Roberts H R, Monroe D M, Oliver J A, Chang J Y, Hoffman M
Center for Thrombosis and Hemostasis, University of North Carolina at Chapel Hill, USA.
Haemophilia. 1998 Jul;4(4):331-4. doi: 10.1046/j.1365-2516.1998.440331.x.
In this report we describe an in vitro model of blood coagulation reactions that mimics as closely as possible the in vivo condition. Our model indicates that the tissue factor-factor VIIa complex initiates coagulation by activating small amounts of both factor IX and factor X in the environment of the tissue factor bearing cell. Factor Xa and factor IXa formed in the initial reaction then play very distinct roles in the subsequent interactions of the clotting mechanism leading to a burst of thrombin generation on the platelet surface. Our results also indicate that factor XI can be activated by thrombin in the absence of factor XII and that the function of factor XI is simply to enhance conversion of factor IX to factor IXa resulting in enhanced thrombin generation on the platelet surface.
在本报告中，我们描述了一种尽可能模拟体内情况的血液凝固反应体外模型。我们的模型表明，组织因子-因子VIIa复合物通过在携带组织因子的细胞环境中激活少量的因子IX和因子X来启动凝血。在初始反应中形成的因子Xa和因子IXa随后在凝血机制的后续相互作用中发挥非常不同的作用，导致血小板表面大量生成凝血酶。我们的结果还表明，在没有因子XII的情况下，因子XI可被凝血酶激活，并且因子XI的功能仅仅是增强因子IX向因子IXa的转化，从而导致血小板表面凝血酶生成增加。
