EFFECTS OF ALCOHOL ON PLATELET FUNCTIONS

Recent epidemiologic studies have consistently shown that moderate int ake of alcoholic beverages protect against morbidity and mortality fro m coronary heart disease and ischemic stroke. By contrast, alcohol dri nking may also predispose to cerebral hemorrhage. These observations s uggest an effect of alcohol similar to that of aspirin. Several studie s in humans and animals have shown that the immediate effect of alcoho l, either added in vitro to platelets or 10 to 20 min after ingestion, is to decrease platelet aggregation in response to most agonists (thr ombin, ADP, epinephrine, collagen). Several hours later, as, in free-l iving populations deprived of drinking since the previous day it is mo stly secondary aggregation to ADP and epinephrine and aggregation to c ollagen that are still inhibited in alcohol drinkers. By contrast, in binge drinkers or in alcoholics after alcohol withdrawal, response to aggregation, especially that induced by thrombin, is markedly increase d. This rebound phenomenon, easily reproduced in rats, may explain isc hemic strokes or sudden death known to occur after episodes of drunken ness. The platelet rebound effect of alcohol drinking was not observed with moderate red wine consumption in man. The protection afforded by wine has been recently duplicated in rats by grape tannins added to a lcohol. This protection was associated with a decrease in the level of conjugated dienes, the first step in lipid peroxidation. In other wor ds, wine drinking does not seem to be associated with the increased pe roxidation usually observed with spirit drinking. Although further stu dies are required, the platelet rebound effect of alcohol drinking cou ld be associated with an excess of lipid peroxides known to increase p latelet reactivity, especially to thrombin.