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目的探讨硒对急性缺血心肌保护作用的机制。方法采用结扎大鼠心肌左冠状动脉复制心肌缺血模型。ＳＤ大鼠１００只，分为正常对照组（Ｃ）、缺血组（ＭＩ）及硒组（ＭＩ＋Ｓｅ）。硒组按每日补硒８０μｇ·ｋｇ－１，连续７ｄ。观察硒对心肌缺血后３０、６０、９０ｍｉｎ肌浆网（ＳＲ）、线粒体（Ｍｉｔ）Ｃａ２＋－ＡＴＰ酶活性动态变化及缺血６０ｍｉｎ肌膜（ＳＬ）Ｎａ＋－Ｋ＋－ＡＴＰ酶活性和线粒体膜磷脂含量变化的影响。结果与正常对照组比较，心肌缺血不同时点，Ｍｉｔ、ＳＲ、Ｃａ２＋－ＡＴＰ酶活性均有不同程度降低，且呈随缺血时间延长进行性下降的趋势；缺血６０ｍｉｎＭｉｔ磷脂含量和ＳＬＮａ＋－Ｋ＋－ＡＴＰ酶活性也明显降低。但无论任何时点，硒组Ｍｉｔ、ＳＲＣａ２＋－ＡＴＰ酶、ＳＬＮａ＋－Ｋ＋－ＡＴＰ酶活性和Ｍｉｔ磷脂含量均显著高于缺血组。结论硒在一定程度上能减轻或延缓缺血对心肌细胞Ｃａ２＋转运功能的损害作用，可能是硒保护急性缺血心肌作用机制之一。
Objective To explore the protective mechanism of selenium on acute ischemic myocardium. Methods The model of myocardial ischemia was established by ligation of the left coronary artery in rats. 100 SD rats were divided into normal control group (C), ischemia group (MI) and selenium group (MI + Se). Selenium group according to daily selenium 80μg · kg-1, continuous 7d. The changes of sarcoplasmic reticulum (SR), mitochondrial Ca2 + -ATPase activity and the activities of Na + -K + -ATPase in mitochondria and mitochondrial membrane phospholipid at 60, 60, 90min after myocardial ischemia were observed. The impact of changes in content. Results Compared with the normal control group, the activities of Mit, SR and Ca2 + -ATP decreased at different time points after myocardial ischemia, and decreased with the prolongation of ischemic time. The contents of phospholipid and SLNa + K + -ATP enzyme activity is also significantly reduced. However, at any time, Mit, SRCa2 + -ATPase, SLNa + -K + -ATPase activity and Mit phospholipid content in selenium group were significantly higher than those in ischemic group. Conclusion Selenium can reduce or delay the damage of Ca2 + transport function of myocardial cells to a certain extent, which may be one of the mechanisms of action of selenium on acute myocardial ischemia.