摘要
用血小板聚集、粘附、释放实验和出血时间测定观察L 精氨酸·L 门冬氨酸盐 (DR)对血小板功能的作用。实验结果显示 :DR 15mg/kg静脉给药 ,可明显抑制腺苷二磷酸 (ADP)诱导的大鼠血小板聚集 (P <0 0 1) ;15mg/kg单次口服给药可明显抑制ADP诱导的家兔血小板聚集 ;其药效可持续 8h以上 (P <0 0 1) ;DR 7 5、15、3 0mg/kg灌胃给药 (Bid× 3 5d) ,可明显抑制ADP、胶原或凝血酶诱导的大鼠血小板聚集 (P <0 0 1) ,并延长出血时间 (P <0 0 5 )。DR 3 0mg/kg可明显抑制大鼠血小板粘附 ,并促进血管内皮释放前列环素 (PGI2 ) ,但对活化的血小板释放血拴素 (TXA2 )无明显影响。本研究发现 ,DR可抑制血小板聚集和粘附功能 ,其作用机制不同于阿司匹林。这些作用部分是由于DR增加了血管内皮PGI2 的释放。此结果为血小板功能的调节提供了新线索。
The effects of L arginine·L aspartate salt (DR) on platelet aggregation, adhesion and release were investigated. Platelet aggregation induced by adenosine 5′ diphosphate (ADP) was significantly inhibited ( P <0 01) by intravenous injection of DR (15 mg/kg) in rats or oral administration (15 mg/kg) in rabbits, the inhibitory effect on rabbit platelet aggregation lasting for more than 8 h ( P <0 01). Platelet aggregation induced by ADP, collagen or thrombin in rats was all markedly inhibited by 7 5, 15 or 30 mg/kg of DR (bid for 3 5 d, ig, P <0 01). Platelet adhesion to foreign objects was inhibited by 30 mg/kg of DR (ig). Bleeding time in rat tails was prolonged by 30 mg/kg of DR ( P <0 05). Furthermore, PGI 2 released from the vascular wall was increased in DR treated rats ( P <0 05), however, TXA 2 released from platelets was not affected. These data demonstrate the inhibitory effect of DR on platelet function, suggesting that its action target may be different from that of acetylsalicylic acid, and that the increase of PGI 2 release may be responsible partly for this effect. It is suggested that DR may probably be used as a new agent for regulating platelet function.
出处
《生理学报》
CAS
CSCD
北大核心
2001年第4期303-306,共4页
Acta Physiologica Sinica