Hoffman Maureane
Department of Pathology, Duke University Medical Center and Durham VA Medical Center, Durham, NC 27705, USA.
J Thromb Thrombolysis. 2003 Aug-Oct;16(1-2):17-20. doi: 10.1023/B:THRO.0000014588.95061.28.
The concept of a coagulation cascade describes the biochemical interactions of the coagulation factors, but has flaws as a model of the hemostatic process in vivo. For example, the model cannot explain why hemophiliacs bleed when they have an intact factor VIIa/tissue factor ("extrinsic") pathway. Hemostasis requires the formation of an impermeable platelet and fibrin plug at the site of vessel injury, but it also requires that the powerful procoagulant substances activated in this process remain localized to the site of injury. This control of blood coagulation is accomplished by localizing the procoagulant reactions to events on specific cell surfaces to keep coagulation from spreading throughout the vascular system. A consideration of the critical role of cells allows us to construct a model of coagulation that better explains bleeding and thrombosis in vivo. This cell-based model suggests that the "intrinsic" and "extrinsic" pathways are in fact not redundant systems, but operate in parallel on different cell surfaces.
凝血级联反应的概念描述了凝血因子的生化相互作用，但作为体内止血过程的模型存在缺陷。例如，该模型无法解释为什么血友病患者在其因子VIIa/组织因子（“外源性”）途径完整时仍会出血。止血需要在血管损伤部位形成不可渗透的血小板和纤维蛋白凝块，但还需要在此过程中激活的强大促凝血物质局限于损伤部位。这种对血液凝固的控制是通过将促凝血反应定位到特定细胞表面的事件来实现的，以防止凝血扩散到整个血管系统。对细胞关键作用的考虑使我们能够构建一个更好地解释体内出血和血栓形成的凝血模型。这个基于细胞的模型表明，“内源性”和“外源性”途径实际上并非冗余系统，而是在不同细胞表面并行运作。
