摘要
[目的]观察HQSM对垂体后叶素所致急性心肌缺血大鼠血浆PGI2／TXA2的影响。[方法]84只大鼠，随机分成7组：正常对照组、模型对照组、IIQSM组（210mg／kg、150mg／kg、105mg／kg）、阳性对照组（黄芪生脉饮、地奥心血康）。采用灌胃给药，每天1次，连续30d。末次给药后1h．尾静脉给予垂体后叶素造成急性心肌缺血模型。1h后取血，分离血浆，测定各组PGI2、TXA2的代谢产物6-Keto-PGF1α、TXB2，分析PGI2／TXA2比值。[结果]大鼠给予垂体后叶素后，血浆中TXB2升高，6-Keto—PGF1α／TXB2比值降低（P〈0．05～0．01）。与模型对照组比较，HQSM（210mg／kg、150mg／kg）明显降低垂体后叶素所升高的TXB2，升高6-Keto—PGF1α／TXB2比值（P〈0．01）。[结论]HQSM抗垂体后叶素致大鼠心肌缺血作用机制之一是通过抑制升高的血浆TXA2，纠正PGI2／TXA2失衡。
[Objective] To observe the effect of HQSM on PGI2/TXA2 in blood plasma of acute myocardial ischemia rats caused by injecting pituitrin. [Methods] 84 SD rats were divided into seven groups at random： normal control group,model control group, three HQSM groups（ 210mg/kg, 150mg/kg, 105mg/kg）, Huangqi Shengmaiyin and DI ＇ ao Xinxuekang. Intragastric administration was adopted once a day for 30 days. Acute myocardial ischemia model rat was established by injecting pituitrin from tail vein lh after the last administration, and blood plasma was separated to be determined the activity of 6-Keto-PGF1α and TXB2, which is the rnetabolitc of PGI2 and TXA2 in blood plasma of SD rats. [Results] Having heen injected pituitrin,the activity of TXB2 upgraded while 6 Keto PGI1α/TXB2 decreased（ P〈0.05 - 0.01 ）. Compared with model group, HQSM （210mg/kg, 150mg/kg） group could decrease the activity of TXB2 and increase the ratio of 6 Keto-PGF1α/TXB2 （P〈0.01）. [Conclusion] One of the action mechanisms of HQSM amacliorating myocardial ischemia eaused by pituitrin is that it can increase the ratio of 6- Keto PGF1α/TXB2 through decreasing the activity of TXA2.
出处
《浙江中医药大学学报》
CAS
2006年第6期607-608,611,共3页
Journal of Zhejiang Chinese Medical University
基金
国家十五重大科技攻关专项863计划(No:2003AA2Z3254)~~
