W G Mayhan1, S P Didion. 1. Department of Physiology and Biophysics, University of Nebraska Medical Center, Omaha 68198-4575, USA.
Abstract
BACKGROUND AND PURPOSE: Previous studies have suggested that acute exposure of large peripheral arteries to ethanol impairs endothelium-dependent relaxation. The goal of the present study was to determine the acute effects of ethanol exposure on responses of cerebral resistance arterioles in vivo. METHODS: We prepared a cranial window in rats to expose the cerebral (pial) microcirculation. We measured the diameter of pial arterioles in vivo in response to agonists that presumably stimulate the synthesis/release of nitric oxide from the endothelium (ADP, acetylcholine, and histamine) or neurons (N-methyl-D-aspartate [NMDA]) before and after topical application of various concentrations of ethanol 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: Before application of ethanol, ADP, acetylcholine, histamine, NMDA, and nitroglycerin produced dose-related dilatation of pial arterioles. Application of the various concentrations of ethanol did not alter the baseline diameter of pial arterioles. However, application of 80 and 100 mmol/L ethanol inhibited dilatation of pial arterioles in response to agonists that stimulate the synthesis/release of nitric oxide. Dilatation of pial arterioles in response to nitroglycerin was not altered by application of ethanol. CONCLUSIONS: The findings of the present study suggest that acute exposure of cerebral arterioles to modest-to-moderate 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 (80 and 100 mmol/L) can produce specific impairment of dilatation to agonists that stimulate the synthesis/release of nitric oxide from endothelium and neurons.
BACKGROUND AND PURPOSE: Previous studies have suggested that acute exposure of large peripheral arteries to ethanol impairs endothelium-dependent relaxation. The goal of the present study was to determine the acute effects of ethanol exposure on responses of cerebral resistance arterioles in vivo. METHODS: We prepared a cranial window in rats to expose the cerebral (pial) microcirculation. We measured the diameter of pial arterioles in vivo in response to agonists that presumably stimulate the synthesis/release of nitric oxide from the endothelium (ADP, acetylcholine, and histamine) or neurons (N-methyl-D-aspartate [NMDA]) before and after topical application of various concentrations of ethanol 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: Before application of ethanol, ADP, acetylcholine, histamine, NMDA, and nitroglycerin produced dose-related dilatation of pial arterioles. Application of the various concentrations of ethanol did not alter the baseline diameter of pial arterioles. However, application of 80 and 100 mmol/L ethanol inhibited dilatation of pial arterioles in response to agonists that stimulate the synthesis/release of nitric oxide. Dilatation of pial arterioles in response to nitroglycerin was not altered by application of ethanol. CONCLUSIONS: The findings of the present study suggest that acute exposure of cerebral arterioles to modest-to-moderate 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 (80 and 100 mmol/L) can produce specific impairment of dilatation to agonists that stimulate the synthesis/release of nitric oxide from endothelium and neurons.