1225

catheter was reaspirated without blood. Thus the renalcirculation had completely ceased. Shortly after theremoval of the catheter the patient recovered fromshock.

We have no knowledge of the oxygen content of thearterial blood of this patient before shock, but we haveno reason to assume it was not normal. The oxygenof the venous blood both in the right auricle (8-51) andin the renal vein was normal. The sudden and sharprise of the venous oxygen and bicarbonates duringshock can be explained only by a striking readjustment ofthe renal circulation during shock. The following ratioserves to explain the exclusion of the functional renaltissue in shock when the circulation through the kidneyis maintained :

Renal arteriovenous difference in 00. x blood-flow.

Renal arteriovenous difference in 0. x blood-flow.

No other explanation seems possible than the presencem the human kidney, under conditions of shock, of ashunt such as that described by Trueta and his associates-an arrangement whose existence in man has beendoubted.The complete suppression of the blood-flow through

the renal vein at the more severe stages of shock seemsto accord with Van Slyke’s concept of the sacrificeof the renal circulation. We are not in a position toexplain the levels of extraction of Na and K, but wemust remark that the latter appeared in a slightly higherconcentration in the blood of the renal vein, as if Khad been liberated by the anoxic tubular cells.In this case we were not able to detect spurting of the

renal venous blood, but in another patient under shockspurting was noted. In this case the arteriovenous

oxygen difference was normal.P. MÉRIELF. GALINIERJ. M. SUCM. DESANDRE.

Department of Clinical Medicine,Hôpital Purpan, Toulouse.

1. Wright, J. T. Quart. J. Med. 1955, 24, 95.2. Maynert, E. W., van Dyke, H. B. Pharmacol. Rev. 1949, 1, 217.

A BARBITURATE ANTAGONIST

F. H. SHAWN. E. W. MCCALLUM.University of Melbourne,

Australia.

SiR—When one of us (F. H. S.) replied to Dr. McElligott(April 16), the excellent article of Dr. Wright was notavailable for perusal. However, the statement (May 7)" that little barbiturate would remain in the body aftersix days " was not a generality but was based on theexperience of one of us (N. E. W. McC.) who has beenstudying barbiturate metabolism for some years past.Dr. Wright has found that phenobarbitone disappears

from the plasma at the rate of 15% per day and calcu-lates that after the ingestion of 72 grains of the com-pound, there would be 27 grains present at the end ofsix days. This calculation appears to imply that pheno-barbitone is removed from the body solely by renalexcretion, whereas it has been established that some

80% of administered phenobarbitone cannot be recoveredfrom the urine.In one of our patients who was known to have ingested

at least 100 grains of phenobarbitone, traces of com-

pounds showing a spectrophotometric absorption similarto barbiturate absorption were present in serum andurine eight days later. We have, however, spectro-photometric and other evidence which strongly suggeststhat phenobarbitone was not the only compound whichwas contributing to the absorption. This evidence wassupported in experiments with dogs.As we have said, it has been established that only some

20% of ingested phenobarbitone is excreted as such inthe urine.2 The larger proportion is metabolised in someunknown fashion, but from what we know of the destruc-tion of other barbiturates it is likely that the ring structureremains intact at first. We also have evidence that at

least one of the possible decomposition products ofphenobarbitone has an absorption similar to that of theparent substance. In view of the fact of such destructionof phenobarbitone in the body I would suggest thatsome of the material estimated spectrophotometrically byDr. Wright 1 is of metabolic origin. In other words, inthe absence of detailed knowledge of phenobarbitonemetabolism the results of analyses obtained by spectro-photometric methods should be interpreted with caution.

Also we do not agree that the worth of new barbiturate

antagonists can be evaluated by a measurement of druglevels in the blood. The only test is the pragmatic one ofa lessening of the duration of coma and the mortality-rate. The suggestion that barbiturate intoxication isbest treated by conservative methods will be the subjectof another paper.

3. Counihan, T. B., Evans, B. M., Milne, M. D. Clin. Sci. 1954,13, 583.

4. Maren, T. H., Wadsworth, B. C., Yale, E. K., Alonso, L. G.Bull. Johns Hopk. Hosp. 1954, 95, 277.

ELECTRIC BLANKETS

AUSTIN STRUTT.Home Office,

London, S.W.1.

SIR,-The attention of the Standing Interdepart-mental Committee on Accidents in the Home, of whichI am Chairman, has been drawn to the letter by Dr.Maddison in your issue of April 16, giving directions formaking an electric blanket. The committee think itdesirable that your readers should be warned thatblankets of this kind may be dangerous unless certainprecautions are taken, which Dr. Maddison would nodoubt have wished to mention, had space permitted.These include the incorporation of thermostats and

secondary fuses as a protection against overheatingand the use of a transformer embodying a safeguardagainst a fault developing between the primary andsecondary windings, which would otherwise have theeffect of making the blanket live at mains voltage.

In addition it should be borne in mind that the

repeated folding of conductors of the type suggestedwould in time cause deterioration of the insulation and

breaking of the conductors themselves, giving rise torisk of burns and shock.

Since considerable technical experience is necessaryto make the above precautions effective it may be unwisefor anyone without proper qualifications to attempt theconstruction of an article which requires highly specialisedknowledge for its successful production.

DIURESIS FROM CARBONIC ANHYDRASEINHIBITION

SiR,-Your leader of April 2 was remarkable in its

scope and balance, and certainly represents the bestavailable statement in this complex and controversialfield. May I be permitted a few comments on severalof the technical questions raised ?

(1) The maximal rate of HC03 excretion following acetazo-leamide (’ Diamox ’) may show a logarithmic relation to dose,but this is only in the range 0-1 mg. per kg. to 5-0 mg. perkg.3 4 Above this range and at clinical levels the dose-responsecurve is flat; there is little difference between HCÛ3- excretionrates following 5 or 100 mg. per kg. orally.4 This suggeststhat inhibition of renal carbonic anhydrase is essentiallycomplete at the therapeutic dose range of 5-10 mg. per kg.The total amount of bicarbonate excreted after a single dose,however, is a function of dose in the 5-100 mg. per kg. range,since the dose determines the duration and hence the finalmagnitude of effect.

(2) The diuretic effect of acetazoleamide is not necessarilydependent on plasma HCû3- concentration in the range12-22 m.eq. per litre. Lowering of plasma HC03 by hyperven-tilation or by a moderate single dose of acetazoleamide itselfdoes not block the renal response, since in these situations