Acute ethanol ingestion increases platelet reactivity: is there a relationship to stroke?
The effects of ethanol ingestion on ADP-induced platelet aggregation and associated thromboxane formation were studied in the platelet-rich plasma of 10 healthy male volunteers, each serving as his own control. Ethanol caused a transient decrease in threshold concentration of ADP to produce irreversible aggregation. Over a wide range of ADP total platelet aggregation was increased. In the presence of irreversible aggregation, formation of thromboxane B2 rose from 303 +/- 56 to 950 +/- 212 fmol per 10(7) platelets (p less than 0.01). The effects lasted as long as ethanol was present in blood, did not significantly correlate to blood ethanol levels and exhibited great individual variation. It remains to be proved, whether these observations could contribute to the increased risk of ischemic brain infarction associated with acute ethanol ingestion.
D000244:Adenosine Diphosphate / Q000494:pharmacology; D000328:Adult; D002561:Cerebrovascular Disorders / Q000097:blood* / Q000503:physiopathology; D000431:Ethanol / Q000097:blood / Q000494:pharmacology*; D006801:Humans; D066298:In Vitro Techniques; D008297:Male; D010974:Platelet Aggregation / Q000187:drug effects*; D010976:Platelet Count; D013928:Thromboxane A2 / Q000096:biosynthesis; D013997:Time Factors
D000431:Ethanol; D013928:Thromboxane A2; D000244:Adenosine Diphosphate