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目的：观察预缺氧对急性缺氧大鼠心肌线粒体功能及ＡＴＰ含量的影响。方法：实验大鼠分三组。１常氧对照组；２急性缺氧组；３预缺氧组。测定了心肌ＡＴＰ含量及线粒体呼吸功能，以荧光偏振法测定线粒体膜流动性。结果：经预缺氧处理的大鼠遭受急性缺氧后ＡＴＰ含量从（３１８±２４２）ｍｇ１·ｇ－１增加到（６０５５±３．５２）ｍｇ－１·ｇ－１（Ｐ＜００１）；线粒体呼吸控制率（ＲＣＲ）从１８４±０５８上升到４５５±０３２（Ｐ＜００１）；线粒体膜流动性（ＭＭＦ）明显增加（Ｐ＜００５），Ｆ０Ｆ１－ＡＴＰ酶及Ｎａ＋－Ｋ＋－ＡＴＰ酶活性分别提高６６％和２５％。结论：预缺氧可有效改善缺氧大鼠心肌能量代谢，其作用环节可能和提高线粒体膜流动性，改善线粒体呼吸功能有关。
Objective: To observe the effect of hypoxia on myocardial mitochondrial function and ATP content in acute hypoxia. Methods: Experimental rats were divided into three groups. 1 normoxia control group, 2 acute hypoxia group, 3 pre-hypoxia group. The myocardial ATP content and mitochondrial respiratory function were measured, and the mitochondrial membrane fluidity was measured by fluorescence polarization method. Results: The ATP content increased from (318 ± 242) mg1 · g-1 to (6055 ± 3.52) mg-1 · g) in acute hypoxia-treated rats -1 (P <001). The mitochondrial respiratory control rate (RCR) increased from 1.84 ± 0.58 to 4.55 ± 0.32 (P <0.01), and the mitochondrial membrane fluidity (MMF) (P <005), F0F1-ATPase and Na + -K + -ATPase activity increased by 66% and 25% respectively. CONCLUSION: Hypoxia can effectively improve the myocardial energy metabolism in hypoxic rats, which may be related to the enhancement of mitochondrial membrane fluidity and mitochondrial respiratory function.