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用结扎大鼠冠状动脉左室支造成心肌缺血及再灌注损伤模型，观察苄普地尔对其心肌缺血再灌注损伤的影响。苄普地尔（２．５ｍｇ／ｋｇ，ｉｖ）显著降低大鼠室性心动过速发生率（Ｐ＜０．０５），提高其心肌超氧化物歧化酶活性，但统计学处理无显著性差异（Ｐ＜０．０５）。Ｐ＜０．０１２．２对ＳＯＤ活力影响ＮＳ组大鼠心肌缺血区与非缺血区ＳＯＤ活力比值为０．６９±０．０９（ｎ＝６），Ｖｅｒ组与Ｂｅｐ组分别为０．８８±０．１５（ｎ＝６）及０．７６±０．１９（ｎ＝６），前者与ＮＳ组比较Ｐ＜０．０５，后者则Ｐ＞０．０５。提示Ｂｅｐ对缺血再灌后大鼠心肌ＳＯＤ活力与ＮＳ组比较无显著性差异。３讨论从以上实验可看出，Ｂｅｐ组心律失常发生率显著低于ＮＳ组，与国外文献［５·６］报道一致，ＳＯＤ活力比值高于ＮＳ组，但无显著性差异。我们还同时观察了心肌超微结构（见后文，发表于徐州医学院学报１９９４年第２期）Ｂｅｐ组心肌细胞损伤程度略轻于ＮＳ对照组。因此实验结果提示，在我们的实验条件下，Ｂｅｐ对结扎在体大鼠心脏冠状动脉左室支造成心肌缺血再灌注损伤有部分缓解作用，但能否达到理想疗效，有待进一步证实。心肌缺血再灌时形成大量超氧自由基，可以损伤膜通道，导致细胞外?
Myocardial ischemia-reperfusion injury was induced by ligation of the left coronary artery in rats and the effect of beupiplarn on myocardial ischemia-reperfusion injury was observed. Bepridil (2.5mg / kg, iv) significantly decreased the incidence of ventricular tachycardia (P <0.05) and increased the activity of myocardial SOD, but there was no statistical difference (P <0.05). P <0.012.2 Effect on SOD activity The ratio of SOD activity in ischemic area and non-ischemic area in NS group was 0.69 ± 0.09 (n = 6), and 0 in group Ver and Bep respectively. 88 ± 0.15 (n = 6) and 0.76 ± 0.19 (n = 6), P <0.05 in the former group and P> 0.05 in the latter group. Tip Bep on myocardial SOD activity after ischemia-reperfusion in rats compared with the NS group no significant difference. 3 Discussion From the above experiments we can see, Bep group arrhythmia incidence was significantly lower than the NS group, consistent with foreign literature [5,6], SOD activity ratio was higher than the NS group, but no significant difference. We also observed myocardial ultrastructure (see later, published in Journal of Xuzhou Medical College, No. 2, 1994) Bep group of myocardial cell injury was slightly lighter than the NS control group. Therefore, the experimental results suggest that under our experimental conditions, Bep can partially relieve the myocardial ischemia-reperfusion injury caused by ligation of the left ventricular branches in the rat coronary heart, but whether this effect can be achieved remains to be confirmed. Myocardial ischemia and reperfusion form a large number of superoxide radicals, can damage the membrane channel, leading to extracellular?