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探讨一氧化氮合成酶（ＮＯＳ）、一氧化氮（ＮＯ）、超氧化物歧化酶（ＳＯＤ）、丙二醛（ＭＤＡ），在急性低压缺氧时含量变化。将４８只ｗｉｓｔａｒ大鼠分为实验组和对照组。实验组进行模拟高空缺氧，以３０ｍ／ｓ速度直接上升至７５００ｍ高度，分１０ｍｉｎ、３０ｍｉｎ、６０ｍｉｎ三个暴露组。对照组于低压舱内，不上升高度。对缺氧不同时间心肌组织和血清ＮＯＳ、ＮＯ、ＳＯＤ和ＭＤＡ含量进行测定。结果：大鼠急性低压缺氧３０ｍｉｎ、６０ｍｉｎ组心肌组织ＮＯＳ显著高于１０ｍｉｎ组及对照组Ｐ＜０．００１；血清ＮＯ１０ｍｉｎ、３０ｍｉｎ组显著高于６０ｍｉｎ组及对照组Ｐ＜０．０１；ＳＯＤ，低压缺氧１０ｍｉｎ、３０ｍｉｎ血清和心肌组织中ＳＯＤ水平显著高升，而６０ｍｉｎ后降之对照组水平。缺氧时间越长，血清、心肌组织中ＭＤＡ含量增加越明显。大鼠急性低压缺氧时，诱导诱生酶（ｉＮＯＳ）的表达，ｉＮＯＳ产生大量的ＮＯ造成心肌损伤。
To investigate the changes of nitric oxide synthase (NOS), nitric oxide (NO), superoxide dismutase (SOD) and malondialdehyde (MDA) in acute hypobaric hypoxia. 48 wistar rats were divided into experimental group and control group. The experimental group simulated altitude hypoxia, with 30m / s speed rose directly to 7500m height, 10min, 30min, 60min three exposure groups. The control group in the low pressure cabin, does not rise height. The contents of NOS, NO, SOD and MDA in myocardial tissue and serum at different times of hypoxia were determined. Results: The rats in acute hypobaric hypoxia 30min, 60min group NOS was significantly higher than the 10min group and control group P <0.001; serum NO10min, 30min group was significantly higher than 60min group and control group P <0.01; SOD, Low pressure hypoxia 10min, 30min serum and myocardial SOD levels were significantly elevated, while 60min after the fall of the control group. The longer the hypoxia time, the more obvious the increase of MDA content in serum and myocardium. Rat acute hypobaric hypoxia induced the expression of inducible enzyme (iNOS), iN OS produced a large number of NO myocardial damage.