Effect of ethanol on thromboxane and prostacyclin synthesis by fetal platelets and umbilical artery

The effect of ethanol (10–500 mmol/1) on platelet thromboxane production and on vascular thromboxane and prostacyclin was studied in human fetal tissues. The release of thromboxane B2 (a metabolite of thromboxane A2) during thrombin-induced spontaneous aggregation of fetal platelets was inhibited by ethanol concentrations of 50 mmol/1 or higher. Ethanol at concentration from 100 mmol/1 also inhibited umbilical artery production of thromboxane B2 and that of 6-keto-prostagladin F1a (a metabolite of prostacyclin). However, it stimulated the conversion of exogenous arachidonic acid to thromboxane B2 in fetal platelets and to 6-keto-prostaglandin F1a in the umbilical artery. This suggests that ethanol inhibits phospholipase A2, but stimulates the enzymes distal from phospholipase A2 in the prostaglandin-synthesizing enzyme cascade.