Bara L, Samama M, Bilski-Pasquier G, Bloch M F, Rochas S
Pathol Biol (Paris). 1977 Dec;25 Suppl:48-54.
Our aim in this work has been to obtain precisions on the bleeding mechanism during fibrinolysis induced by streptokinase in the rabbit. Haemostasis was studied in vivo by the method oh Honour and Russell. The injection of 40 000 u/kg of streptokinase in 10 minutes induces rapidly fibrinolysis, which lasts for approximately one hour which is not accompanied by changes either in coagulation factors, or in platelet function. In vivo : . the adhesion of platelets to the vascular lesion is normal; . platelet aggregation is normal as is the formation of intravascular thrombi; . on the other hand the intra mural platelet thrombus is unstable. The embolization of the intravascular thrombi is responsible for new hemorrhages which can be correlated with the intensity of fibrinolysis. Thus, even in the absence of fibrinogenolysis, of fibrinogen degradation products FPD, of abnormal thrombin generation and of altered platelet function, the fibrinolytic activity induced by streptokinase could alone be responsible for bleeding episodes, occuring during thrombolytic treatment by streptokinase in man.
我们这项工作的目的是要明确链激酶诱导家兔纤维蛋白溶解过程中的出血机制。采用Honour和Russell的方法在体内研究止血情况。10分钟内注射40000单位/千克链激酶可迅速诱导纤维蛋白溶解,持续约1小时,此过程中凝血因子和血小板功能均无变化。在体内:. 血小板对血管损伤的黏附正常;. 血小板聚集正常,血管内血栓形成也正常;. 另一方面,壁内血小板血栓不稳定。血管内血栓的栓塞导致新的出血,这与纤维蛋白溶解的强度相关。因此,即使不存在纤维蛋白原溶解、纤维蛋白原降解产物(FPD)、异常凝血酶生成以及血小板功能改变,链激酶诱导的纤维蛋白溶解活性本身就可能是人类链激酶溶栓治疗期间出血发作的原因。