Differential Effects of Alcohols on Intracerebral Arterioles. Ethanol Alone Causes Vasoconstriction

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Abstract
We compared the effect of the acute application of ethanol, methanol, 1-propanol, 1-butanol, urea, and mannitol (1–100 mM) on the basal tone of isolated–cannulated rat intracerebral arterioles to determine if the response of these arterioles to ethanol could be attributed to alteration of membrane fluidity or changes in osmolality. These arterioles spontaneously developed tone to 62.0 ± 8.4% of passive diameter (44.2 ±11.9 vs. 70.9 ± 14.7 μm). Ethanol caused a dose-dependent reduction in arteriolar diameter starting at 3 mM (p = 0.03), reaching a diameter of 81.4 ± 3.0% of basal tone at 100 mM. In comparison, all other agents tested caused the arterioles to dilate, with the exception of 1-propanol, which produced inconsistent vessel responses. At 100 mM concentration, methanol, 1-butanol, urea, and mannitol dilated intracerebral arterioles by 116.1 ± 12.7, 151.5 ± 12.4, 131.1 ± 17.0, and 149.8 ± 6.6%, respectively. Thus, in a concentration range associated with acute intoxication, ethanol causes constriction of isolated intracerebral arterioles. The mechanism of action of ethanol cannot be accounted for solely based upon its physicochemical characteristics of osmolality or lipid solubility, but rather may reflect a more specific action on one or more cellular mechanisms responsible for determining basal intracerebral arteriolar tone. The characterization of the response of intracerebral arterioles to ethanol is important in view of epidemiologic links between ethanol consumption and cerebrovascular disease.