Louis L. Battey, M.D.; Alberta Heyman, M.D.; John L. Patterson Jr.
JAMA. 1953;152(1):6-10. doi:10.1001/jama.1953.03690010012002.
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The ingestion of ethyl alcohol is known to produce dilatation of the blood vessels in the skin and, to a lesser extent, those in other tissues. For this reason, it has been advocated for the treatment of peripheral vascular disease and angina pectoris.1 Its use as a cerebral vasodilator has also been recommended,2 because of the dilatation of pial vessels observed in animals given large amounts of ethyl alcohol intravenously. The symptoms of acute alcoholic intoxication are generally believed to be caused by depression of the central nervous system. In vitro studies have shown, however, that alcohol in concentrations up to 2% produces an increase in oxygen consumption, while in concentrations greater than this it produces a decrease.3 A decrease in cerebral arteriovenous oxygen difference has been found during alcoholic intoxication, but this has been attributed to a reduction in cerebral oxygen utilization rather than to an


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