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through the water for long distances with the same governedair exchange and conservation of energy.

LORNA LAKE.Paddington and Kensington Chest Clinic,

14, Newton Road,London, W.2.

EFFECT OF ’MILTON’ ON CANCER CELLS

SiR,—The article by Mr. Oates and his colleagues 1deserves comment in view of differences between their findingsand our earlier ones.2 They concluded that Milton ’ was aneffective anti-tumour-cell irrigant for subcutaneous wounds,but produced evidence that, in the system they used, it

appeared to enhance tumour growth after intraperitonealadministration. There were, however, several variations inmethod which should be considered in comparing theirresults with ours. Firstly, they used the Walker 256 carcino-sarcoma in rats, and we used the Ehrlich ascites tumour inmice. Most of the reports of enhanced peritoneal " take "with halogenated compounds have been based on the use ofthe Walker 256 tumour or the Guerin adenocarcinoma,3 4and the generality of these results has not been established.Secondly, they diluted the milton with sodium bicarbonatesolution, and not with water as recommended by the manu-facturers ; thirdly, they used intraperitoneal rather than etheranaesthesia, and there is a possibility of interaction betweenanaathetic and irrigant-these two points may seem improbableexplanations of the differences between their results and ours,but they should none the less have been considered.There is no doubt that the tumour " take " reported by

Mr. Oates and his colleagues was greater in hypochlorite-treated animals than in controls, even though no statisticalanalysis of the results was provided. It should be pointed out,however, that all the experiments in our paper and not onlythose on irrigation, were with intraperitoneal inoculation.Under these conditions a significant prolongation of survivaland delay in tumour onset was observed in treated animals.This raises the possibility that the Walker 256 carcinosarcomain the rat does not behave the same, with hypochlorite treat-ment, as the Ehrlich ascites tumour in the mouse. Evidenceof a variation between the 2 systems is in fact provided byMr. Oates and his colleagues in their table VI, which fails toshow any significant difference in " take rate betweenmilton-treated mice and controls (x2 = 0-2372 for 1 degree offreedom); apart from being at variance with our findings,2this difference is also at variance with their own findings ofan increased " take " rate with the Walker 256 tumour.

We used the Ehrlich ascites tumour as a system to test the

capacity of milton against free tumour cells, rather than as aspecific model of intraperitoneal cancer spread in humansurgery. The continued study of milton was advocated incancer surgery in general, and not, as erroneously cited byMr. Oates and his colleagues, in abdominal cancer surgery inparticular. We concluded that milton did have an anti-tumour-cell effect, and this was confirmed by the results of Mr. Oatesand his colleagues in their subcutaneous system. We agreethat, in the present state of indecision, milton should not beused as a peritoneal irrigant until it can be determinedwhether enhancement of tumour " take " is observed generallyin animal tumours, or whether it occurs in only a few typesof experimental cancer.

Finally, it is regretted that Mr. Oates and his colleaguesallowed their discussion of the intraperitoneal effects ofmilton irrigation to obscure their own finding that, for othertypes of cancer surgery, a cheap, stable, and effective hypo-chlorite irrigant is now available.

P. C. VINCENTT. S. REEVEANNETTE NICHOLLS.

Wellcome Research Laboratories,Royal North Shore Hospital,

Crows Nest,and Department of Surgery,

University of Sydney,New South Wales, Australia.

1. Oates, G. D., Mehigan, J. T., Hoppe, E. T. Lancet, 1965, i, 1241.2. Vincent, P. C., Reeve, T. S., Nicholls, A. Cancer, N. Y. 1964, 17, 997.3. Vernick, J. J., Magell, J., Hoppe, E. T. Surg. Forum, 1964, 15, 336.4. McKibbin, B., Gazet, J. C. Br. J. Surg. 1964, 51, 693.

THE NURSE’S LOAD

SIR,-The old proverb of the cobbler’s child being the worstshod has obviously had a parallel in the report that the nurse’sback seems to have been the least cared for. Your leadingarticle (Aug. 28) is a salutary reminder to the medical andnursing professions of the price that is paid in wear and tearof nurses’ backs. You rightly stress the awkwardness of thehuman body as a load, and the intolerable demands which areoften made by the physical environment and working equip-ment. Nursing staff are expected to lift and handle these loadsas routine.

The nurses’ attitude of " making do ", although aware ofthe stresses and strains imposed on them by their handlingtasks, is characteristic of their traditional devotion to duty andself-sacrifice. Cannot this " making do " be replaced by a farmore active policy of " loadproofing " during student training.This means that, in addition to improving designs of beds andequipment, the dissemination of knowledge of lifting andhandling methods should be accompanied by enlightenedpractical instruction. You cannot learn and practise safe liftingand handling by visual aids only; theoretical instruction shouldbe accompanied by spells of practical instruction in suitableclothing. The instructor should be well versed in the bodymechanics of handling, and the key factors of attention tostance, hold, and arm, neck, and spinal positions, with use ofbody-weight, should be emphasised.The importance of the relation of lumbar spine disorders to

heavy manual work and lifting was admirably presented byDr. Troup.l He pointed out the need for epidemiological studyof low-back disorders, and showed how the knowledge of thephysiology of lifting and similar heavy work was in its infancy.It does appear that the nursing profession would present anideal group for epidemiological study, and that their manualtasks would be valuable subjects for " job analysis ". AsDr. Troup claims, it is only by investigations of this type thatthe dangers inherent in some types of manual work can beproperly understood.

JOHN M. JACKSON.National Dock Labour Board,

Popple Street, Hull.

HALOTHANE

SIR,-Your leading article (Sept. 4) suggested that the cardiacarrhythmias of halothane anaesthesia were not in accord withaccepted aetiology, for you stated that " the distinction betweenrelatively innocent disturbances of cardiac rhythm of vagalorigin, such as nodal rhythm, and more serious indications ofventricular irritability may not have as sound a physiologicalbasis as it once appeared to have ".

It is known that the primary (sino-atrial [s.-A.]), the

secondary (atrioventricular [A.v.]), and the tertiary (ventricular)pacemakers of the heart are susceptible to the mutally anta-gonistic influences of the sympathetic and the parasympatheticnervous systems. Sympathetic (adrenergic) stimulation mayprovoke the A.v. node into pacemaker activity, which is usuallypreceded by S.-A. nodal tachycardia and followed by ventriculartachycardia when the stimulus is adequate. One of the criteriaby which the cause of an A.v. nodal rhythm is recognised duringanaesthesia is the fact that the rate of a nodal rhythm ofadrenergic origin is faster than the previous sinus-rate.Blockade of the &bgr;-adrenergic receptors with propranolol(’ Inderal’) protects the pacemakers from adrenergic stimuli,but exposes them to unopposed vagal inhibition. The ultimateeffect of vagal inhibition of the heart, which you describe as" relatively innocent", may be cardiac arrest in asystole.Vagal (cholinergic) inhibition of the heart usually causes A.v.

nodal escape at a rate which is slower than the previous sinus-rate. Atropine insulates the pacemakers from the vagalinhibition, but exposes them to the effects of adrenergicstimuli, to which the tertiary centres are particularly susceptibleduring anaesthesia with " catecholamine sensitising

"

agents.The heart which is under the influence of propranolol andatropine is essentially denervated. Anaesthesia with halothane-

1. Troup, J. D. G. Lancet, 1965, i, 857.