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目的评价地高辛抗血清对心肌缺氧损伤的保护作用与机制。方法制备心肌组织缺氧损伤模型 ,观察不同剂量的地高辛抗血清对缺氧损伤心肌组织内源性洋地黄样因子水平和心肌细胞膜ATP酶活性的影响。结果缺氧损伤可使心肌组织内源性洋地黄样因子水平明显升高 ,心肌细胞膜ATP酶活性明显下降 ;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 ,使酶活性得到恢复。结论缺氧损伤所致心肌组织内源性洋地黄样因子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源性洋地黄样因子的作用 ,减轻缺氧所致心肌损伤 ,对缺氧损伤心肌具有保护作用
Objective To evaluate the protective effect and mechanism of digoxin antiserum on myocardial hypoxia injury. Methods The hypoxia injury model of myocardial tissue was prepared and the effects of different doses of digoxin antiserum on endogenous digitalis-like factor and myocardial ATPase activity in myocardial cells were observed. Results After hypoxia injury, the level of endogenous digitalis-like factor in myocardium was significantly increased and the activity of ATPase in myocardial cell membrane was significantly decreased. Digoxin antiserum could obviously antagonize the inhibitory effect of hypoxia on the ATPase activity of myocardial cell membrane, Activity has been restored. Conclusion The increased level of endogenous digitalis-like factor in myocardial tissue induced by hypoxia is the molecular basis of hypoxia-mediated myocardial injury. Anti-digoxin antiserum can reduce the deficiency of endogenous digitalis-like factor Oxygen-induced myocardial injury, hypoxic myocardial injury has a protective effect