Comparative effects of ethanol, acetaldehyde and acetate on arterioles and venules in skeletal muscle: direct in situ studies on the microcirculation and their possible relationship to alcoholic myopathy.

The precise effects ethanol (ETOH), acetaldehyde (ACT) and acetate (AC) exert on microscopic resistance and capacitance vessels in skeletal muscle is unknown. In-situ studies on the skeletal (cremaster) microvasculature of the rat, using high-resolution television microscopy, were undertaken. Acute administration (topical, intra-arterial or iv) of ethanol (0.001-10%) to young rats produced a concentration-related vasoconstriction of arterioles (18-45 microns) and muscular venules (25-50 microns), ranging from a 7 to 80% reduction in microvessel lumen sizes. Acute administration of either ACT or AC, however, produced concentration-related vasodilatation of these same microvessels. No known amine or opiate pharmacologic antagonist or cyclooxygenase inhibitor could attenuate or prevent ETOH, ACT and AC from eliciting their unique microvascular responses. These new, direct in-situ microcirculatory findings clearly demonstrate: 1) ETOH exerts constrictor, and not dilator, effects on skeletal muscle microscopic resistance and capacitance vessels; 2) both ACT and AC exert dilator, and not constrictor, effects on these muscle microvessels; and 3) the effects of alcohol can not be due to metabolism to ACT or AC. A progressive increase in ischemia of the skeletal muscle microscopic resistance and capacitance vessels, over a period of time (weeks to years), could result in the well-known syndrome of alcoholic myopathy.