Broze G J
Division of Hematology, Jewish Hospital, Washington University Medical Center, St. Louis, MO 63110, USA.
Curr Opin Hematol. 1996 Sep;3(5):390-4. doi: 10.1097/00062752-199603050-00010.
Thrombin generation during coagulation affects the fibrinolysis resistance of clots. This phenomenon is mediated at least in part by a plasma carboxypeptidase that has been called carboxypeptidase-U, carboxypeptidase-R, pro-carboxypeptidase-B, and thrombin-activatable fibrinolysis inhibitor. Carboxypeptidase-U circulates as an inactive proenzyme and is activated by thrombin in a process that is dramatically enhanced by the cofactor thrombomodulin. Clots formed in hemophilic plasma in the presence of a plasminogen activator lyse prematurely and this defect can be correlated by the addition of the missing coagulation factor or thrombomodulin. Thrombin-dependent inhibition of fibrinolysis, which is demonstrable in artificial systems in vitro, may help explain certain in vivo observations, including the delayed bleeding often seen in individuals with hemophilia.
凝血过程中凝血酶的生成会影响血凝块的纤溶抗性。这种现象至少部分是由一种血浆羧肽酶介导的，该羧肽酶被称为羧肽酶 -U、羧肽酶 -R、前羧肽酶 -B和凝血酶激活的纤溶抑制物。羧肽酶 -U以无活性的酶原形式循环，在辅因子血栓调节蛋白显著增强的过程中被凝血酶激活。在纤溶酶原激活剂存在的情况下，血友病血浆中形成的血凝块会过早溶解，并且通过添加缺失的凝血因子或血栓调节蛋白可以关联这种缺陷。在体外人工系统中可证实的凝血酶依赖性纤溶抑制，可能有助于解释某些体内观察结果，包括血友病患者中常见的延迟性出血。
