抑肽酶对血小板粘附功能保护作用的实验研究

Reserch on Protective Effect of Aprotinin for Platelet Adhesion

在正常人富血小板血浆中加入尿激酶后,激活瑞斯托霉素诱导的血小板凝集率下降到对照值的31.7%,表明血小板粘附功能受到明显损伤。这种作用可能与活化的纤溶系统对血小板膜糖蛋白Ⅰ受体的水解有关。事先经抑肽酶孵育的富血小板血浆中加入相同浓度的尿激酶,瑞斯托霉素诱导的血小板凝集率下降不明显,表明抑肽酶可有效地抑制尿激酶的损伤作用,保护血小板的粘附功能。

By adding urokinase to PRP of normal subjects, ristocetin induced platelet agglutination declined to 31.7% of control value, indicating the damage in platelet adhesive function, which may be attributed to the hydrolysis of platelet GPI caused by fibrinolysis. However, when the same does of urokinase was added to aprotinin pretreated PRP, the decline of platelet agglutination was not demonstrated. The results showed that aprotinin could protect the platelet adhesive function effectively by inhibiting fibrinolysis.