中文摘要：

目的：探讨高原低压缺氧暴露过程中大鼠心肌能量代谢及腺苷酸转位酶活性变化特点。方法：雄性Wistar大鼠随机分为正常对照组、缺氧1d组、5d组、15d组和30d组。缺氧组于模拟海拔5000m高原低压舱内连续缺氧23h／d。提取心室肌线粒体，Clark氧电极法测定线粒体氧化呼吸活性；HPLC法测量线粒体内腺苷酸含量；[^3H]-ADP掺入法测量线粒体ANT转运活性。结果：大鼠经缺氧1d、5d、15d后，ST3和RCR显著降低，缺氧30d时ST3仍显著低于对照组，ST4在缺氧1d、5d、15d时显著升高，缺氧30d时降低，RCR在30d时接近正常。缺氧1d和5d心肌线粒体ATP含量、ANT活性明显下降，缺氧15d时接近正常，缺氧30d时则再次降低。结论：缺氧对心肌线粒体氧化呼吸功能的抑制是导致线粒体内ATP含量下降的主要原因。缺氧过程中ANT活性与线粒体内ATP含量成协调变化。

英文摘要：

AIM： To explore the changes of myocardial energy metabolism and adenine nueleofide transiocase activity in mitochondria in rats exposed to hypoxia. METHODS： Adult male Wistar rats were exposed to simulated high altitude at 5 000 m for control （0 d）, 1 d, 5 d, 15 d, 30 d in hypobaric chamber. Myocardial mitochondria were isolated by centrifugatinn. Mitochondria respiratory function was measured by Clark oxygen electrode. The size of adenine nucleotides pool （ ATP, ADP, AMP） in mitochondria were separated and measured by HPLC. ANT activity was measured by [^3H] - ADP incorporation. RESULTS： Compared to control, mitochondria state Ⅲ respiratory （ST3） and RCR decreased and ST4 increased sharply at 1 d, 5 d and 15 d, ST3 still lower than that in control at 30 d, while RCR level restored. ATP contents and ANT activity decreased at 1 d and 5 d, then restored to control level at 15 d, then decreased again at 30 d. CONCLUSION： The inhibition of mitochondria respiratory function is the main reason that makes ATP contents decrease during hypoxic exposure. ANT activity and ATP content change cooperatively.