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目的 观察L 精氨酸L 门冬氨酸盐 (DR)对动物血栓形成模型的影响并初步探讨其作用机制。方法 用大鼠颈动脉血栓模型、动静脉旁路血栓模型和小鼠肺栓塞模型评价DR的抗血栓作用 ;测定血浆TXA2 、PGI2 和NO水平 ,测定血管内皮释放PGI2 水平 ,以探讨DR的作用机制。结果 DR 7 5、15、3 0mg·kg-1单次灌胃给药 ,可减轻大鼠颈动脉血栓重量 (P <0 0 1) ;7 5、15、3 0或 60mg·kg-1均可显著抑制血小板在动静脉旁路中丝线上的沉积 (P <0 0 5或P <0 0 1) ;但对花生四烯酸引起的小鼠肺栓塞死亡无明显作用。DR 3 0mg·kg-1单次给药 (ig) ,对大鼠血浆TXA2 水平无明显影响 ;使PGI2 有升高趋势。而相同剂量阿司匹林 (ASA)可明显抑制二者水平。DR 3 0mg·kg-1给药 (ig) 7次 ,每日 2次 ,可明显促进血管内皮释放PGI2 ;并使血浆NO水平有明显升高。结论 DR可明显抑制动脉血栓形成 ,其作用可能与血管内皮释放PGI2 和NO有关 ,而与血小板花生四烯酸代谢途径无关。
Objective To observe the effect of L-arginine L-aspartate (DR) on animal thrombosis model and to explore its mechanism. Methods The carotid artery thrombosis model, arteriovenous bypass thrombosis model and mouse pulmonary embolism model were used to evaluate the antithrombotic effect of DR. The levels of plasma TXA2, PGI2 and NO were measured and the levels of PGI2 released from the vascular endothelium were measured to explore the mechanism of DR . Results A single intragastric administration of DR 7, 5, 15, 30 mg · kg -1 could reduce the carotid artery thrombosis weight (P <0.01), and all of 7, 15, 15 or 60 mg · kg -1 (P <0.05 or P <0.01). However, there was no significant effect on arachidonic acid induced pulmonary embolism death in mice. DR 3 0mg · kg-1 single administration (ig) had no significant effect on plasma TXA2 level in rats; PGI2 increased. The same dose of aspirin (ASA) can significantly inhibit both levels. DR 3 0mg · kg-1 administered (ig) 7 times, twice daily, can significantly promote the release of PGI2 endothelium; and plasma NO levels were significantly increased. Conclusion DR can significantly inhibit arterial thrombosis, which may be related to the release of PGI2 and NO in vascular endothelium, but not to the platelet arachidonic acid metabolic pathway.