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作 者:谭家庆[1] 丁春华[1] 索晓华[1] 凌亦凌[1] 刘笑然[1] 张俊毅[1]
机构地区:[1]河北医科大学病理生理学教研室,河北石家庄050017
出 处:《中国应用生理学杂志》2007年第1期92-96,I0006,共6页Chinese Journal of Applied Physiology
摘 要:目的:研究内毒素休克时内源性一氧化碳(CO)对肺组织和肾组织的保护作用及其机制;方法:采用盲肠结扎穿孔(CLP)的方法建立大鼠内毒素休克模型,通过免疫组化、光镜下组织形态学观察及超氧化物岐化酶活性、丙二醛含量的测定进行研究;结果:治疗组肺组织和肾组织病变明显减轻,炎症反应及脂质过氧化程度减轻;结论:内毒素休克时内源性CO对肺组织和肾组织具有保护作用,且此保护作用与其抑制炎症反应和抗氧化作用有重要关系。Aim: To study the protective role of endogenous carbon monoxide to lung and kidney tissues during septic shock and its mechanism, Methods: A rat model of CLP was built by using the method of CLP. The malondialdehyde(MDA) content and the activity of uuperoxide dematase(SOD) in blood, lung and kidney were detected by immunohistochemical technique and light microscope. Restilts: Pathological changes of lung and kidney in CLP+ Hemin group were lighter than CLP group, inflammatory reaction and lipid peroxidation were also lighter, conclusion: Endogenous CO can protect lung and kidney from the oxidative injury. It can suppress inflammation and the oxidative injury caused by activated inflammatory cells, it is probably an important mechanism of its protective effects.
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