维心脉抗心肌缺血的实验研究

 目的研究维心脉对实验性急性心肌缺血的保护作用及可能的机制。方法阻断犬冠状动脉前降支造成急性心肌缺血模型,测量心外膜心电图(ECG)、Ⅱ导联心电图[ECG(Ⅱ)]、平均动脉压(MBP)、心肌耗氧指数及心肌梗死面积;以体内血栓形成仪刺激大鼠血栓形成,二磷酸腺苷(ADP),花生四烯酸及胶原诱导血小板聚集,测量血栓形成时间和血小板聚集抑制百分率。结果维心脉1.5和3.0g·kg^-1可明显降低心肌梗死犬的∑ST,NST及心肌氧耗指数,缩小心肌梗死范围,降低血压而对心率无明显影响。维心脉3个剂量组:2.0,4.0和8.0g·kg^-1能显著推迟大鼠实验性动脉血栓形成时间,抑制ADP,花生四烯酸及胶原诱导的血小板聚集。结论维心脉可通过降低心肌耗氧量,抑制血小板聚集和血栓形成从而较好的保护缺血心肌。

Effect of Weixinmai on myocardial ischemia

OBJECTIVE To study the effects and possible mechanism of Weixinmai against the experimental acute myocardial ischemia. METHODS The experimental acute myocardial ischemic model was established by ligating the anterior descending coronary artery in dogs. Thrombosis was caused by thrombosis instrument in vivo. Platelet aggregation was induced by ADP, arachidonic acid and collagen, respectively. The effect of Weixinmai on myocardial ischemia was investigated by measuring Σ ST and NST of epicardial ECG, HR, MBP, myocardial oxygen consumption index,time for thrombosis, and inhibitory percentage of platelet aggregation. RESULTS Weixinmai reduced ΣST, NST, myocardial oxygen consumption index, myocardial infarction size and lowed the blood pressure without significant influence of heart rate at 1.5 and 3.0 g·kg^-1. Weixinmai also delayed the thrombosis and inhibited platelet aggregation induced by ADP, arachidonic acid and collagen at 2.0,4.0,and 8.0g·kg^-1 .CONCLUSION Weixinmai effectively protected ischemic myocardium by lowing myocardial oxygen constimption, inhibiting thrombosis and platelet aggregation.