产科DIC的病理生理学.docVIP

Pathophysiology of DIC in obstetric disorders 产科DIC的病理生理学 It is important to understand the normal coagulation process in order to characterise the abnormalities observed during DIC. 为了描述DIC的异常特征，理解正常的凝血过程十分重要。 The coagulant response begins with exposure of tissue factor (TF) and binding of factor VIIa to activate factor X for conversion of pro-thrombin to thrombin.[1] 凝血反应始于组织因子（TF）的暴露以及VIIa与Xa结合使凝血酶原转变为凝血酶[1]。 Thrombin generation is further propagated through the intrinsic pathway and the explosive burst of thrombin results in cleavage of ?brinogen into ?brin.[2] 凝血酶通过内源性途径进一步生成，凝血酶的爆发式生成导致了纤维蛋白原裂解为纤维蛋白[2]。 Clot formation is homeostatically regulated to achieve the desired haemostatic effect and this involves a number of regulatory responses that are spatially and temporally differentiated. 血块的形成是自稳性调节而获得理想的止血效果，这涉及了大量的时空特异性的调解节反应。 Normal endothelium at the margins of injury switches from thrombin procoagulant to anticoagulant activity via its binding to the endothelial receptor, thrombomodulin (TM).[3] 伤口边缘的正常内皮通过与内皮受体凝血酶调节蛋白（TM）结合，由促凝变为抗凝[3]。 The thrombin–TM complex activates protein C bound to the endothelial protein C receptor (EPCR).[4] 凝血酶-凝血酶调节蛋白复合物激活结合与内皮蛋白C受体(EPCR)上的蛋白C[4]。 The generated activated protein C (APC) degrades activated factor V and VIII with co-factor support from protein S to inhibit further clot formation.[5] 产生的活化的蛋白C在来自于蛋白S的辅助因子的支持下降解Va 和VIIIa，抑制血块的进一步形成。 Other important anticoagulants involved are anti thrombin and tissue factor pathway inhibitor (TFPI). The former inactivates thrombin and factor Xa whilst TFPI forms a quaternary complex with tissue factor, factor VIIa and Xa to inhibit the cascading effect towards thrombin generation.[6] 涉及的其它的抗凝血物质是抗凝血酶（AT）和组织因子途径抑制剂（TFPI）。前者灭活凝血酶和Xa，而TFPI与组织因子、VIIa 、Xa形成四聚体抑制凝血酶生成的级联效应。 Normal clot formation is followed by its own regulated dissolution. This process of ?brinolysis involves thrombin-induced tissue plasminogen activator (t-PA) dependent generation of plasmin from plasminogen.[7] 正常的血块