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目的 观察左旋精氨酰 谷氨酸二肽 (L Arg Glu)对大鼠血小板聚集、血栓形成、血液流变性、凝血纤溶系统及血浆NO、cGMP、PGI2 的影响。方法 2 4只SD大鼠随机分为3组 ,分别灌服阿斯匹林 36mg·kg-1·d-1,Arg Glu 6 1.4mg·kg-1·d-1及同体积对照液 ,8d后检测血流变、凝血纤溶指标 ;2 4只SD大鼠随机分为 2组 ,处理相同 ,比浊法测定血小板聚集活性 ,放免法测定血浆cGMP、PGI2 水平 ,分光光度法测定一氧化氮浓度 ;另 2 4只SD大鼠分为两组 ,处理相同 ,以颈总动脉 颈外静脉旁路模型观察血栓湿重。结果 L Arg Glu与对照组相比可明显降低全血表观黏度、还原黏度、红细胞压积和血浆黏度 ,延长血浆复钙时间、白陶土部分凝血活酶时间及凝血酶原时间 (P <0 0 5 ) ,可使大鼠血小板聚集活性降低 (ADP及AA诱导 ) ,血栓湿重降低 ,血浆NO和cGMP升高 ,PGI2 有升高趋势 ,但差异无统计学意义。结论 Arg Glu二肽有抗血栓、改善血液流变性、抑制血小板聚集活性 ,可视为一NO前体 ;其作用机制推测除可能由精氨酸 一氧化氮 环磷酸鸟苷酸代谢通路 (Arg NO cGMPpathway)所介导外 ,尚有其它作用机制参与。
Objective To observe the effects of L-arginine glutamate on platelet aggregation, thrombosis, hemorheology, coagulation and fibrinolysis system, plasma NO, cGMP and PGI2 in rats. Methods Twenty four SD rats were randomly divided into three groups: aspirin 36 mg · kg -1 · d -1, Arg Glu 6 1.4 mg · kg -1 · d -1 and the same volume of control solution for 8 days And then the indexes of blood rheology and coagulation and fibrinolysis were detected. Twenty four SD rats were randomly divided into two groups and were treated identically. The platelet aggregation activity was measured by turbidimetric method. Plasma levels of cGMP and PGI2 were determined by radioimmunoassay. Nitric oxide The other 24 SD rats were divided into two groups and treated identically. The wet weight of thrombus was observed by external jugular vein venous bypass model. Results Compared with the control group, L Arg Glu significantly reduced whole blood apparent viscosity, reduction viscosity, hematocrit and plasma viscosity, prolonged plasma calcium re-Ca, kaolin partial thromboplastin time and prothrombin time (P <0 0 5) could decrease the platelet aggregation activity (induced by ADP and AA), the thrombus wet weight, the plasma NO and cGMP, and the PGI2 increased, but the difference was not statistically significant. Conclusion The Arg Glu dipeptide has antithrombotic, improving hemorheology and inhibiting platelet aggregation activity, which can be regarded as a precursor of NO. Its mechanism of action suggests that Arg NO may be caused by Arg NO cGMPpathway) mediated, there are other mechanisms of action involved.