急性缺氧对大鼠脑线粒体能量代谢的影响  

EFFECTS OF ACUTE HYPOXIA ON BRAIN MITOCHONDRIAL ENERGY METABOLISM IN RATS

作　　者：高文祥[1] 柳君泽[1] 罗德成[1] 蔡明春 

机构地区：[1]第三军医大学基础部,400038

出　　处：《高原医学杂志》1999年第3期13-17,共5页Journal of High Altitude Medicine

基　　金：国家自然科学基金面上项目!(No.39600171);全军九.五青年基金

摘　　要：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。To explore the effects of acute hypoxia on brain mitochondrial oxidative phosphorylation,rats were exposed to simulated 4 000m high altitude for 72 hours before experiments,Methods:Rats were sacrificed by decapitation under normoxic and hypoxic conditions respectively and then mitochondria isolated.Respiratory function and F 0F 1-ATPase activity were observed with the methods of Clark oxide electrode and oligomycin depression respectively.Mitochondrial ATP,ADP and AMP contents and ATP production rate were measured with high performance liquid chromatography(HPLC).Results:Brain mitochondrial ST 4 was increased and respiratory control rate,mitochondrial ATP content,ATP production rate and F 0F 1-ATPase activity were decreased respectively during acute hypoxia.Conclusions:Our data suggested that acute hypoxic depressed brain mitochondrial respiratory activity and F 0F 1-ATPase activity,ATP content was decreased in brain tissue and brain mitochondrial oxidative phosphorylation function was suppressed.$$$$

关 键 词：缺氧 线粒体 氧化磷酸化 脑 能量代谢 

分 类 号：R364.4[医药卫生—病理学] R594.3[医药卫生—基础医学]