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Ethanol produces coronary vasospasm: evidence for a direct action of ethanol on vascular muscle
Author(s) -
Altura B.M.,
Altura B.T.,
Carella A.
Publication year - 1983
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1983.tb09389.x
Subject(s) - coronary arteries , ethanol , phentolamine , methysergide , vascular smooth muscle , chemistry , acetaldehyde , medicine , propranolol , cardiology , dilator , phenoxybenzamine , endocrinology , pharmacology , anesthesia , artery , receptor , biochemistry , smooth muscle , antagonist
The effects of ethanol and acetaldehyde on basal tension of canine small and large coronary arteries were examined in vitro. Ethanol in a concentration as little as 8.5 m m can induce threshold contractions of coronary arteries. High concentrations of ethanol produce concentration‐dependent coronary vasospasms equivalent to those induced by supra‐maximal concentrations of KCl. Acetaldehyde (10 −5 to 10 −2 m ) resulted in concentration‐dependent relaxation of basal tone. Use of a variety of pharmacological antagonists (i.e., phentolamine, methysergide, diphenhydramine, metiamide, propranolol and indomethacin) did not attenuate or prevent the spasmogenic actions of ethanol. These findings could help to explain why alcohol can induce cardiac depression, arrhythmias, cardiomyopathy and the higher than normal incidence of sudden death observed in ‘binge’ drinkers.