Uotila P, Matintalo M, Dahl M L
Prostaglandins Leukot Med. 1983 Nov;12(3):299-303. doi: 10.1016/0262-1746(83)90008-2.
Addition of arachidonic acid (AA) to human platelet rich plasma caused a reversible platelet aggregation and a concomitant formation of thromboxane B2 (TXB2). Both AA-induced platelet aggregation and TXB2 formation were inhibited by OKY-1581 and the amounts of PGE2 and PGF2 alpha formed were correspondingly increased. The formation of 6-keto-PGF1 alpha was smaller and was increased only slightly by OKY-1581. ADP-induced platelet aggregation did not result in the formation of TXB2 and it was inhibited only slightly by OKY-1581. When ADP was added to platelet rich plasma six minutes after the addition of AA, the ADP-induced aggregation was greatly decreased in the presence and absence of OKY-1581. The present study indicates that the AA-induced platelet aggregation is inhibited by OKY-1581 and that OKY-1581 is a specific inhibitor of thromboxane synthesis in platelet rich human plasma.
向富含人血小板的血浆中添加花生四烯酸(AA)会导致血小板可逆性聚集,并伴随血栓素B2(TXB2)的形成。OKY - 1581可抑制AA诱导的血小板聚集和TXB2形成,同时PGE2和PGF2α的生成量相应增加。6 - 酮 - PGF1α的生成量较少,OKY - 1581仅使其略有增加。ADP诱导的血小板聚集不会导致TXB2形成,且仅被OKY - 1581轻微抑制。在添加AA六分钟后向富含血小板的血浆中添加ADP,无论有无OKY - 1581,ADP诱导的聚集都会大幅降低。本研究表明,OKY - 1581可抑制AA诱导的血小板聚集,且OKY - 1581是富含人血小板血浆中血栓素合成的特异性抑制剂。