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Canadian Journal of Anesthesia, Vol 17, 574-590, Copyright © 1970 by Canadian Anesthesiologists' Society

Effect of Gallamine on Cholinergic Receptors

FLORA J. RATHBUN M.SC.1 and JOHN T. HAMILTON PH.D.2

1 Department of Pharmacology, University of Western Ontario
2 University of Western Ontario, London, Ontario

Gallamine triethiodide causes tachycardia thought to be due to a specific vagolytic action. Recently, Brown and Crout have shown that gallamine may cause increased inotropic and chronotropic activity due to the release of catecholamines from cardiac sympathetic nerves. As a further analysis of the mechanisms, experiments were performed on pithed rats and spinally transected, brain-destroyed cats in vivo pretreated with hexamethonium and/or propranolol to determine the nature of the antiacetylcholine action of gallamine on the heart.

A significant antagonism by gallamine of the negative chronotropic action of acetylcholine on the heart of the pithed rat in vivo, pretreated with hexamethonium and/or propranolol, has been demonstrated. Similarly, gallamine was shown to have a significant antiacetylcholine activity on the heart of the spinal cat preparation. The effect of hexamethonium on the cat, however, differed from that on the rat, as in the former it caused a significant decrease in the apparent affinity constant of gallamine. The possible mechanisms whereby this is caused and the clinical implications, should the cat be similar to man in this regard, are discussed.

This antiacetylcholine activity of gallamine on the heart (negative chronotropic response to acetylcholine) fulfils many of the requirements for competitive antagonism. Parallel results were obtained with atropine except on the hexamethonium-treated cat. Thus, if atropine acts on the acetylcholine receptor in a competitive manner, it is likely that gallamine does also.

Experiments on the isolated guinea pig ileum in vitro have re-demonstrated the remarkable selectivity of the parasympatholytic activity of gallamine with respect to the cardiovascular system and an interesting antihistaminic action which deserves further study.

As the observed anticholinergic actions of gallamine on the heart of both species were obtained with doses necessary for muscle relaxation, it is conceivable that a true atropine-like action may complement any sympathomimetic action of gallamine in producing the tachycardia encountered in clinical practice.

Note:

Supported in part by a grant-in-aid from the Ontario Heart Foundation of Canada, grant 3-15, and in part from the Medical Research Council of Canada, grant MA 1216.






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Copyright © 1970 by the Canadian Anesthesiologists' Society.