Kontula K, Viinikka L, Ylikorkala O, Ylikahri R
Life Sci. 1982 Jul 19;31(3):261-4. doi: 10.1016/0024-3205(82)90587-2.
To investigate the effects of acute ethanol administration on the production of proaggregatory thromboxane A2 (TxA2) and antiaggregatory prostacyclin (PGI2), ethanol (1.5 g/kilogram body weight) was given to eight healthy nonsmoking men, and the stable metabolites thromboxane B2 (TxB2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), respectively, measured by radioimmunoassay from serial blood samples before drinking and during the ensuing 18 hours. Each subject was studied as his own control on another occasion when only an equivalent volume of water was given. Serum TxB2 level decreased (p less than 0.01) from 206 +/- 31 ng/ml (mean +/- S.E.) to 167 +/- 24 and 161 +/- 23 ng/ml (two and four hours after beginning of the drinking, respectively) concomitantly with the attainment of maximal blood ethanol concentrations (about 120 mg/100 ml), whereas no changes occurred in plasma 6-keto-PGF1 alpha concentrations. Our results may provide an explanation for known effects of ethanol on platelet aggregation. They also raise speculation whether TxA2-inhibition and the antiatherogenic effect of alcohol intake are somehow related.
为研究急性给予乙醇对促聚集血栓素A2（TxA2）和抗聚集前列环素（PGI2）生成的影响，对8名健康不吸烟男性给予乙醇（1.5克/千克体重），并通过放射免疫分析法，从饮酒前及随后18小时内的系列血样中分别测定稳定代谢产物血栓素B2（TxB2）和6-酮-前列腺素F1α（6-酮-PGF1α）。在另一次仅给予等量水时，将每位受试者作为自身对照进行研究。血清TxB2水平从206±31纳克/毫升（均值±标准误）降至167±24和161±23纳克/毫升（分别在开始饮酒后2小时和4小时），同时达到最大血乙醇浓度（约120毫克/100毫升），而血浆6-酮-PGF1α浓度无变化。我们的结果可能为乙醇对血小板聚集的已知影响提供解释。它们还引发了关于TxA2抑制与饮酒的抗动脉粥样硬化作用是否存在某种关联的推测。
