Vermylen J, Chamone D A, Verstraete M
Lancet. 1979 Mar 10;1(8115):518-20. doi: 10.1016/s0140-6736(79)90944-9.
Ingestion of 1.2 g Bay g 6575 daily for 1 week by six healthy volunteers had no effect on blood-coagulation, fibrinolysis, or platelet aggregation in vitro, but it seemed to inhibit platelet aggregation in vivo (shown by a smaller reduction in the platelet aggregate ratio after venous occlusion). Plasma drawn from five volunteers after ingestion of a single dose of 1.2 g of the drug stimulated prostacyclin release from slices of rat aorta which had been washed until they stopped releasing anti-aggregating substances, whereas plasma from the same individuals before ingestion of the substance did not. Administration of either Bay g 6575 or dipyridamole alone had no effect on platelet aggregation in vitro, but combined administration resulted in a striking and prolonged inhibition of A.D.P.-induced platelet aggregation. It is proposed that the previously described antithrombotic properties of Bay g 6575 in animals are due to stimulation of prostacyclin release from the vessel wall, and that this effect is also demonstrable in man.
6名健康志愿者连续1周每天摄入1.2克Bay g 6575，对体外血液凝固、纤维蛋白溶解或血小板聚集没有影响，但似乎在体内抑制了血小板聚集（静脉闭塞后血小板聚集率降低幅度较小表明了这一点）。5名志愿者在摄入单剂量1.2克该药物后采集的血浆，刺激了已冲洗至停止释放抗聚集物质的大鼠主动脉切片释放前列环素，而在摄入该物质之前同一受试者的血浆则没有这种作用。单独给予Bay g 6575或双嘧达莫对体外血小板聚集没有影响，但联合给药导致对ADP诱导的血小板聚集有显著且持久的抑制作用。有人提出，先前描述的Bay g 6575在动物体内的抗血栓形成特性是由于刺激血管壁释放前列环素，并且这种作用在人体中也可得到证实。
