Effects of Ethanol on Terminal Arterioles and Muscular Venules: Direct Observations on the Microcirculation

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Abstract

Summary:

The present experiments, using an image-splitting television microscope recording system, show for the first time the quantitative effects of topical, intra-arterial, and intravenously administered ethanol on terminal arterioles (15–23 μm i.d.) and muscular venules (28–39 μm i.d.), in situ, in a splanchnic terminal vascular bed. Irrespective of the route of administration, ethanol (0.05–10%) dose-dependently dilated both terminal arterioles and muscular venules. These ethanol-induced dilator responses were not modified by cholinergic, histaminergic (neither H1- nor H2-blockers), serotonergic, or prostaglandin synthetase antagonists. β-Adrenergic blockade significantly enhanced the vasodilator effects of the alcohol. In addition, locally as well as systemically administered ethanol dose-dependently inhibited the constrictor effects of catecholamines (epinephrine and norepinephrine), angiotensin, vasopressin, and barium chloride on the microscopic resistance and capacitance vessels. Catecholamine-, angiotensin-, and vasopressin-induced constrictor responses on terminal arterioles were more sensitive to inhibition by ethanol than were the agonist-induced contractile responses on muscular venules. The sensitivity of barium chloride responses to ethanol inhibition, in the two types of muscular microvessels, was the reverse of that observed with the other agonists. The duration of the arteriolar constrictor responses to catecholamines was reduced significantly upon application of ethanol, whereas the duration of Ba2--induced venular constrictions was increased after application of the alcohol. Low doses of ethanol (i.e., 0.01–0.05%) did not potentiate constrictor responses to norepinephrine, epinephrine, angiotensin, vasopressin, or Ba2+ These findings indicate that ethanol can (i) exert direct effects on microvascular smooth muscle: (ii) attenuate microvascular constrictor responses induced by vasoactive substances; and (iii) possibly interfere with microvascular smooth muscle cell inactivation or disposition of catecholamines and Ba2+. It is suggested that the direct vasodepressant actions on microscopic resistance and capacitance vessels may play a significant role in alcohol-induced peripheral vasodilatation seen in man and animals.

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