内源性一氧化碳在脓毒性休克期间对肺和肾组织的保护作用
[Protective role of endogenous carbon monoxide to lung and kidney tissues during septic shock].
作者信息
Tan Jia-Qing, Ding Chun-Hua, Suo Xiao-Hua, Ling Yi-Ling, Liu Xiao-Rao, Zhang Jun-Yi
机构信息
Department of Pathophysiology, Hebei Medical University, Shijiazhuang 050017, China.
出版信息
Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2007 Feb;23(1):92-6.
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 superoxide dematase (SOD) in blood, lung and kidney were detected by immunohistochemical technique and light microscope.
RESULTS
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 in flammation and the oxidative injury caused by activated inflammatory cells, it is probably an important mechanism of its protective effects.
目的
研究内源性一氧化碳在脓毒性休克时对肺和肾组织的保护作用及其机制。
方法
采用盲肠结扎穿孔法建立大鼠脓毒症模型。采用免疫组化技术和光学显微镜检测血液、肺和肾中丙二醛（MDA）含量及超氧化物歧化酶（SOD）活性。
结果
氯高铁血红素干预组肺和肾的病理改变较模型组轻，炎症反应及脂质过氧化程度也较轻。
结论
内源性一氧化碳可减轻肺和肾的氧化损伤，抑制炎症反应及炎症细胞激活所致的氧化损伤，可能是其发挥保护作用的重要机制。
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