Succinylcholine, cholinoceptors and catecholamines: proposed mechanism of early adverse haemodynamic reactions.

Abstract

An hypothesis is proposed to account for the occurrence of adverse haemodynamic reactions to succinylcholine. Interaction of succinylcholine with cholinergic receptors is postulated to result in release of endogenous catecholamines (predominantly norepinephrine). The occurrence and the clinical manifestations of the adverse reactions would be dependent on the extent of the release. Based on literature reports of findings in experimental animals with nicotinic and muscarinic agents, a mechanism for the release of norepinephrine is outlined. Interaction of succinylcholine with muscarinic and nicotinic receptors is proposed to result in an initial activation which is followed by a phase of chemical insensitivity. Activation of the presynaptic nicotinic receptors on the postganglionic sympathetic terminals leads to a short-lasting release of norepinephrine. Activation of the presynaptic muscarinic receptors produces attenuation of the norepinephrine release. In the majority of patients these opposing actions are balanced and the net result is small, variable, and of little clinical importance. An unbalanced response leading to clinical manifestations can be expected if the two types of the presynaptic cholinoceptors are differentially activated.