L-精氨酸L-门冬氨酸盐对血栓形成的影响及其机制  

The effect of L-arginine L-aspartate on arterial thrombosis model and its mechanism

作　　者：王银叶[1] 刘晓岩[1] 王景燕 王超[2] 李春波 毛伟 彭师奇[2] 

机构地区：[1]北京大学药学院药理学系,北京100083 [2]北京大学药学院药物化学系,北京100083 [3]浙江新昌制药厂

出　　处：《中国药理学通报》2001年第5期528-531,共4页Chinese Pharmacological Bulletin

摘　　要：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。AIM To study the effects of L arginine L aspartate on arterial thrombosis in animal model and to explore its action mechanism. METHODS Jugular artery thrombosis model and A V by pass thrombosis model in rats; pulmonary embolism model in mice; PGI 2 and TXA 2 assay in serum,Tests of PGI 2 in aorta segment and cAMP in platelets with radio immunological assay; NO in serum assay with reduction method. RESULTS 7 5, 15, 30 mg·kg -1 of DR (ig) significant reduced wet thrombus weight when stimulated by FeCl 3 ( P <0 01); 7 5, 15, 30, 60 mg·kg -1 of DR(ig bid×3 5 d) reduced wet or dry thrombus weight on the thread segment in A V by pass ( P< 0 05 or P <0 01). However, DR did not affect the mortality of mouse induced by pulmonary embolism induced by AA. In addition, DR significantly enhanced the release of PGI 2 from the aorta wall ( P <0 05), and also increased NO level in serum ( P <0 05). CONCLUSION DR inhibited arterial thrombosis in rats, this efficacy can be partly due to stimulating PGI 2 and NO release from vessel wall and was not related with arachidonic acid metabolic way in platelets.

关 键 词：L-精氨酸L-门冬氨酸盐 动脉血栓形成 血栓素 前列环素 一氧化氮 

分 类 号：R543[医药卫生—心血管疾病] R973.2[医药卫生—内科学]