摘要
目的:应用内源性一氧化碳诱导剂,观察内源性一氧化碳在肝缺血再灌注损伤中的作用机制。方法:72只SD大鼠随机分为3组,对照组,生理盐水组,氯化血红素组。建立肝缺血再灌注模型后,即刻经尾静脉分别注入生理盐水和氯化血红素。于再灌注后不同时间点处死动物,测量血清中CO ,ET的水平,及肝组织的病理变化。结果:生理盐水组与氯化血红素组CO水平均随着再灌注时间延长而增高,但氯化血红素组增高明显,与生理盐水组比较有显著性差异(P <0 . 0 5)。在生理盐水组ET水平与对照组比较增高明显(P <0. 0 5) ,氯化血红素组ET水平则明显降低,与对照组比较有显著性差异(P <0 . 0 5)。结论:内源性CO对大鼠肝缺血再灌注损伤具有保护作用。
Objective:To observe the effects of endogenous carbon monoxide on hepatic ischemia reperfusion injury in rats and discuss the mechanism.Methods: The model of hepatic ischemia reperfusion was established.72 SD rats were randomly divided into three groups: sham group, saline group, hemin group. The animals were executed after different reperfusion time. The activity of CO and ET were checked , as well as the pathologic changes in the tissue of liver.Results: In saline and hemin groups, the activity of CO were higher, but in the hemin group increased obviously ( P <0.05). Compared with the sham group, the activity of ET was lower in saline group ( P <0.05),but increased in hemin group ( P <0.05).Conclusion: The endogenous carbon monoxide has a protective effect for hepatic ischemia reperfusion injury of rats.
出处
《医学理论与实践》
2005年第5期504-506,共3页
The Journal of Medical Theory and Practice
