Kumada T, Abiko Y
Thromb Res. 1984 Oct 15;36(2):153-63. doi: 10.1016/0049-3848(84)90337-2.
For understanding the physiological role of rat alpha 2-plasmin inhibitor (alpha 2-PI), the effect of alpha 2 PI deficiency on the fibrinolytic system was studied in rats in vitro and in vivo. Selective removal of alpha 2 PI from plasma was achieved in vitro and in vivo by immune complex formation with specific anti-rat alpha 2 PI rabbit gamma-globulin and the F(ab')2 fragments derived from specific anti-rat alpha 2 PI rabbit IgG, respectively. Depletion of alpha 2 PI from plasma resulted in almost complete loss of the fast-acting antiplasmin activity of the plasma and in a marked acceleration of urokinase-induced plasma clot lysis. A similar acceleration of thrombus dissolution was also observed, when a thrombus isolated from a thrombosed rat was incubated in alpha 2 PI-deficient serum in vitro. The effect was found to be inversely proportional to the alpha 2 PI levels in plasma or serum. When alpha 2 PI deficiency was induced in rats with experimental venous thrombosis, thrombus size was markedly decreased in association with elevation of serum fibrin degradation products and reduction of plasma plasminogen, indicating enhanced fibrinolysis in vivo. In addition, alpha 2 PI deficiency for a longer period induced a mild bleeding tendency at the sites of venipuncture. These results indicate that alpha 2 PI plays an important role as a stabilizer of fibrin in rats, as in humans.
为了解大鼠α2-纤溶酶抑制剂（α2-PI）的生理作用，我们在体外和体内研究了α2-PI缺乏对大鼠纤溶系统的影响。分别通过与特异性抗大鼠α2-PI兔γ球蛋白和源自特异性抗大鼠α2-PI兔IgG的F(ab')2片段形成免疫复合物，在体外和体内实现了从血浆中选择性去除α2-PI。血浆中α2-PI的消耗导致血浆快速起效的抗纤溶酶活性几乎完全丧失，并显著加速尿激酶诱导的血浆凝块溶解。当从血栓形成的大鼠中分离出的血栓在体外α2-PI缺乏的血清中孵育时，也观察到血栓溶解有类似的加速现象。发现这种作用与血浆或血清中的α2-PI水平成反比。当在实验性静脉血栓形成的大鼠中诱导α2-PI缺乏时，血栓大小显著减小，同时血清纤维蛋白降解产物升高，血浆纤溶酶原降低，表明体内纤溶增强。此外，长时间的α2-PI缺乏在静脉穿刺部位诱导了轻度出血倾向。这些结果表明，与人类一样，α2-PI在大鼠中作为纤维蛋白的稳定剂发挥着重要作用。
