1956
DOI: 10.1093/bja/28.4.159
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Dual Action of Suxamethonium Chloride

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Cited by 43 publications
(18 citation statements)
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“…Thus a tetanus and anticholinesterase drugs exert some antagonistic action, and tubocurarine augments the paralysis. Numerous reports have indicated that the blocks produced in man by the depolarizing type of muscle relaxant (for example decamethonium, suxamethonium and carbolonium) often change in type after prolonged administration (Grant, 1952;Guerrier & Huxley-Williams, 1954;Hodges, 1955;Argent, Dinnick & Hobbiger, 1955;Hodges & Foldes, 1956;Brennan, 1956;Foldes, Wnuck, Hodges, Thesleff & de Beer, 1957;Churchill-Davidson & Christie, 1959;Wiemers & Overbeck, 1960). Because, at a late stage of the block produced by these depolarizing drugs, a tetanus and neostigmine exert some antagonism, while tubocurarine augments the paralysis, many anaesthetists have concluded that the depolarization phase in man may give way to a competitive phase.…”
Section: Discussionmentioning
confidence: 99%
“…Thus a tetanus and anticholinesterase drugs exert some antagonistic action, and tubocurarine augments the paralysis. Numerous reports have indicated that the blocks produced in man by the depolarizing type of muscle relaxant (for example decamethonium, suxamethonium and carbolonium) often change in type after prolonged administration (Grant, 1952;Guerrier & Huxley-Williams, 1954;Hodges, 1955;Argent, Dinnick & Hobbiger, 1955;Hodges & Foldes, 1956;Brennan, 1956;Foldes, Wnuck, Hodges, Thesleff & de Beer, 1957;Churchill-Davidson & Christie, 1959;Wiemers & Overbeck, 1960). Because, at a late stage of the block produced by these depolarizing drugs, a tetanus and neostigmine exert some antagonism, while tubocurarine augments the paralysis, many anaesthetists have concluded that the depolarization phase in man may give way to a competitive phase.…”
Section: Discussionmentioning
confidence: 99%
“…It may be assumed that a certain degree of membrane depolarization due to succinylcholine, made it possible for a reduced and nearly insufficient end-plate potential to reach the trigger level more safely, and so facilitate transmission. The absence of change in MIPI and the increase in jitter, effects normally seen after succinylcholine, may be due to a competitive action between curare and succinylcholine, which has been clinically and experimentally documented ( BRENNAN 1956). Higher doses of succinylcholine would perhaps have produced the effects described in the untreated end-plate.…”
Section: Results ( B )mentioning
confidence: 92%
“…Several studies have documented potentiation of phase I block and antagonism of phase I1 block by anticholinesterases (1)(2)(3). With the advent of train-of-four monitoring, it became apparent that train-of-four fade could be used to separate phase I from phase I1 block (3,4).…”
mentioning
confidence: 99%