Nomura S, Nagata H, Suzuki M, Iwata K, Kawakatsu T, Kido H, Fukuroi T, Yamaguchi K, Yanabu M, Soga T
First Department of Internal Medicine, Kansai Medical University, Osaka, Japan.
Thromb Res. 1992 Jan 1;65(1):95-104. doi: 10.1016/0049-3848(92)90229-4.
We analyzed the effects of ticlopidine on platelet aggregation and on microparticle (MP) formation when platelets were exposed to a monoclonal anti-CD9 antibody (NNKY1-19) in vitro. Even when NNKY1-19-induced platelet aggregation was completely inhibited by preincubation with anti-GPIIb/IIIa antibody or Arg-Gly-Asp-Ser, or by using washed platelets from a Glanzmann's thrombasthenia patient, the formation of MP was still observed. Prostaglandin E1 and protein kinase C antagonists (H-7 and staurosporine) inhibited both NNKY1-19-induced aggregation and MP formation. Ticlopidine or aspirin plus apyrase scarcely affected NNKY1-19-induced platelet aggregation, except to prolong the lag time. However, ticlopidine significantly inhibited MP formation (p less than 0.01). These results suggest that ticlopidine inhibits NNKY1-19-induced MP formation by a different mechanism to that of the other antagonists, and that this mechanism is unrelated to the inhibition of platelet aggregation.
我们在体外分析了噻氯匹定对血小板聚集以及血小板暴露于单克隆抗CD9抗体（NNKY1-19）时微粒（MP）形成的影响。即便通过与抗GPIIb/IIIa抗体或精氨酸-甘氨酸-天冬氨酸-丝氨酸预孵育，或使用来自血小板无力症患者的洗涤血小板，完全抑制了NNKY1-19诱导的血小板聚集，但仍观察到了MP的形成。前列腺素E1和蛋白激酶C拮抗剂（H-7和星形孢菌素）抑制了NNKY1-19诱导的聚集和MP形成。噻氯匹定或阿司匹林加腺苷双磷酸酶几乎不影响NNKY1-19诱导的血小板聚集，只是延长了延迟时间。然而，噻氯匹定显著抑制了MP的形成（p小于0.01）。这些结果表明，噻氯匹定通过与其他拮抗剂不同的机制抑制NNKY1-19诱导的MP形成，且该机制与血小板聚集的抑制无关。
