Effect of ethanol on platelet function.
Epidemiological studies have linked an inhibition of platelet function by ethanol, among other factors, to the cardioprotective effects of moderate ethanol consumption. Platelet defects have been noted in alcoholics and in human experimental studies. Importantly, in in vivo experimental settings, ethanol diminishes thrombus formation on damaged arterial walls. Ethanol inhibits platelet activation in vitro in response to diverse agonists. Phospholipase A2 is a major site for ethanol inhibition, corresponding to a reduction in the formation of stimulatory arachidonate metabolites. Additional signal transduction pathways are likely targets for ethanol including phosphoinositide-specific phospholipase C and cyclic AMP. The role of additional cofactors in the inhibition of platelet responses by ethanol is discussed.
Rubin
R
R
Department of Pathology, Anatomy, and Cell Biology, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA.
D000428:Alcohol Drinking / Q000453:epidemiology; D000818:Animals; D001161:Arteriosclerosis / Q000503:physiopathology; D000431:Ethanol / Q000494:pharmacology*; D006801:Humans; D010741:Phospholipases A / Q000187:drug effects*; D054467:Phospholipases A2; D015539:Platelet Activation / Q000187:drug effects*; D015398:Signal Transduction / Q000187:drug effects
D000431:Ethanol; D010741:Phospholipases A; D054467:Phospholipases A2