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目的：评价地高辛抗血清对抗心肌缺氧损伤的作用与机制。方法：制备心肌组织缺氧模型，观察不同剂量的地高辛抗血清对缺氧损伤心肌组织内洋地黄素水平和心肌细胞膜ＡＴＰ酶活性的影响。结果：缺氧损伤时心肌组织内洋地黄素水平明显高于正常对照组，心肌细胞膜ＡＴＰ酶活性明显低于正常对照组；地高辛抗血清能明显拮抗缺氧对心肌细胞膜ＡＴＰ酶活性的抑制作用。结论：缺氧所致心肌组织内洋地黄素水平升高是缺氧介导心肌损伤的分子生物学基础，地高辛抗血清通过拮抗内洋地黄素的作用，减轻缺氧所致心肌损伤，对缺氧心肌具有保护作用。
Objective: To evaluate the effect and mechanism of digoxin antiserum against myocardial hypoxia injury. Methods: The model of myocardial hypoxia was prepared and the effects of different doses of anti-digoxin antiserum on endoxin and myocardial ATPase activity in myocardium were observed. Results: The hypoxia-induced myocardial ischemia-reperfusion injury was significantly higher than that of the normal control group, and the activity of ATPase in myocardium was significantly lower than that in the normal control group. Digoxin antiserum significantly inhibited the inhibition of ATPase activity in myocardial cells by hypoxia effect. CONCLUSION: Hypoxia-induced increase of endoxin in myocardium is the molecular basis of hypoxia-mediated myocardial injury. Digoxin antiserum can reduce myocardial damage caused by hypoxia by antagonizing endoxin, Hypoxic myocardium has a protective effect.