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凝血因子XI(FXI)作为凝血接触激活途径的一员首先被大家认识。然而随着研究的深入,人们对传统的瀑布凝血理论进行了修正,修正的理论认为:FXI可被凝血酶激活,并且在持续不断的凝血酶的生成和纤维蛋白溶解的抑制中发挥作用。FXI在血栓形成和止血中发挥不成比例的作用,人类先天FXI缺乏者一般只有轻度的受伤后出血,FXI缺乏或FXI抑制的动物出血也不受影响,说明FXI的放大途径对体内正常止血的作用不大。但是最近的动物实验揭示,FXI在病理性血管内凝血过程中起着重要的作用。本文将要讨论
As a member of the coagulation pathway, coagulation factor XI (FXI) was first recognized. However, with the deepening of research, the traditional theory of waterfall coagulation has been revised. The revised theory holds that FXI can be activated by thrombin and plays a role in the continuous generation of thrombin and inhibition of fibrinolysis. FXI plays a disproportionate role in thrombosis and hemostasis. Hypothyroidism in people with FXI deficiency generally results in mild post-traumatic hemorrhage. FXI deficiencies or FXI-suppressed animal haemorrhaging are also not affected, indicating that FXI’s amplification pathway is essential for normal hemostasis in the body not so useful. However, recent animal experiments revealed that FXI plays an important role in the pathological intravascular coagulation. This article will be discussed