957)128. Good, A. L., and Sellers, A. F., Am. J. Physiol., 188, 451 (1957)129. Graf, W., and Graf, K., Acta Physiol. Scand., 41~ 140 (1937)130. Grant, W. L., S. African Mech. Eng., 6, 109 (1956)131. Grayson, J., and Mendel, D., J. Physiol. (London), 133, 334 (1956)132. Haddy, F. J., Fleishman, M., and Scott, J. B., Jr., Circulation Research, 5~ 58

(1957)133. Hahn, P., Physiol. Bohemosloven., 5~ 291 (1956)134. Hahn, P., K~e~ek, J., and Kt~e~kov~l, J., Physiol. Bohemosloven., 5, 283 (1956)135. Hale, F. Q., Westland, R. A., and Taylor, C. L., J. Appl. Physiol., 12~ 20 (1958)136. Hale, H..B., Sayers, G., Sydnor, K. L., Sweat, M. L., and Van Fossan, D. D.,

J. Clin. Invest., 36, 1642 (1957)137. Hall, J. F., Jr., and Polte, J. W., J. Appl. Physiol., 8~ 539 (1955/36)138. Hammel, H. T., Am. J. Physiol., 182, 369 (1953)139. Hammel, H. T., J. Mammal., 37, 37~ (1956)140. Hannon, J. P., J. Appl. Physiol., 12, 211 (1938)141. Hannon, J. P., Proc. Soc. ExplI. Biol. Med., 97, 368 (1958)142. Hannon, J. P., Am. J. Physiol., 192, 253 (1958)143. Harmon, J. P., and Covino, B. G., Am. J. Physiol., 192, 121 (1958)144. Hansen, A. T., Haxholdt, B. F., Husfeldt, E., Lassen, N. A., Munch, O.,

S~rensen, H. R., and Winkler, K., Scand. Y. Clin. & Lab. Invest., 8~ 182 (1956)145. Hardenbergh, E., and Bamberg, P. G., Am. Y. Physiol., 188, 461 (1957)146. Hardy, J, D., Hammel, H. T., and Murgatroyd, D., Y. Appl. Physiol., 9~ 257

(1956)147. Hardy, J, D., Stoll, A. M., Cunnlngham, D., Benson, W. M., and Greene, L.,

Am. J, Physiol., 189, 1 (1957)148. Hart, J. S., Rev. can. biol., 16, 133 (1957)149. Hellman~, K., Collins, K. J., Gray, C. H., Jones, R. M., Lunnon, J. B., and

Weiner, J. S., J, Endocrinol., 14~ 209 (]956)150. Hellon, R. F., and Lind, A. R., J. Physiol. (London), 133~ 132 (1956)


Ann

u. R

ev. P

hysio

l. 19

59.2

1:91

-116

. Dow

nloa

ded

from

arjou

rnals.

annu

alrev

iews.o

rgby

Uni

vers

idad

Nac

iona

l de

Colo

mbi

a-se

de M

edel

lin o

n 10

/20/

06. F

or p

erso

nal u

se o

nly.

112 HENSEL

151. Hellon, R. F., and Lind, A. R., J. Physiol. (London), 141, 262 (1958)152. Hemingway, A., and Birzis, L., J. Appl. Physiol., 8, 577 (1955/56)153. Hendler, E., Crosbie, R., and Hardy, J. D., J. Appl. Physiol., 12, 177 (1958)154. Henneman, D. H., Bunker, J. P., and Brewster, W. R., Jr., J. Appl. Physiol.,

12, 164 (1958)155. Hensel, H., Ergeb. Physiol., biol. Chem. u. exp. Pharmakol., 47, 166 (1952)156. Hensel, H., Arch. ges. Physiol., 257, 371 (1953)157. Hensel, H., Z. vergleich. Physiol., 37, 509 (1955)158. Hensel, H., Arch. ges. Physiol., 263, 48 (1956)159. Hensel, H., Arch. ges. Physiol., 264, 228 (1957)160. Hensel, H., and Krfiger, F. J., Arch. ges. Physiol., 268, 72 (1958)161. Hensel, H., and Zotterman, Y., J. Neurophysiol., 14, 377 (1951)162. Hertzman, A. B., J. Appl. Physiol., 10, 242 (1957)163, Hiestand, W. A., Stemler, F. W., and Jasper, R. L., Proc. Soc. Exptl. Biol. Med.,

88, 94 (1955)164. Hillermann, J. P., and Wilson, W. O., Am. J. Physiol., 180, 591 (1955)165. Holub, A., Forman, Z., and Je~kov~., D., Nature, 180~ 858 (1957)166. Hong, S. K., Am. J. Physiol., 188~ 137 (1957)167. Horvath, S. M., Radcliffe, C. E., Hurt, B. K., and Spurr, G. B., J. Appl.

Physiol., 8, 145 (1955/56)168. Horvath, S. M., Spurt, G. B., Hurt, B. K., and Hamilton, L. H., J. Appl.

Physiol., 8, 595 (1955/56)169. Hsieh, A. C. L., and Carlson, L. D., Am. J. Physiol., 190, 243 (1957)170. Hsieh, A. C. L., Carlson, L. D., and Gray, G., Am. J. Physiol., 190, 247 (1957)171. Hiigin, F., and Verz~tr, F., Gerontologia, 1~ 91 (1957)172. Iampietro, P. F., Bass, D. E., and Buskirk, E. R., J. Appl. Physiol., 10, 398

(1957)173. Iampietro, P. F., Buskirk, E. R., Bass, D. E., and Welch, B. E., J. Appl.

Physiol., 11, 349 (1957)173a. Iggo, A., J. Physiol. (London), 143, 47P (1958)174. Imig, C. J., Roberson, W. J., and Hines, H. M., Am. J. Physiol., 186, 35 (1956)175. Irving, L., and Hart, J. S., Can. J. Zool., 35, 497 (1957)176. Irving, L., Schmidt-Nielsen, K., and Abrahamsen, N. S. Ft., Physiol. Zo~l., 30,

93 (1957)177. Itoh, S., Nagoya J. Med. Sci., 19, 239 (1957)178. Itzhaki, S., and Wertheimer, E., Circulation Research, 5~ 451 (1957)179. Jacquez, J. A., Huss, J., McKeehan, W., Dimitroff, J. M., and Kuppenhelm,

H. F., J. Appl. Physiol., 8, 297 (1955/56)180. Jaequez, J. A., Kuppenheim, H. F., Dimitroff, J. M., McKeehan, W., and Huss,

J., J. Appl. Physiol., 8, 212 (1955/56)181. Kandror, I. S., and Rapoport, K. A., Fiziol. Zhur. S.S.S.R., 43, 60 (1957)182. Kanter, G. S., Am. J. Physiol., 188, 443 (1957)183. Kanter, G. S., and Lubinski, R. H., Am. J. Physiol., 180, 559 (1955)184. Kantner, M., Acta Neuroveget. (Vienna), 15, 223 (1957)185. Kanwisher, J. W., Biol. Bull., 109, 56 (1955)186. Kanwisher, J., and Leivestad, H., Norweg. Whaling Gazette, 1~ 1 (1957)187. Kassenaar, A. A. H., Lameyer, L. D. F., and Querido, A., Acta Endocrinol., 21~

37 (1956)188. Kaufmann, W., Thauer, R., and Z611ner, G., Arch. ges. Physiol., 261, 189 (1955)189. Kayser, C., Rev. can. biol., 16, 303 (1957)


Ann

u. R

ev. P

hysio

l. 19

59.2

1:91

-116

. Dow

nloa

ded

from

arjou

rnals.

annu

alrev

iews.o

rgby

Uni

vers

idad

Nac

iona

l de

Colo

mbi

a-se

de M

edel

lin o

n 10

/20/

06. F

or p

erso

nal u

se o

nly.

HEAT AND COLD 113190. Kayser, C., Arch. sd. physiol., 11, 7 (1957) 191. Kayser, C., Coraboeuf, E., and Gargouil, ., Compt. rend. soc. biol., 150, 1789

(1957)192. Keatinge, W. R., J. Physiol. (London), 139, 497 (1957)193. Kerslake, D. McK., J. Physiol. (London), 127, 280 (1955)194. Krelder, M. B., and Buskirk, E. R., J. Appl. Physiol., 11, 339 (1957)194a. Kuhn, W., Helv. Chim. Acta, 39, 1071 (1956)195. Kundt, H. W., Brt~ck, K., and Hensel, H., Arch. ges. Physiol., 264, 97 (1957)196. Kundt, H. W., Brtick, K., and Hensel, H., Naturwissenschaften, 44, 496 (1957)197. Kuno, ., Human Perspiration, (Charles C Thomas, Publisher, Springfield, Ilk,

416 pp., 1956)198. Kyle, R. H., and Kirby, C. K., Arch. Surg., 74, 136 (1957)199. Ladell, W. S. S., J. Physiol. (London), 127, 11 (1955)200. LAllemand, H., Brendel, W., and Usinger, W., Anaesthesist, 4, 36 (1955)201. Landgren, S., Acta Physiol. Scand., 40, 202 (1957)202. Landgren, S., Acta Physiol. Scan&, 40, 210 (1957)203. LeBlanc, J. A., J. Appl. Physiol., 9, 395 (1956)204. LeBlanc, J. A., J. Appl. Physiol., 10, 281, (1957)205. LeBlanc, J. A., and Rosenberg, F. J., d. Appl. Physiol., 11, 344 (1957)206. LeBlanc, J. A., and Rosenberg, F. J., Proc. Soc. Exptl. Biol. Med., 96, 234 (1957)207. Lee, D. H. K., King Ranch Centennial Conference: Breeding beef cattle for un-

favorable environments, 21 (University of Texas Press, Austin, Tex., 1955)208. Lee, D. H. K., Europ. Assoc. Animal Production, Publ. No. 5, Gen. Rept. No. 1,

7 (1957)209. Lee, D. H. K., Climate and Economic Development in the Tropics (Harper

Brothers, New York, N. Y., 1957)210. Leldlg, R., and Gray, G. M., Am. J. Physiol., 188, 507 (1957)211. Lele, P. P., J. Physiol. (London), 126, 191 (1954)212. Lele, P. P., Weddell, G., and Williams, C. M., J. Physiol. (London), 126, 206

(1954)213. Levitt, J., in Protoplasmalogia, Handbuch der Protoplasmaforschung, 8, Part 6

(Springer-Verlag, Vienna, Austria, 100 pp., 1958)214. Lichton, I. J., J. Appl. Physiol., 11,422 (1957)215. Lim, P. K., and Grodins, F. S., Am. J. Physiol., 180, 445 (1955)216. Lind, A. R., and Hellon, R. F., J. Appl. Physiol., 11, 35 (1957)217. Lind, A. R., Hellon, R. F., Weiner, J. S., and Jones, R. M., Brit. J. Ind. Med.,

12, 296 (1955)218. Lovelock, J. E., and Smith, A. U., Proc. Roy. Soc. (London), 145, 427 (1956)219. Lyburn, St. John E. F. J. Physiol. (London), 134, 207 (1956)220. Lynch, H. F., and Adolph, E. F., J. Appl. Physiol., 11, 192 (1957)221. MacFarlane, W. V., Med. J. Australia, 43. Vol. II. 139 (1956)222. Malmejac, J., Plane, P., and Bogaert, E., Compt. rend., 242, 2764 (1956)223. Marshall, J. M., Circulation Research, 5, 664 (1957)224. Marshall, J. M., and Williams, E. M. V., J. Physiol. (London), 131, 186 (1956)225. Maruhashi, J., Mizlguchi, K., and Tasakl, I., J. Physiol. (London), 117, 129

(1952)226. Masoro, E. J., Asuncion, C. L., Brown, R. K., and Rapport, D., Am. J. Physiol.,

190, 177 (1957)227. Masoro, E, J., Felts, J. M., and Panagos, S. S., Am, J. Physiol., 189, 479 (1957)


Ann

u. R

ev. P

hysio

l. 19

59.2

1:91

-116

. Dow

nloa

ded

from

arjou

rnals.

annu

alrev

iews.o

rgby

Uni

vers

idad

Nac

iona

l de

Colo

mbi

a-se

de M

edel

lin o

n 10

/20/

06. F

or p

erso

nal u

se o

nly.

114 HENSEL228. Masoro, E. J., Panagos, S. S., Cohen, A. I., and Rapport, D., Am. J. Physiol.,

186, 24 (1956)229. Masterton, J. P., and Lewis, H. E., Brit. J. Nutrition, 2, 346 (1957)230. Matiushklna, N. A., Fiziol. Zhur. S.S.S.R., 42, 939 (1956)231. Matsuda, K., Hoshi, T., and Kameyama, S., TOhoku J. R.xptl. Med., 63, 318

(1956)232. Mayor, G. E., Harder, R. A., McEvoy, R. K., McCoord, A. B., and Mahoney,

E. B., Am. J. Physiol., 185, 515 (1956)233. McCance, R. A., Ungley, C. C., Crosfill, J. W. L., and Widdowson, E. M.,

Med. Research Council (Brit.), Spec. Rept. Ser., 291, 1 (1956)234. McMurrey, J. D., Bernhard, W. F., Taren, J. A., and Bering, E. A., Jr., Surg.,

Gyneeol. Obstet., 102~ 75 (1956)235. Meehan, J. P., Alaskan Air Command, Arctic Aerom. Lab., Ladd Air Force Base,

Proj. No. 7-7951, Rept. No. g (1955)236. Meryman, H. T., Science, 124, 515 (1956)237. Meryman, l-I. T., Physiol. Revs., 37, 233 (1957)238. Miller, A. T., Jr., and Blyth, C. ~., J. Appl. Physiol., 12, 17 (1958)239. Mills, A. W., J. Appl. Physiol., 9, 447 (1956)240. Morales, P., Carbery, W., Morello, A., and Morales, G., Ann. Surgery, 145, 488

(1957)241. Mtiller, E. A., and Wenzel, H.-G., Intern. Z. angew. Physiol., 16, 373 (1957)242. Murray, R. W., Nature, 176, 698 (1955)243. Murray, R. W., J. Exptl. Biol., 33, 798 (1956)244. Murray, R. W., Nature, 170, 106 (1957)245. Niazi, S. A., and Lewis, F. J., y. Appl. Physiol., 10, 137 (1957)246. Nicholls, D., and Rossiter, R. J., Am. J. Physiol., 187, 11 (1956)247. Nicolai, L., Arch. ges. Physiol., 263, 453 (1956/57)248. Nicolai, L., Arch. ges. Physiol., 266, 308 (1958)249. Osiba, S., Japan. J. Physiol., 7~ 355 (1957)250. Otis, A. B., and Jude, J., Am. J. Physiol., 188, 355 (1957)251. Pearcy, M., Robinson, S., Miller, D. I., Thomas, J. T., Jr., and DeBrota, J.,

J. Appl. Physiol., 8, 621 (1955/56)252. Petrunj, N. M., Doklady Akad. Nauk S.S.S.R., 111, 228 (1956)253. Pichotka, J., H6fler, W., and Reissner, J., Arch. exptl. Pathol. u. Pharmakol.,

Naunyn-Schmiedebergs, 223, 217 (1954)254. Precht, H., Christophersen, J., and Hensel, H., Temperatur und Leben (Springer-

Verlag, Berlin, GCttingen, Heidelberg, Germany, 514 pp., 1955)255. Ralll, E. P., Kuhl, W. J., Jr., Gershberg, H., Beck, E. M., Street, E. R., and

Laken, B., Metabolism, Clan. and Exptl., ~, 170 (1956)256. Randall, W. C., Cox, J. W., Alexander, W. F., Coldwater, K. B., and Hertzman,

A. B., Y. Appl. Physiol., 7, 688 (1954/55)257. Raths, P., Z. Biol. 110, 62 (1958)258. Redisch, W., Tangco, F. T., Wertheimer, L., Lewis, A. J., and Steele, J. M.,

Circulation, 15, 518 (1957)259. Reissmann, K. R., and Kapoor, S., Am. J. Physiol., 184, 162(1956)260. Rennle, D. W., and Adams, T., J. Appl. 29hysiol., 11~ 201 (1957)261. Riberl, A., Siderys, H., and Shumacker, H. B., Jr., Ann. Surg., 143, 216 (1956)262. Richards, J. B., and Egdahl, R. H., Am. Y. Physiol., 186, 435 (1956)263. Riley, P. A., Jr., Mixon, B. M., Jr., and Barila, T. G., Surgery, 42, 936 (1957)


Ann

u. R

ev. P

hysio

l. 19

59.2

1:91

-116

. Dow

nloa

ded

from

arjou

rnals.

annu

alrev

iews.o

rgby

Uni

vers

idad

Nac

iona

l de

Colo

mbi

a-se

de M

edel

lin o

n 10

/20/

06. F

or p

erso

nal u

se o

nly.

HEAT AND COLD 115

264. Robinson, K. W., Howard, B., and MacFarlane, W. V., Med. J. Australia, 42,II, 756 (1955)

265. Robinson, K. W., and MacFarlane, W. V., Australian J. Biol. Sci., 9, 130 (1956)266. Robinson, K. W., and MacFarlane, W. V., J. Appl. Physiol., 12, 13 (1958)267. Robinson, S., Maletich, R. T., Robinson, W. S., Rohrer, B. B., and Kunz,

A. L., J. Appl. Physiol., 8, 615 (1955/56)268. Rodahl, K., Alaskan Air Command, Arctic Aeromed. Lab., Ladd Air Force Base,

Tech. Rept. 57-21 (1957) 269. Rodahl, K., and Bang, G., Alaskan Air Command, Arctic Aeromed. Lab., Ladd

Air Force Base, Tech. Rept. 57-36 (1957)270. Rodahl, K., and Rennie, D. W., Alaskan Air Command, Arctic Aeromed. Lab.,

Ladd Air Force Base, Proj. 8-7951, Rept. 7 (1957)271. Roddie, I. C., and Shepherd, J. T., Clin. Sci., 15, 433 (1956)272. Roddie, I. C., and Shepherd, J. T., J. Physiol. (London), 131,657 (1956)273. Roddie, I. C., Shepherd, J. T., and Whelan, R. F., J. Physiol. (London), 134,

444 (1956)274. Roddie, I. C., Shepherd, J. T., and Whelan, R. F., J. Physiol. (London), 136,

489 (1957)275. Roddie, I. C., Shepherd, J. T., and Whelan, R. F., J. Physiol..(London), 138,

445 (1957)276. Roddle, I. C., Shepherd, J. T., and Whelan, R. F., Clin. Sci., 16, 67 (1957)277. Sarajas, H. S. S., Am. Heart J., 51, 298 (1956)278. Sarajas, H. S. S., Nyholm, P., and Suomalalnen, P., Nature, 181,.612 (1958)279. Schmldt-Nielsen, B., Schmldt-N[elsen, K., Houpt, T. R., and Jarnum, S. A:,

Am. J. Physiol., 185, 185 (1936)280. Scholander, P. F., van Dam, L., Kanwlsher, J. W., Hammel, H. T., and Gordon,

M. S., J. Cellular Comp. Physiol., 49, 5 (1957)280a. Scholander, P. F., Hammel, H. T., Hart, J. S., .LeMesurier,. D. H., and

Steen, J., J. Appl. Physiol., 13, 211 (1958)281. Scholander, P. F., Hammel, H. T., Lange Andersen, K., and Leyning, Y.,

J. Appl. Physiol., 12, 1 (1958)282. Scholander, P. F., and Krog, J., J. Appl. Physiol., 10, 405 (1957)283. Scholander, P. F., Lange Andersen, K., Krog, J., Vogt Lorentzen, F., and

Steen, J., J. Appl. Physiol., 10, 231 (1957)284. Schreider, E., Nature, 179, 915 (1957)285. Schwartz, I. L., and Thaysen, J. H., J. Clin. Invest., 35, 114 (1956)286. Segar, W. E., Riley, P. A., Jr.; and Barila, T. G., Am. J. Physiol., 185, 528 (1956)287. Sellers, E. A., and You, R. W., Brit. Med. J., 1, 815 (1956)288. Severinghaus

annurev.ph.21.030159

Documents

heat capacity of living

heat exc

skin surface

heat transfer of living

used skin temperature

radiant temperature

general problems of

thermal properties