Ethanol-Induced Inhibition of Platelet Aggregation in Whole Blood from Healthy Donors

Ethanol is known to inhibit platelet aggregation. In order to examine effects of ethanol on platelet aggregation, isolated platelet-rich plasma and platelet suspension are often used. However, it remains to be clarified whether and how ethanol affects platelet aggregation in whole blood. In this concise study, we examined effects of ethanol on platelet aggregation induced by different stimulants in whole blood by using the screen filtration pressure method. Thapsigargin and 1-oleoyl-2-acetyl-sn-glycerol (OAG), which cause Ca2+ entry into platelets through the storeoperated Ca2+ channels and the diacylglycerol-dependent Ca2+ channels, respectively, were used for inducing platelet aggregation. Thapsigargin-induced platelet aggregation was markedly inhibited by ethanol at 0.25% or higher, and OAG-induced platelet aggregation was significantly inhibited by ethanol at 1% or higher. These results indicate that inhibitory effect of ethanol was more prominent on thapsigargin-induced aggregation than on OAGinduced aggregation. Thus, ethanol inhibits thapsigarginand OAG-induced platelet aggregation in whole blood, and the effect of ethanol on platelet aggregation through the store-operated Ca2+ channels is thought to be stronger than that on aggregation through the diacylglycerol-dependent Ca2+ channels.