ALTHOUGH CURARE has come into wide use a general anaesthesia, the problem of reversing il There is no doubt that neostigmine is antagoni, depolarizing neuromuscular blockad@ but ma with Foldes -~ that the safest course is to assist tion is inadequate at the conelusion of operat only with hesitancy and in small doses, if it is us ; a relaxant in conjunction with s effects has not yet been solved. tie to curare and can reverse nonay anaesthesiologists would agree :espiration if tl~e patient's ventilaon. Neostigmine bromide is used ~d at all. We have, therefore, attempted to study the effects of relatively large doses of atropine and neostigmine upon the heart to d~termine whether this unquestionably useful technique may be safely employed. HISTOIRYThe first reports of death associated with tt~e administration of atropine and neostigmine appeared in the British literatnr~in 1949. 3'4,5 In these three eases, ! eardiovascular collapse followed very shortly after the administration of neostigrnine and atropine. The doses were 2.5 mg. neos;tigmine with 0.65 rag. atropine, 3 2.0 rag. neostigmine with 0.65 rag. atropine, 4 and, in a 3-kg. infant, 0.25 rag. neostigmine with 0.-o2 mg. atropine. ~ In cacti case the two drugs were given simultaneously.Shortly afterward, Bain and Broadbent 6 postulated the mechanism of these deaths, pointing out that atropine can cause an increase in cardiac vagal tone centrally before it causes a decrease in tone peripherally. Thus, they said, instead of preventing neostigmine's undesirable effects, atropine may potentiate the N. Moreover, they felt atropine would have,little effect on a neostigmine-indueed bradyeardia because "the peripheral anti-aeetyleholine effects of atropine take some 20 to 30 minutes to become fully established." The authors admitted, however, that they were speaking of subcutaneous doses of atropine and had "no experience" with the effects of intravenous administration.Since neostigmine has been implicated,in other eases of cardiac arrest] ,s it is easy to see how the current dis~-ust of thi~ agent came about. There is a considerable body of evidence, on the other hand; which makes this view hard for some investigators to accept. In the first place, studies involving the intravenous administration of atropine in man show that there is no central vagal stimulating effect; the pulse rate rises and reaches its maximum in 3 to 5 minutes. 9 Hunter 1~ found that when atropine and neostigmine were administered together intravenously the pulse rate rose to a peak within 5 minutes ~nd then fell slowly, the greatest ~Department
HYPERGLYCAEMIA has long been recogmzed as one of. the chmf responses to the metabohc stress of anae~thesaa Dlethyl ether especmlly will produce increases 1 n the blood sugar of ut to 100 per cent during the fllrst half-hour to 45 minutes o[~anaeskhesaa and for th~s reason ats effect on carbohy[drat{, metabohsm has been s~Ldled extensively 1 Experiments done on dogs m th~l' 192,0 s seemed to mdmate that thus hyperglycaemm was related to, or caused by, a profound metabohe aeLdosls which appeared qmte early during the adm~l~astratmn of ether 2 a 4 This e:cplanaaon was w,~dely accepted as applying to man until Beecher and his co-workers demonstrated that ~her~ is no slgmficant metabohe acidosis during the admmastrahon of efher to adults, although some degree of acidosis does occur m children 5 e Prior to Beecher's reports, at hgd been shown m rabbats that both adrenalectom)i and spinal anaesthesaa prelducmg a T4 sensory level woutd protect against hyperglycaemaa during ether anaesthesm 7 This observation has been confirmed repeatedly by the use of beth local anaesthetms and a,drenergm blocking agents s 0 Today, therefore, it ~as generally concluded that ihe hyperglycaemm produced by ether anaesthesm as mostly the result of the hberatton of catecholammes ~oOther general anaestheaes are also capable of p~loduemg a hyperglycaemm l esponse Cyclopropane anaesthesm m man cheats an increase m the Mood sugar %ompa~able to that reduced by ether" according to Greene al Reports concernmg "the effect of halothane are somewhat davergent Some studms have shown no effect on blood sugar during halothane anaesthe,,m, while other evaluatmns have shown that there as some hype~:glycaemm response to halothane m This, however, as not as great as that seen wath ether and cyelopropane ~ ~4 It is of anterest to note that the hyperglycaem~a produced by these agents seems to para~el thear effect on sympathetic actrvlty, for~ at has been shown that both ether and cyclowopane produce a marked increase m the level of circulating cateeholammes, wh~le halothane does not ~5 Methox),flurane combines some of the structural and anaesthetm charactenstacs of both dlethyl ether and halothane, smee at as a halogenated methyl ethyl e~mr Its effect on carbohydrate metabohsm, however, has not yet been studmd care}ully In one early report of a chmeal trml of methoxyflu~ane in 20~ patmnts the b]ood sugar was measured an ~ In 8 of these a moderate rise of about 85 mg ~g occurred 1~ Another study with dogs indicated that Mood sugar was unchanged during spontaneous respiration but decreased wath a~s~sted resp~ratmn ~7 ~From the Department of Anesthesiology, 'The Umverslty of Mmhlgan MedmaI School, Veterans Administration Hospital, Ann Arbor, Michigan 7 Can Anaes S~c J, vo] 11, no 1, Jam~ary, !964
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