Effect of ethanol on thromboxane and prostacyclin synthesis by fetal platelets and umbilical artery.
The effect of ethanol (10-500 mmol/l) 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/l or higher. Ethanol at concentration from 100 mmol/l also inhibited umbilical artery production of thromboxane B2 and that of 6-keto-prostaglandin F1 alpha (a metabolite of prostacyclin). However, it stimulated the conversion of exogenous arachidonic acid to thromboxane B2 in fetal platelets and to 6-keto-prostaglandin F1 alpha 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.
D015121:6-Ketoprostaglandin F1 alpha / Q000096:biosynthesis* / Q000097:blood; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000378:metabolism; D001792:Blood Platelets / Q000187:drug effects / Q000378:metabolism*; D000431:Ethanol / Q000494:pharmacology*; D005260:Female; D005312:Fetal Blood / Q000187:drug effects; D006801:Humans; D007231:Infant, Newborn; D007700:Kinetics; D011247:Pregnancy; D013929:Thromboxane B2 / Q000096:biosynthesis* / Q000097:blood; D014469:Umbilical Arteries / Q000187:drug effects / Q000378:metabolism*
D001095:Arachidonic Acids; D016718:Arachidonic Acid; D000431:Ethanol; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha