PubMed · 391339
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
J A Lee. 1979-11-10. Anaesthesia.. https://doi.org/10.1136/bmj.2.6199.1192
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
The hypothesis that histamine H2 receptor blockade adversely affects neuromuscular function was tested, in vivo, in rats anaesthetised with urethane during mechanical pulmonary ventilation. Succinylcholine was administered as a bolus and constant-rate infusion to maintain 49.2% (+/- 1.5 SEM) twitch suppression in 19 rats. Cimetidine iv, 3.2, 7.5, 10, 17.8, 23.7, 31.6, or 56.2 mg.kg-1 was then administered in groups of two to three rats. Cimetidine produced an immediate potentiation of twitch suppression followed by a transient reversal and then a continued potentiation. Peak potentiation occurred within 19.0 (+/- 2.7) sec and was maintained in 11 rats at steady-state. Reversal was evident 4.1 (+/- 0.4) min after cimetidine administration. There was a good relationship between peak potentiation and serum cimetidine concentration with 50% potentiation occurring at 46.5 (+/- 4.6) micrograms.ml-1. Potentiation at steady-state was not correlated to serum cimetidine concentration but there was a weak relationship between reversal and serum cimetidine concentration. These results support reports from patients of an interaction between cimetidine and succinylcholine.
Explore the source record for details and available documents.
The mechanisms of action of intravenous anaesthetics are not yet completely elucidated. Until recently, most of the studies had focused on the interactions between anaesthetics and lipid bilayers. It has been proposed that loss of consciousness is produced by disorganization of the lipid phase of nerve membranes, which impairs the action potential propagation. However, new data obtained with sophisticated neuropharmacological tools such as the patch clamp technique have recently contributed to challenge this hypothesis. Indeed, several lines of evidence suggest that intravenous anaesthetics are thought to induce loss of consciousness by blocking the excitatory synaptic transmission. This can be achieved presynaptically, by inhibiting glutamate release from nerve endings via alterations in the gating properties of voltage-dependent calcium channels. Blockade of excitatory synaptic transmission can also occur at the postsynaptic level by antagonizing the glutamate receptors of the N-methyl D-aspartate subtype. Some anaesthetic agents including ketamine also block the nicotinic receptors, however the relevance of this finding with respect to clinical anaesthesia requires further investigation. Preliminary data also suggest that propofol and etomidate elicit uncoupling of gap junctions between astrocytes, which represent a major nonneuronal cell population in the central nervous system. This phenomenon might indirectly contribute to the hypnotic action of these compounds. Whether loss of consciousness involves preferential target structures within the brain remains to be delineated. A better understanding of the mechanisms of action of general anaesthetics might contribute to generate new agents with more pharmacological selectivity and less undesirable side-effects.