Study On Effects Of No And Selective Inhibitor Of INOS In Rat During Intestine Ischemia-reperfusion Period

Objective: To establish animal model of rat with intestine ischemia-reperfusioninjury, and study on the change of NO production during the period.Methods: Divided 18 rats into 3 groups randomly and averagely. Group A wascontrol group; Group B: Anesthetized rats underwent 135 minutes of superiormesenteric artery occlusion; Group C: Anesthetized rats underwent 45 minutes ofsuperior mesenteric artery occlusion follow by 90 minutes of reperfusion. Studypathological changes of small intestine with light microscopy and eyes, and plasmaMDA . SOD NO contents were measured.Result: Plasma MDA, NO contents increased in group A, B C gradually(F =49.62, P<0.01; F=26.56, P<0.01), while the differences between groups weresignificant. The activity of SOD decreased gradually (F= 134.57, P<0.01), and thedifferences between groups were significant too.Conclusion: Animal model of rat with small intestine ischemia-reperfusion injurycould be created by superior mesenteric artery occlusion in felicitous period of time.The increasing of NO indicates that small intestine ischemia-reperfusion injury islikely to be induced by NO partly.Dissertation TwoA study of the relationship between No and intestine ischemia-reperfusion injury in ratObjective: To observe the changes of NO and expression of iNOS during intestineischemia-reperfusion period, and clarify the relationships among plasma NOcontents, expression of iNOS, pathologic change of intestine.Methods: To establish intestine ischemia-reperfusion animal model of Wistar rat.Plasma NO content expression of iNOS pathologic change of intestine weremeasured at different times.The relationships among them would be deduced bystatistic method.Result: Both pathologic change of intestine and expression of iNOS wereincreasing gradually and significantly during intestine ischemia-reperfusionperiod(F=287.13, PO.01; F=62.484, P<0.01). NO increased remarkably just inreperfusion phase(F=38.667, P<0.01).Conclusion: The expression of iNOS had been activated with ischemia andenhanced in reperfusion phase. NO, which was synthesized by iNOS, inducedintestine ischemia-reperfusion injury in great part.Objective: To investigate the influence of selective inhibitor of iNOS on intestine ischemia-reperfusion injury, and clarify the causalities among expression of iNOS in intestine plasma NO content pathologic change of intestine during the period. Methods: To establish intestine ischemia-reperfusion model of Wistar rat. AG was injected and plasma NO content, expression of iNOS pathologic change of...