Kawamura T, Kitani T, Okajima Y, Okuda S, Urano S, Watada M, Nakagawa M, Ijichi H
Prostaglandins Med. 1980 Aug;5(2):113-21. doi: 10.1016/0161-4630(80)90098-1.
Prostacyclin (PGI2) has been reported to be a labile but potent inhibitor of platelet aggregation and a powerful vasodilator. This paper reports the effect of trapidil on PGI2 generation in rat aorta by means of bioassay system. The aortic ring was incubated in 0.05 M Tris HCl buffer (pH 7.5) for 10 min. This incubation medium was added into human PRP, and then incubated at 37 degrees C for 2 min., and ADP was added. PGI2 activity was assayed by the inhibitory percentage of ADP induced platelet aggregation. When the aortic ring was incubated in a medium containing trapidil, PGI2 generation was accelerated. This acceleration was inhibited by pretreatment with indomethacin. Moreover, the aortas of rats intravenously injected with 30 mg/kg of trapidil were incubated in the same way, and PGI2 activity in the medium was estimated. More potent PGI2 activity was observed in the aortas of rat treated with trapidil compared with the controls. These results indicate that acceleration of PGI2 generation from aorta by trapidil is involved in the mode of action of this drug of thrombus formation.
据报道，前列环素（PGI2）是一种不稳定但有效的血小板聚集抑制剂和强力血管扩张剂。本文通过生物测定系统报道了曲匹地尔对大鼠主动脉中PGI2生成的影响。将主动脉环在0.05 M Tris HCl缓冲液（pH 7.5）中孵育10分钟。将该孵育培养基加入人富血小板血浆中，然后在37℃孵育2分钟，再加入ADP。通过ADP诱导的血小板聚集抑制百分比来测定PGI2活性。当主动脉环在含有曲匹地尔的培养基中孵育时，PGI2的生成加速。这种加速被吲哚美辛预处理所抑制。此外，将静脉注射30 mg/kg曲匹地尔的大鼠的主动脉以同样的方式孵育，并测定培养基中的PGI2活性。与对照组相比，在接受曲匹地尔治疗的大鼠主动脉中观察到更强的PGI2活性。这些结果表明，曲匹地尔加速主动脉中PGI2的生成与该药物的血栓形成作用方式有关。
