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取大鼠３０只分为正常对照组、模型对照组及川芎嗪组，ｉｐ乌拉坦麻醉，监测肢体Ⅱ导联心电图。正常对照组冠脉左室支下只穿线不结扎，另两组均结扎冠脉左室支，结扎后心电图ＳＴ段明显抬高，３０ｍｉｎ后松解结扎线再灌注６０ｍｉｎ。松扎同时各组分别以恒流泵经股静脉匀速输入生理盐水及川芎嗪生理盐水溶液。测心律失常出现时间川芎嗪组明显迟于模型组。ＳＴ段抬高程度川芎嗪组显著低于模型组。再灌注后心肌细胞内Ｃａ２＋含量及血清ＣＫ－ＭＢ含量川芎嗪组明显低于模型对照组。川芎嗪可明显对抗大鼠心肌再灌注损伤所致的ＳＯＤ、ＧＳＨ－Ｐｘ活性下降和ＭＤＡ含量的升高。说明川芎嗪对再灌注损伤有一定的防护作用，其机理可能与其抑制细胞Ｃａ２＋的内流、保护心肌组织抗氧自由基酶活性、加强清除氧自由基、抑制脂质过氧化等作用有关
30 rats were divided into normal control group, model control group and ligustrazine group, ip urethane anesthesia, limb Ⅱ lead electrocardiogram monitoring. In the control group, left ventricular branches of the coronary arteries were only ligated without ligating. The other two groups were ligated with left ventricular branches of the coronary artery. The ST segment of the electrocardiogram was significantly elevated after ligation, and the ligature of the ligature was released for 60 minutes after 30 minutes. At the same time, the rats in each group were given normal saline and ligustrazine normal saline solution by constant flow pump at the same time through the femoral vein. Arrhythmia time TMP group was significantly later than the model group. The level of ST elevation in the ligustrazine group was significantly lower than that in the model group. After reperfusion, intracellular Ca2 + content and serum CK-MB content in ligustrazine group was significantly lower than that in model control group. Ligustrazine can obviously antagonize the decrease of the activity of SOD, GSH-Px and the increase of MDA content caused by myocardial reperfusion injury in rats. This shows that tetramethylpyrazine has a protective effect on reperfusion injury, and its mechanism may be related to its inhibition of influx of Ca2 +, protection of myocardial tissue of free radical antioxidant enzyme activity, enhance scavenging oxygen free radicals, inhibition of lipid peroxidation and so on