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目的：本文旨在了解急性缺氧时大鼠脑线粒体氧化磷酸化功能的改变。方法：大鼠经模拟４ ０００ｍ 高原急性缺氧７２小时后分离脑线粒体。用氧电极法分析线粒体呼吸功能并检测Ｆ０Ｆ１－ ＡＴＰ酶活性，运用高效液相色谱技术（ＨＰＬＣ）测定脑线粒体腺苷酸含量以及线粒体ＡＴＰ生成率。结果：与对照组相比，急性缺氧使动物脑线粒体ＩＶ态呼吸（ＳＴ４）显著升高，呼吸控制率（ＲＣＲ）明显降低；线粒体ＡＴＰ含量、ＡＴＰ生成率和Ｆ０Ｆ１－ＡＴＰ酶活性显著降低。结论：急性缺氧可抑制脑线粒体呼吸功能和Ｆ０Ｆ１－ ＡＴＰ酶活性，脑组织ＡＴＰ含量下降，脑线粒体氧化磷酸化功能降低。
Objective: This article aims to understand the acute hypoxia changes in rat brain mitochondrial oxidative phosphorylation. Methods: The mitochondria were isolated from the rats exposed to simulated hypoxia at 4 000 m altitude for 72 hours. The mitochondrial respiratory function was assayed by the oxygen electrode method and the F0F1-ATPase activity was measured. The content of mitochondrial adenine acid and mitochondrial ATP formation rate were determined by high performance liquid chromatography (HPLC). Results: Compared with the control group, the acute hypoxia significantly increased the level of IV of ST4 and reduced the respiratory rate (RCR). The mitochondrial ATP content, ATP production rate and F0F1-ATPase activity were significantly decreased. CONCLUSION: Acute hypoxia can inhibit the mitochondrial respiratory function and F0F1-ATPase activity, reduce the content of ATP in brain tissue and reduce the mitochondrial oxidative phosphorylation.