大鼠肠缺血再灌注损伤病理生理动态改变的实验研究

The Pathophysiological Changes of Intestinal Ischemia-reperfusion was Induced in Rats

目的探讨大鼠肠缺血再灌注损伤的病理生理改变及其机理。方法采用夹闭大鼠肠系膜动脉制作肠缺血再灌注病理模型,研究大鼠肠缺血45 min再灌注后肠粘膜谷光甘肽(GSH)、氧化代谢产物 (MDA)抗氧化酶及肝肾功能的动态改变。结果肠缺血45 min后再灌注2、4、8 h,GSH明显减少;MDA 水平明显升高。肠粘膜CAT、SOD和GSH-PX活性未见明显改变。血清ALT和BUN明显升高。结论大鼠肠缺血再灌注可致肠粘膜严重氧化性损伤,并引起远隔器官(肝肾)功能受损,其损伤程度与再灌注时间呈现动态性改变。

Objectives To investigate the pathological changes of intestinal ischemia-reperfusion in rats. Methods The intestinal ischemia-reperfusion in rats with clamping superior mesenteric artery for 45 min followed by reperfusion. The levels ofMDA, GSH, the activities ofantioxidant enzymes in the gut mucosa including CAT, SOD, GSH-Px and serum ALT, AST, BUN, Cr were assayed at 2, 4, 8, 12, 24 h after reperfusion. Results The levels of MDA and GSH in the gut mucosa increased and decreased significantly at 2 h of reperfusion. The activities of CAT, SOD and GSH-Px did not show significant changes in rats after intestinal ischemia-reperfusion. Serum ALT, AST, BUN and Cr increased significantly at 2 h of reperfusion, Conclusion This study showed that intestinal ischemia for 45 min followed by reperfusion diminished GSH level and increased MDA level and caused liver and renal reversible damage.