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目的：探讨缺氧大鼠心肌线粒体呼吸功能和心肌能量代谢的变化。方法：通过Ｃｌａｒｋ氧电极法和生化方法测定线粒体功能和ＦｏＦ１－ＡＴＰ酶活力，运用高效液相色谱技术（ＨＰＬＣ）测定心肌组织ＡＴＰ含量。结果：急性缺氧大鼠心肌线粒体呼吸功能，ＦｏＦ１－ＡＴＰ酶活力以及１－苯胺基，８－萘磺酸镁（ＡＮＳ）相对荧光强度明显降低（Ｐ＜０．０１），表明：ＦｏＦ１－ＡＴＰ酶构象发生改变。心肌组织ＡＴＰ含量明显减少（Ｐ＜０．０１）。慢性缺氧上述指标不同程度有所恢复，但仍明显低于平原水平。经相关分析表明：ＡＴＰ含量与线粒体呼吸控制率（ＲＣＲ），ＦｏＦ１－ＡＴＰ酶活力及ＰａＯ２呈明显正相关（Ｐ＜０．０１）。结论：急性缺氧动物心肌能量代谢障碍可能与心肌线粒体呼吸功能降低，ＦｏＦ１－ＡＴＰ酶活力降低有关系。慢性缺氧后能量代谢的改善，可能是缺氧适应的机理之一。
Objective: To investigate the changes of myocardial mitochondrial respiratory function and myocardial energy metabolism in hypoxia rats. METHODS: Mitochondrial function and FoF1-ATPase activity were determined by Clark’s oxygen electrode method and biochemical methods. The ATP content in myocardial tissue was determined by HPLC. RESULTS: The mitochondrial respiratory function, FoF1-ATPase activity and the relative fluorescence intensity of 1-anilino and 8-naphthalenesulfonate (ANS) were significantly decreased in acute hypoxia rats (P <0.01) The conformation of the enzyme changes. The content of ATP in myocardium decreased significantly (P <0.01). The indicators of chronic hypoxia restored to varying degrees, but still significantly lower than the plain level. Correlation analysis showed that ATP content was positively correlated with mitochondrial respiratory control rate (RCR), FoF1-ATPase activity and PaO2 (P <0.01). Conclusion: Myocardial dysfunctions in acute hypoxic animals may be related to the decrease of mitochondrial respiratory function and the decrease of FoF1-ATPase activity. Improvement of energy metabolism after chronic hypoxia may be one of the mechanisms of hypoxia adaptation.