Effects of acute, moderate ethanol consumption on human platelet aggregation in platelet-rich plasma and whole blood.

摘要

BACKGROUND: Platelet-inhibitory effects of alcohol potentially contribute to the reduced risk of coronary heart disease associated with moderate drinking. However, few studies have directly examined the effects of acute consumption of a moderate dose of alcohol on aggregation of platelets from healthy human subjects. In the present study, we examined those effects, with the use of multiple platelet agonists and two aggregation measurement techniques, as part of an ongoing series of studies that evaluate the actions of ethanol on platelet function. METHODS: Human subjects consumed alcohol at a dose equivalent to one drink (0.25 ml/kg) or two drinks (0.5 ml/kg). One hour after ingestion, anticoagulated blood was collected and agonist-induced aggregation of platelets was measured in both whole blood and in platelet-rich plasma. RESULTS: Inhibition of aggregation by ethanol consumption was observed in whole blood (measured as maximum change in impedance) and reached statistical significance (p < 0.05) in the 0.5 ml/kg alcohol group for two collagen concentrations (0.625 and 1.25 microg/ml) as well as for the highest concentration of adenosine diphosphate tested (p < 0.05). Inhibition was 15.4%, 22.6%, and 10.5%, respectively, for these three situations. In platelet-rich plasma, after consumption of 0.5 ml/kg ethanol, aggregation (measured as maximum change in optical density) in response to 1.25 microg/ml collagen was significantly inhibited (p < 0.05); no other significant inhibition was observed at either dose of alcohol in any other cases with platelet-rich plasma. In comparison of male and female subjects, there was a statistically significant difference (p < 0.05) in the degree of inhibition by ethanol consumption (0.5 ml/kg) of whole-blood platelet aggregation induced by collagen, whereby female aggregation was inhibited to a greater extent than male. CONCLUSIONS: This study shows that alcohol, at physiologically relevant doses, below those investigated in most previous human studies, has a dose-dependent inhibitory effect on platelet aggregation. Such an effect could potentially contribute to the beneficial effects of alcohol consumption against coronary artery disease. The inhibitory action is most readily measured with whole-blood platelet aggregometry, with the use of collagen as the agonist. This observation is consistent with the view that alcohol reduces platelet sensitivity to thrombotic stimuli by inhibition of arachidonic acid release and, therefore, subsequent thromboxane synthesis.