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目的 :研究缺血及缺血再灌注后肠组织内NO代谢产物的变化。方法 :建立大白鼠肠系膜上动脉阻断模型 ,采用荧光法测定回肠组织内NO-2 含量。结果 :缺血后 3 0min ,肠组织NO-2 上升 ,2h达高峰。缺血再灌注组 ,在复灌 3 0min、60min、12 0min、180min时NO-2 含量均明显高于单纯缺血组。缺血前腹腔给予iNOS抑制剂氨基胍 (AG)可明显降低缺血及缺血再灌时肠组织NO-2 含量。结论 :肠缺血及缺血再灌注后肠组织内NO-2 含量发生明显改变 ,iNOS抑制剂AG对缺血及缺血再灌所致iNOS活性增高有明显抑制作用。NO参与了肠缺血再灌注的损伤过程。
Objective: To study the changes of NO metabolites in intestinal tissue after ischemia and reperfusion. Methods: The rat model of superior mesenteric artery occlusion was established. The content of NO-2 in ileal tissue was measured by fluorescence method. Results: At 30 min after ischemia, NO-2 in intestinal tissue increased and peaked at 2h. The content of NO-2 in ischemia-reperfusion group was significantly higher than that in ischemia group at 30 min, 60 min, 120 min and 180 min respectively. Intraperitoneal administration of iNOS inhibitor aminoguanidine (AG) before ischemia significantly reduced the content of NO-2 in the intestine during ischemia and reperfusion. CONCLUSION: The content of NO-2 in intestinal tissue changes remarkably after intestinal ischemia and reperfusion. The iNOS inhibitor AG significantly inhibits the increase of iNOS activity induced by ischemia and reperfusion. NO participates in the process of intestinal ischemia-reperfusion injury.