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机构地区:[1]军事医学科学院毒物药物研究所,北京100850
出 处:《军事医学科学院院刊》1999年第4期263-265,268,共4页Bulletin of the Academy of Military Medical Sciences
摘 要:目的:探讨NO2 致急性肺损伤机理。方法:大鼠静式吸入染毒,观测肺组织病理变化及肺泡灌洗液中蛋白和LDH 含量,同时测定肺组织抗氧化物及丙二醛(MDA)的含量。结果:大鼠吸入NO2 后,肺组织明显损伤,同时GSH-PX、SOD、维生素E、总巯基含量显著降低,MDA 含量也明显下降,肺损伤越重,各指标下降越明显,随着肺损伤的修复,各指标也恢复正常。结论:NO2Objective: To study the mechanism of acute lung injury induced by NO 2. Methods: A chamber without air diffusion was used for NO 2 exposure. Pathology of lung, contents of protein and lactate dehydrogenase in bronchioalveolar lavage fluid and contents of antioxidant and malondialdehyde(MDA) in lungs were examined after rats were exposed to NO 2. Results: After exposure to NO 2, lungs were injured , contents of glutathione peroxidase, superoxide dismutase, vitamin E and sulfhydryl in lungs decreased significantly, and so did MDA. All changes showed dose effect relatim and returned to control level with lungs repaired. Conclusion: These results suggest that decreases in antioxidants may have contribution to acute lung injury caused by NO 2.
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