276
Correspondence
If we accept that man is no different from other animals in this context, except perhaps in degree, then current views are correct, there’s an end to the matter and there is no need for ‘real evidence’. But I have the impression man, and especially a sick man, is not always the same as the experimental animal. Whilst oxygen breathing can produce very abnormal changes in lung function, this does not necessarily prove there is histological damage. The brain is depressed by anaesthetics, and the heart by &blockers, and lung function is often gravely impaired in status asthmaticus, without these organs being damaged. I accept as Dr Smith says, we cannot ethically obtain the histological information in healthy volunteers to resolve this argument. Accepting that excessive oxygen can, indeed, produce lung damage, the crucial question remains, which is more important, arterial oxygen or the inspired oxygen fraction? Dr Smith cites work which incriminates the F I O ~ as the dominant factor. My argument was based on admittedly earlier work which blames the Pao2.1*2 There is also evidence that the primary lesion is in the capillary ~ a l l l . as ~ *in~retrolental fibroplasia, and not in the alveolus. In retrolental fibroplasia the arterial and not the alveolar arterial oxygen tension is the crucial factor, and experimentally (sic) hypoxaemia is protective.s If the damaged lung is somewhat resistant to oxygen poisoning, is this because the venous end of the well-ventilated capillary contains markedly desaturated blood, or is it because damage in the susceptible well-perfused,
well-ventilated areas is masked by non-susceptible areas with other types of damage? I was until recently unaware of work by Kapanci and his colleagues,6 which strongly supports the view that excessive oxygen does, indeed, produce damage in healthy human lung, which seems to settle one of these issues. On the other hand, has the incidence of so-called ’respirator lung’ fallen with the recent avoidance of excessive oxygen therapy, one of the factors previously blamed? National Heart Hospital, Westmoreland Street, London, W I M 8BA
ALANGILSTON
References
oxygen toxicity at atmospheric pressure, Acra Medico Srandinaricn, Suppl. 1, loo.
1. OHLSSON, W.T. (1947) A study of
2. BENDIXEN, H.H., EGBERT, L.D., HEDLEY-WHYTE, J.. LAVER, M.B. & PONTOPPIDAN, H. (1965) Respiratory Care, Ch. 14. C.V. Mosby, St Louis. 3. PRATT,P.C. (1965) The reaction of the human lung to enriched oxygen atmosphere. Annals New York Academyof Sciences, 121,809. 4. STAUB,N.C. (1969) Respiration. Annual Rerieiv of Physiology, 31, 173. 5. YANAFF, M., MILLER, W.W. & WALDHAUSEN, J.A. (1970) Oxygen poisoning of the eyes, Archirw o / Oprhalmology, 84,627. 6. KAPANCI,Y., Tosco, R . , EGGERMAN, J . & GOULO, V.E. (1972) Oxygen pneumonitis in man: Light and, electron microscopic morphometric studies. Chesr. 62, 162.
A new museum of anaesthesia During the past year the Department of Anaesthesia at St Bartholomew’s Hospital, London, has been assembling a collection of historic anaesthetic apparatus. The collection is now on display in the Department’s own lecture theatre which was, until the Second World War, an operating theatre; it is the place in which Boyle and Langton Hewer unpacked and then used the first Boyle anaesthetic machine early in the spring of 1917. This collection is not intended to duplicate the Charles King Collection or any other museum of anaesthetic apparatus. Its purpose is to illustrate the continuing process of evolution of anaesthetic equipment from the early days right up to the present time. All forms of apparatus are included from intravenous needles to ventilators and from airways to vapourisers; there is also a selection of early
textbooks on anaesthesia. Due to the interest and generosity of many doctors throughout the United Kingdom the Department has already acquired many fascinating and unique specimens. However, a collection such as this can never be complete and any old apparatus no longer in use (regardless of its condition) and textbooks of any age would be welcome for inclusion in the museum. I believe that it is only by assembling such a collection that irreplaceable pieces of apparatus and textbooks will be preserved for the benefit of present day anaesthetists and for the future. Department of Anaesthesia, D.J. WILKINSON St Bartholomew’s Hospital, London ECI A 7BE
Plasma lorazepam estimation in neonates Since publishing our method for the extraction and estimation of plasma lorazepam by gas-liquid
chromatography (Anaesthesia, 1977, 32, 767) it has become necessary to analyse samples from neonates.
Correspondence This means that only very small amounts of plasma are available for analysis, which led to a revision of our published method. In this modification 0.1 ml of plasma is added to 0.1 nil potassium chloride and extracted with 1.5 ml of benzene with 20 bI of the internal standard added. 1 ml of the benzene layer is evaporated to dryness reconstituted with 50pl benzene and 2.5 pl
271
injected into the chromatograph. This has produced analyses which compare favourably with the original method and has the added economic advantage. Department of Anaesthetics. P.J. HOWARI) The Queen’s Unii>ersirvof Belfast, W. TONER 97 Lisbirrn Road, Belfast BT9 7BL
Acute cardiac obstruction from a Bjork-Shiley valve It was with great interest we read Dr Gilston’s letter concerning acute cardiac obstruction from a BjorkShiley valve (Anaesthesia, 1977, 32, 810). However, in our experience the problem of the valve sticking has been due not to an inherent problem of the valve manufacture but due to chordae being trapped and jamming the valve from the ventricular side (one case) or a too-long suture end being trapped and
jamming the valve from the atrial side (one case). However, unlike the case described by Dr Gilston our cases occurred in the late postoperative stage and resuscitation was not successful. Groby Road Hospital, Croby Road, Leicester, LE3 9 Q E
I. MCLELLAN J.S. BAILEY
Anticholinesterase action of pancuronium There are plenty of papers about the relationship between anaesthesia and pseudocholinesterase, but little data is available concerning true cholinesterase. Recent investigations of Pilz’ focused attention on the existence of a specific acetylcholinesterase in human serum. Its activity must be differentiated from that of the unspecific cholinesterases’ which can be altered by quite different diseases3 In a previous in vitro study pancuronium was found to inhibit red cell and brain ch~linesterase.~ Attempts have been made by theauthor of the letter to observe the behaviour of the serum acetylcholinesterase, since this variant of the acetylcholinesterase is easier to be determined. The data obtained are presented as a letter to the editor since the validity of the Pilz method is still much debated. A group of forty-three patients was anaesthetised by thiopentone and halothane and received a full apnoeic dose of pancuronium both for tracheal intubation and for the surgical requirements. A similar group was anaesthetised in the same way, but without a muscle relaxant. The serum acetylcholinesterase activity was found to be depressed at 15 min. and the levels remained low for 10 h. The changes were not significant statistically, but the reduction was more pronounced in the group receiving pancuronium. These findings suggest an additive antiacetylcholinesterase action of pancuronium. This action
could probably explain the clinical observation that in patients anaesthetised using pancuronium as the only muscle relaxant a more pronounced degree of miosis is to be o b s e r ~ e d . ~ University Hospital, Cluj-Napoca, Romania
EMILCARDAN
References 1. PILZ,W. (1959) Untersuchungen iiber Fermente des menschlichen Blutes. I l l . Zur vermeintlichen
Identitat der Acethylcholin und Tributir in spaltenden Fermente des menschlichen Serums. Zeitschri/i fur die gesamte experimentelle Medizin, 132, 3 10. 2. PILZ,W. (1968) The specific acethyl Cholinesterase of the human serum. In: 6th International Congress of’ Clinical Chemistry, Munich, (Ed. by 0. Wickland). Vol. 2. Clinical Enzymology, p. 121. Karger Basel, New York. 3. KALOW,W. & GENEST,K. (1957) A method for detection of atypical forms of human serum cholinesterade. Determination of dibucaine numbers. Canadian Journal of Biochemistry & Physiology, 35, 339. 4. BIRZU, T., CUPARENCU, B. & CARDAN, E. (1974) The anticholinesterase activity of pancuronium bromide (Pavulon R). Biochenristr.v & Pharmacology, 23, 166. E. (1970) 100 clinical trials with pan5. CARDAN,
curonium bromide. Clinical report for Organon Lab. Ltd, Organon Library.
Correspondence
If we accept that man is no different from other animals in this context, except perhaps in degree, then current views are correct, there’s an end to the matter and there is no need for ‘real evidence’. But I have the impression man, and especially a sick man, is not always the same as the experimental animal. Whilst oxygen breathing can produce very abnormal changes in lung function, this does not necessarily prove there is histological damage. The brain is depressed by anaesthetics, and the heart by &blockers, and lung function is often gravely impaired in status asthmaticus, without these organs being damaged. I accept as Dr Smith says, we cannot ethically obtain the histological information in healthy volunteers to resolve this argument. Accepting that excessive oxygen can, indeed, produce lung damage, the crucial question remains, which is more important, arterial oxygen or the inspired oxygen fraction? Dr Smith cites work which incriminates the F I O ~ as the dominant factor. My argument was based on admittedly earlier work which blames the Pao2.1*2 There is also evidence that the primary lesion is in the capillary ~ a l l l . as ~ *in~retrolental fibroplasia, and not in the alveolus. In retrolental fibroplasia the arterial and not the alveolar arterial oxygen tension is the crucial factor, and experimentally (sic) hypoxaemia is protective.s If the damaged lung is somewhat resistant to oxygen poisoning, is this because the venous end of the well-ventilated capillary contains markedly desaturated blood, or is it because damage in the susceptible well-perfused,
well-ventilated areas is masked by non-susceptible areas with other types of damage? I was until recently unaware of work by Kapanci and his colleagues,6 which strongly supports the view that excessive oxygen does, indeed, produce damage in healthy human lung, which seems to settle one of these issues. On the other hand, has the incidence of so-called ’respirator lung’ fallen with the recent avoidance of excessive oxygen therapy, one of the factors previously blamed? National Heart Hospital, Westmoreland Street, London, W I M 8BA
ALANGILSTON
References
oxygen toxicity at atmospheric pressure, Acra Medico Srandinaricn, Suppl. 1, loo.
1. OHLSSON, W.T. (1947) A study of
2. BENDIXEN, H.H., EGBERT, L.D., HEDLEY-WHYTE, J.. LAVER, M.B. & PONTOPPIDAN, H. (1965) Respiratory Care, Ch. 14. C.V. Mosby, St Louis. 3. PRATT,P.C. (1965) The reaction of the human lung to enriched oxygen atmosphere. Annals New York Academyof Sciences, 121,809. 4. STAUB,N.C. (1969) Respiration. Annual Rerieiv of Physiology, 31, 173. 5. YANAFF, M., MILLER, W.W. & WALDHAUSEN, J.A. (1970) Oxygen poisoning of the eyes, Archirw o / Oprhalmology, 84,627. 6. KAPANCI,Y., Tosco, R . , EGGERMAN, J . & GOULO, V.E. (1972) Oxygen pneumonitis in man: Light and, electron microscopic morphometric studies. Chesr. 62, 162.
A new museum of anaesthesia During the past year the Department of Anaesthesia at St Bartholomew’s Hospital, London, has been assembling a collection of historic anaesthetic apparatus. The collection is now on display in the Department’s own lecture theatre which was, until the Second World War, an operating theatre; it is the place in which Boyle and Langton Hewer unpacked and then used the first Boyle anaesthetic machine early in the spring of 1917. This collection is not intended to duplicate the Charles King Collection or any other museum of anaesthetic apparatus. Its purpose is to illustrate the continuing process of evolution of anaesthetic equipment from the early days right up to the present time. All forms of apparatus are included from intravenous needles to ventilators and from airways to vapourisers; there is also a selection of early
textbooks on anaesthesia. Due to the interest and generosity of many doctors throughout the United Kingdom the Department has already acquired many fascinating and unique specimens. However, a collection such as this can never be complete and any old apparatus no longer in use (regardless of its condition) and textbooks of any age would be welcome for inclusion in the museum. I believe that it is only by assembling such a collection that irreplaceable pieces of apparatus and textbooks will be preserved for the benefit of present day anaesthetists and for the future. Department of Anaesthesia, D.J. WILKINSON St Bartholomew’s Hospital, London ECI A 7BE
Plasma lorazepam estimation in neonates Since publishing our method for the extraction and estimation of plasma lorazepam by gas-liquid
chromatography (Anaesthesia, 1977, 32, 767) it has become necessary to analyse samples from neonates.
Correspondence This means that only very small amounts of plasma are available for analysis, which led to a revision of our published method. In this modification 0.1 ml of plasma is added to 0.1 nil potassium chloride and extracted with 1.5 ml of benzene with 20 bI of the internal standard added. 1 ml of the benzene layer is evaporated to dryness reconstituted with 50pl benzene and 2.5 pl
271
injected into the chromatograph. This has produced analyses which compare favourably with the original method and has the added economic advantage. Department of Anaesthetics. P.J. HOWARI) The Queen’s Unii>ersirvof Belfast, W. TONER 97 Lisbirrn Road, Belfast BT9 7BL
Acute cardiac obstruction from a Bjork-Shiley valve It was with great interest we read Dr Gilston’s letter concerning acute cardiac obstruction from a BjorkShiley valve (Anaesthesia, 1977, 32, 810). However, in our experience the problem of the valve sticking has been due not to an inherent problem of the valve manufacture but due to chordae being trapped and jamming the valve from the ventricular side (one case) or a too-long suture end being trapped and
jamming the valve from the atrial side (one case). However, unlike the case described by Dr Gilston our cases occurred in the late postoperative stage and resuscitation was not successful. Groby Road Hospital, Croby Road, Leicester, LE3 9 Q E
I. MCLELLAN J.S. BAILEY
Anticholinesterase action of pancuronium There are plenty of papers about the relationship between anaesthesia and pseudocholinesterase, but little data is available concerning true cholinesterase. Recent investigations of Pilz’ focused attention on the existence of a specific acetylcholinesterase in human serum. Its activity must be differentiated from that of the unspecific cholinesterases’ which can be altered by quite different diseases3 In a previous in vitro study pancuronium was found to inhibit red cell and brain ch~linesterase.~ Attempts have been made by theauthor of the letter to observe the behaviour of the serum acetylcholinesterase, since this variant of the acetylcholinesterase is easier to be determined. The data obtained are presented as a letter to the editor since the validity of the Pilz method is still much debated. A group of forty-three patients was anaesthetised by thiopentone and halothane and received a full apnoeic dose of pancuronium both for tracheal intubation and for the surgical requirements. A similar group was anaesthetised in the same way, but without a muscle relaxant. The serum acetylcholinesterase activity was found to be depressed at 15 min. and the levels remained low for 10 h. The changes were not significant statistically, but the reduction was more pronounced in the group receiving pancuronium. These findings suggest an additive antiacetylcholinesterase action of pancuronium. This action
could probably explain the clinical observation that in patients anaesthetised using pancuronium as the only muscle relaxant a more pronounced degree of miosis is to be o b s e r ~ e d . ~ University Hospital, Cluj-Napoca, Romania
EMILCARDAN
References 1. PILZ,W. (1959) Untersuchungen iiber Fermente des menschlichen Blutes. I l l . Zur vermeintlichen
Identitat der Acethylcholin und Tributir in spaltenden Fermente des menschlichen Serums. Zeitschri/i fur die gesamte experimentelle Medizin, 132, 3 10. 2. PILZ,W. (1968) The specific acethyl Cholinesterase of the human serum. In: 6th International Congress of’ Clinical Chemistry, Munich, (Ed. by 0. Wickland). Vol. 2. Clinical Enzymology, p. 121. Karger Basel, New York. 3. KALOW,W. & GENEST,K. (1957) A method for detection of atypical forms of human serum cholinesterade. Determination of dibucaine numbers. Canadian Journal of Biochemistry & Physiology, 35, 339. 4. BIRZU, T., CUPARENCU, B. & CARDAN, E. (1974) The anticholinesterase activity of pancuronium bromide (Pavulon R). Biochenristr.v & Pharmacology, 23, 166. E. (1970) 100 clinical trials with pan5. CARDAN,
curonium bromide. Clinical report for Organon Lab. Ltd, Organon Library.
