Mirshahi M, Soria J, Bertrand O, Amiral J, Soria C
INSERM U. 150, IVS Hôpital Lariboisière, Paris, France.
Blood Coagul Fibrinolysis. 1990 Oct;1(4-5):531-6. doi: 10.1097/00001721-199010000-00032.
Clinical data have shown that the evaluation of fibrin degradation products (FbDP) does not reflect the efficiency of thrombolytic therapy in vivo. In this study, we found that the addition of plasminogen activators to normal plasma resulted in generation of FbDP and release of fibrinopeptide A (FpA) as shown by ELISA and HPLC. This FpA release was concomitant with fibrinogen degradation, and was not inhibited by thrombin inhibition or by prothrombin depletion in plasma. Thus, the increase in FpA did not result from coagulation activation and may result from the plasmin-induced release of FpA from fibrinogen degradation product E1. The generation of cross-linked FbDP after tPA addition occurred in normal plasma as well as in factor-XIII-deficient plasma and quickly reached a plateau. It was not inhibited by hirudin. Therefore FbDP in these plasmas probably derived from the plasmin degradation of cellular transglutaminase cross-linked fibrin/fibrinogen derivatives present in plasma.
临床数据表明，纤维蛋白降解产物（FbDP）的评估并不能反映体内溶栓治疗的效果。在本研究中，我们发现向正常血浆中添加纤溶酶原激活剂会导致FbDP的生成以及纤维蛋白肽A（FpA）的释放，这通过酶联免疫吸附测定（ELISA）和高效液相色谱法（HPLC）得以证实。这种FpA的释放与纤维蛋白原降解同时发生，并且不受血浆中凝血酶抑制或凝血酶原消耗的影响。因此，FpA的增加并非由凝血激活所致，可能是由于纤溶酶诱导纤维蛋白原降解产物E1释放FpA。添加组织型纤溶酶原激活剂（tPA）后交联FbDP的生成在正常血浆以及缺乏因子XIII的血浆中均会发生，并且迅速达到平台期。它不受水蛭素的抑制。因此，这些血浆中的FbDP可能源自血浆中细胞转谷氨酰胺酶交联的纤维蛋白/纤维蛋白原衍生物的纤溶酶降解。
