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血小板和组织因子(2)

  血小板TF在凝血过程中的作用

  普遍认为,TF位于血管壁,与血浆中各种凝血因子分隔,从而防止血栓在完整的血管内生成。凝血和血栓生成是在血管损伤后形成的,因为血管损伤后血管壁上的TF暴露于血,与FⅦa结合形成复合物,从而启动凝血级联反应,形成血栓止血。同时,血栓的扩大还需要血小板的黏附,使其聚集于血管壁。血管壁上TF启动的活化凝血因子需要与血小板上的磷脂结合才能形成凝血酶原酶复合物。然而,黏附于血管壁的血小板白色血栓及早期生成的少量纤维蛋白是一道屏障,阻止活化的凝血因子与上层的血小板接触,使血栓不能扩大。即使凝血因子是通过理想的自由扩散运动也要数小时才能到达1 mm血栓的顶端,而损伤血管壁形成的血栓一般有1-3 mm大小。因此如果血细胞或微粒携带TF可以在逐渐形成的血栓表面激活凝血因子,而不需扩散[26],即血小板表面本身能够形成一个纤维蛋白生成体系,使纤维蛋白不断生成,这样就可以稳定和巩固新形成的血栓[27]。问题和展望凝血是一系列凝血因子及其他成分参与相继酶解激活的过程,分子机制极其复杂,临床许多疾病如休克、血栓性疾病都存在凝血功能紊乱。随着研究的深入和现代科学技术的发展,很多作用机制都会得到阐明。在健康人中,TF不仅存在于血管外组织细胞,而且存在于血管壁及血循环中的一些细胞如内皮细胞、平滑肌细胞、白细胞、血小板等。血小板与血液中TF表达的关系是十分密切的,因此对血小板在生理性止血、凝血及血栓性疾病的发病方面起着其他重要的作用,仍需进一步深入研究,只有这样才能了解疾病的发生、发展进程,以利于指导治疗。

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