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首页> 外文期刊>Platelets >Effects of ticlopidine on von Willebrand factor-mediated shear-induced platelet activation and aggregation.
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Effects of ticlopidine on von Willebrand factor-mediated shear-induced platelet activation and aggregation.

机译：噻氯匹定对血管性假血友病因子介导的剪切诱导的血小板活化和聚集的影响。

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Ticlopidine, recently classified as a P2Y(12) ADP receptor blockade, is known to be an effective antiplatelet agent preventing arterial thrombosis, e.g., myocardial infarction or cerebral infarction, but the mechanism of the in vivo antithrombotic effects of ticlopidine is not fully understood. Blood was drawn from seven normal volunteers before and 7 days after consecutive intake of ticlopidine, and 1 day after oral intake of aspirin after 7 days of ticlopidine wash-out period. Effects of drug intake on shear-induced von Willebrand factor (vWF) binding to platelets, platelet activation evidenced by P-selectin surface expression and translocation of GP Ibalpha, and vWF-mediated platelet aggregation, were investigated by using an optically modified cone-plate viscometer and quantitative flow cytometry. The maximum extent of platelet aggregation occurring under a high shear rate of 10800 s(-1), presumably mediated by vWF, was not significantly influenced by either ticlopidine or aspirin. However, significant dissociation of once aggregated platelets occurred in samples obtained after ticlopidine intake (25.4 +/- 9.3%, P = 0.00030) and less significantly after aspirin intake (15.9 +/- 5.7%, P = 0.0013), while only insignificant and modest dissociation occurred in controls (6.3 +/- 4.4%, n.s.). Binding experiments also revealed that the shear-induced vWF binding to platelets was significantly inhibited by ticlopidine, and less significantly by aspirin, although other indicators of platelet activation, such as shear-induced P-selectin expression and GP Ibalpha translocation were not influenced by either ticlopidine or aspirin. We demonstrate here that platelet aggregation mediated by von Willebrand factor (vWF) under a high shear rate of 10800 s(-1) cannot be stabilized and that dissociation occurs readily when ADP receptor stimulation is blocked by continuous intake of ticlopidine, indicating that these effects on platelet thrombus formation may contribute to the in vivo antithrombotic effects of ticlopidine.
机译：噻氯匹定最近被归类为P2Y（12）ADP受体阻滞剂，已知是预防动脉血栓形成（例如心肌梗塞或脑梗塞）的有效抗血小板药，但是尚未完全了解噻氯匹定的体内抗血栓形成作用的机制。在连续服用噻氯匹定之前和之后7天，以及在抽取噻氯匹定7天后口服阿司匹林后1天，从7名正常志愿者那里抽血。使用光学修饰的锥板研究了药物摄入对剪切诱导的von Willebrand因子（vWF）结合血小板，P-选择素表面表达和GP Ibalpha转运所证实的血小板活化以及vWF介导的血小板聚集的影响。粘度计和定量流式细胞仪。可能由vWF介导的10800 s（-1）高剪切速率下发生的血小板聚集的最大程度不受噻氯匹定或阿司匹林的影响。但是，在噻氯匹定摄入后获得的样品中曾经聚集的血小板发生显着解离（25.4 +/- 9.3％，P = 0.00030），而阿司匹林摄入后的血小板显着解离（15.9 +/- 5.7％，P = 0.0013），而仅发生了很小的变化。在对照中发生适度的解离（6.3 +/- 4.4％，ns）。结合实验还显示，噻氯匹定显着抑制了剪切诱导的vWF与血小板的结合，而阿司匹林的抑制作用则较小，尽管其他血小板活化的指标，例如剪切诱导的P-选择素表达和GP Ibalpha易位均不受此影响。噻氯匹定或阿司匹林。我们在这里证明了在10800 s（-1）的高剪切速率下由von Willebrand因子（vWF）介导的血小板凝集无法稳定，当连续摄取噻氯匹定阻断ADP受体刺激时，解离容易发生。对血小板血栓形成的影响可能有助于噻氯匹定的体内抗血栓形成作用。

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