Ethanol and Contraction of Venous Smooth Muscle
作者:
Haydoohi Edgarian,
Burton Altura,
期刊:
Anesthesiology
(OVID Available online 1976)
卷期:
Volume 44,
issue 4
页码: 311-317
ISSN:0003-3022
年代: 1976
出版商: OVID
关键词: Alcohol;venous smooth muscle; Veins;ethanol
数据来源: OVID
摘要:
Low concentrations of ethanol (17 mM) inhibited development of spontaneous mechanical activity (vasomotion) in isolated rat portal veins. Low concentrations of ethanol potentiated, however, contractions induced by epinephrine, but not those induced by angiotensin or potassium. Higher concentrations of ethanol, such as those associated with surgical anesthesia (100–170 mM), resulted in almost complete suppression of spontaneous contractile responses. These higher concentrations of ethanol: a) attenuate contractions induced by epinephrine, angiotensin, and potassium (K+); b) cause noncompetitive displacement of the dose-response curves of these vasoactive compounds; c) attenuate calcium (Ca++)-induced contractions of K+-depolarized portal veins; d) relax drug-induced, as well as Ca++-induced, contractions of portal veins. The profound depressant actions of ethanol are not mimicked by alpha-adrenergic, histaminergic, cholinergic, or serotonergic blocking drugs, nor are they attributable to actions on β-adrenergic receptors. The direct vasodepressant actions of ethanol on isolated venous smooth muscle may play a significant role in alcohol-induced peripheral vasodilatation seen in man and animals.
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