Mizuta T, Imai C
Department of Pharmacology, Meiji Institute of Health Science, Odawara, Japan.
Life Sci. 1988;43(12):955-63. doi: 10.1016/0024-3205(88)90540-1.
The effects of tissue-type plasminogen activator (t-PA) on the platelet aggregation were studied using citrated whole blood and platelet-rich plasma (PRP) obtained from human donors. t-PA suppressed adenosine 5'-diphosphate (ADP)- or collagen-induced platelet aggregation in a dose-dependent manner. The 50% inhibitory concentration (IC50) for t-PA was lower by one order of magnitude than that for urokinase (UK) in whole blood and PRP. The suppression of platelet aggregation was not completely inhibited by alpha-2-antiplasmin. t-PA did not cause the degradation of fibrinogen or fibrin in PRP, whereas UK caused the reduction of fibrinogen and fibrin, and the increase of fibrinogen- and fibrin-degradation products (FDP). These results suggest that the mode of action of t-PA in inhibiting platelet aggregation may be different from that of UK.
使用从人类供体获得的枸橼酸化全血和富血小板血浆（PRP）研究了组织型纤溶酶原激活剂（t-PA）对血小板聚集的影响。t-PA以剂量依赖的方式抑制腺苷5'-二磷酸（ADP）或胶原诱导的血小板聚集。在全血和PRP中，t-PA的50%抑制浓度（IC50）比尿激酶（UK）低一个数量级。α-2-抗纤溶酶不能完全抑制血小板聚集的抑制作用。t-PA不会导致PRP中纤维蛋白原或纤维蛋白的降解，而UK会导致纤维蛋白原和纤维蛋白减少，以及纤维蛋白原和纤维蛋白降解产物（FDP）增加。这些结果表明，t-PA抑制血小板聚集的作用方式可能与UK不同。
