ACUTE EFFECTS OF ETHANOL ON RESPONSES OF CEREBRAL ARTERIOLES

Background and Purpose Previous studies have suggested that acute expo sure of large peripheral arteries to ethanol impairs endothelium-depen dent relaxation. The goal of the present study was to determine the ac ute effects of ethanol exposure on responses of cerebral resistance ar terioles in vivo. Methods We prepared a cranial window in rats to expo se the cerebral (pial) microcirculation. We measured the diameter of p ial arterioles in vivo in response to agonists that presumably stimula te the synthesis/release of nitric oxide from the endothelium (ADP, ac etylcholine, and histamine) or neurons (N-methyl-D-aspartate [NMDA]) b efore and after topical application of various concentrations of ethan ol added to the cerebrospinal fluid (20, 40, 60, 80, and 100 mmol/L). In addition, we examined responses of pial arterioles to nitroglycerin before and 1 hour after topical application of ethanol. Results Befor e application of ethanol, ADP, acetylcholine, histamine, NMDA, and nit roglycerin produced dose-related dilatation of pial arterioles. Applic ation of the various concentrations of ethanol did not alter the basel ine diameter of pial arterioles. However, application of 80 and 100 mm ol/L ethanol inhibited dilatation of pial arterioles in response to ag onists that stimulate the synthesis/release of nitric oxide. Dilatatio n of pial arterioles in response to nitroglycerin was not altered by a pplication of ethanol. Conclusions The findings of the present study s uggest that acute exposure of cerebral arterioles to modest-to-moderat e concentrations of ethanol (20 to 60 mmol/L) does not alter responses of cerebral arterioles. In contrast, exposure of cerebral arterioles to higher concentrations of ethanol (SO and 100 mmol/L) can produce sp ecific impairment of dilatation to agonists that stimulate the synthes is/release of nitric oxide from endothelium and neurons.