摘要
P6A(10^(-6)—10^(-4)mol/L)体外实验显著减弱ADP诱导的大鼠血小板聚集,明显增加血小板的有效解聚率。20～30μmol/kg的 P 6 A动脉注射后,3～6分钟时大鼠血浆t-PA、PAI活性无变化。0.25～1.0μg/ml的P6A亦不能使兔血浆纤维蛋白平板出现溶解。实验结果提示,P 6 A对血栓闭塞性血管再通的作用主要依赖其抗血小板聚集及促血小板解聚的作用。
P 6 A (10^(-6)-10^(-4) mol/L) could slighly inhibit the rate of maximal platelet aggregation and theinitial aggregation in the first and second minute, significantly enhance tlte rate of platelet disaggrega-tion in the third to fifth minute. The aclivities of plasma t-PA and PAI were not altered in 3 to 6minutes after i.a injection of P 6 A (20-30μmol/kg) in rats, The fibrinous plates of rabbit plasmacould not be lysed by P 6 A (0.25-100μg/ml). The results suggest that the reopening of obliteratedvessels induced by peptide 6 A is chiefly due to the fact that P 6 A inhibits the aggregation andpromotes the disaggregation of platlets.
出处
《北京医科大学学报》
CSCD
1992年第3期185-187,共3页
Journal of Peking University(Health Sciences)
关键词
肽6A
纤维蛋白
血小板聚集
Peptide 6 A
Fibrinolysis
Platelet aggregation
