De Gaetano G, Tonolli M C, Bertoni M P, Roncaglioni M C
Haemostasis. 1977;6(2):127-36. doi: 10.1159/000214172.
Ditazole (4,5-diphenyl-2-bis-(2-hydroxyethyl)-aminoxazol) has been shown to be a strong in vitro inhibitor of human platelet aggregation brought about by release reaction inducers; in contrast, it did not significantly affect primary ADP-induced aggregation. Ditazole strongly inhibited the release of platelet-bound 14C-serotonin under the influence of Thrombofax, whereas it did not interfere with the transport and storage of serotonin in nonstimulated platelets. The effect of ditazole was not potentiated by acetylsalicylic acid. Ditazole also inhibited ADP-reptilase clot retraction and modified thrombin-induced clot formation. The inhibition of platelet aggregation exerted by ditazole in plasma could be removed following gel filtration of platelets on Sepharose 2-B gel. This would indicate that ditazole does not act on platelets by a 'hit and run' mechanism.
双苯咪唑(4,5 - 二苯基 - 2 - 双 -(2 - 羟乙基) - 氨基恶唑)已被证明是一种强大的体外抑制剂,可抑制由释放反应诱导剂引起的人体血小板聚集;相比之下,它对原发性ADP诱导的聚集没有显著影响。在血栓传真素的影响下,双苯咪唑强烈抑制血小板结合的14C - 5 - 羟色胺的释放,而它不干扰5 - 羟色胺在未受刺激血小板中的转运和储存。乙酰水杨酸不会增强双苯咪唑的作用。双苯咪唑还抑制ADP - 爬虫酶凝块退缩并改变凝血酶诱导的凝块形成。通过在Sepharose 2 - B凝胶上对血小板进行凝胶过滤,可以消除双苯咪唑在血浆中对血小板聚集的抑制作用。这表明双苯咪唑不是通过“打了就跑”机制作用于血小板的。