Failure of acetaldehyde or acetate to mimic the splanchnic arteriolar or venular dilator actions of ethanol: direct in situ studies on the microcirculation.

The effects of acetaldehyde and sodium acetate on rat mesenteric arterioles (17-25 micron i.d.) and muscular venules (35-50 micron i.d.) were examined in situ, at the microcirculatory level, by use of a high-resolution closed circuit television microscope recording system. Local, intravenous or intra-arterial administration of acetaldehyde (1.8-3600 mumol) and sodium acetate (0.25-250 mumol) to mesenteric arterioles and muscular venules of the anaesthetized rat induced dose-dependent vasoconstriction. Systemic administration of a variety of pharmacological antagonists (i.e., phentolamine, diphenhydramine, methysergide, atropine and indomethacin) did not attenuate or prevent the dose-dependent vasoconstrictor actions of these metabolites of ethanol. Our findings do not support the concept that some or all of the peripheral vasodilator actions of ethanol can be attributed to its metabolites, acetaldehyde and acetate.