Epidemiological studies have linked an inhibition of platelet function by e
thanol, among other factors, to the cardioprotective effects of moderate et
hanol consumption. Platelet defects have been noted in alcoholics and in hu
man experimental studies. Importantly, in in vivo experimental settings! et
hanol diminishes thrombus formation on damaged arterial walls. Ethanol inhi
bits platelet activation in vitro in response to diverse agonists. Phosphol
ipase A(2) is a major site for ethanol inhibition, corresponding to a reduc
tion in the formation of stimulatory arachidonate metabolites. Additional s
ignal transduction pathways are likely targets for ethanol including phosph
oinositide-specific phospholipase C and cyclic AMP. The role of additional
cofactors in the inhibition of platelet responses by ethanol is discussed.