IN-VIVO REVERSAL OF DEPOLARIZING NEUROMUSCULAR BLOCKADE

The antagonism of depolarizing blockers. principally succinylcholine a nd decamethonium, by tetraethyl- and tetrabutylammonium ions in an in vivo neuromuscular preparation in anesthetized cats is described; poss ible mechanisms for these effects are discussed. Tetraethyl- (50-100 m g/kg, i.v.) and tetrabutylammonium (1-5 mg/kg, i.v.) produced sharp re versals of 95-99% succinylcholine and decamethonium blocks. These reve rsals were effective and sustained at any point during the course of t he blockades. Tetraethyl- or tetrabutylammonium, administered 2-3 min before succinylcholine or decamethonium, prevented blockade, an effect compatible with an earlier reported in vitro investigation. The studi es of others disclose the interaction of depolarizing blockers with ac etylcholine receptors. leading to channel opening: channel entry and b inding therein of these blockers. The present studies support this in showing the prevention of succinylcholine and decamethonium block by t he prior administration of tetraethylammonium, which also interacts wi th acetylcholine receptors. It is proposed that a possible mechanism f or tetraethylammonium reversals of succinylcholine and decamethonium b locks may be attributable to the tetraethylammonium reversal of a K+ c urrent block by quaternary ammonium ions such as succinylcholine and d ecamethonium. Tetraethyl- and tetrabutylammonium ions proved to be eff ective antagonists of succinylcholine block following inactivation of plasma cholinesterases by hexafluorenium.