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近年来,随着对血管内皮细胞抗凝血机制研究的进展,人们认识到前列环素、抗凝血酶Ⅲ辅因子和TM(血栓调理蛋白)是血管壁抗血栓形成的主要成分,其中经TM活化产生的APC(活化的蛋白C)具有选择性灭活V_a/Ⅷ_a因子、抑制血小板膜表面凝血酶原的转化和促进纤溶的能力。此外,TM还与前列环素相互协同,共同参与血小板在微循环中的功能调节。 1976年,Kisiel发现体外凝血时,只有极少量的蛋白C活化。1979年该作者又观察到,凝血酶在体外活化蛋白C的速度非常缓慢,而且受生理浓度的钙离子抑制。Comp(1982)用小剂量凝血酶(1U/分每公斤体
In recent years, with the progress of research on anticoagulant mechanism of vascular endothelial cells, it has been recognized that prostacyclin, antithrombin III cofactor and TM (thrombomodulin) are the main components of antithrombotic vessel wall, APC (activated protein C) produced by TM activation has the ability of selectively inactivating V_a / Ⅷ_a factors, inhibiting the transformation of prothrombin on the platelet membrane and promoting fibrinolysis. In addition, TM synergizes with prostacyclin to participate in the functional regulation of platelets in microcirculation. In 1976, Kisiel found that only a very small amount of protein C was activated in vitro. In 1979, the authors observed that thrombin activated protein C in vitro at a very slow rate and was inhibited by physiological concentrations of calcium ions. Comp (1982) with a small dose of thrombin (1U / min per kilogram of body