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目的 探讨肠缺血 再灌流过程中肠局部血管内皮细胞的细胞间粘附分子 1(intercellu laradhesionmolecule 1,ICAM 1)mRNA和蛋白表达的变化与中性粒细胞聚集的关系及其在肠损伤中的作用。方法 采用肠系膜上动脉夹闭的方法制作大鼠肠缺血 再灌流模型 ,应用逆转录 聚合酶链反应及免疫组织化学的方法观察小肠ICAM 1表达的变化 ,同时检测组织髓过氧化物酶活性及反映肠功能的指标D 乳酸、二胺氧化酶活性的变化。结果 肠缺血 0 5～ 1 5h ,小肠ICAM 1mRNA表达增加 ,免疫组织化学显示其蛋白表达在肠缺血 1h及再灌流 1h时增多 ;肠组织髓过氧化物酶活性同时升高 (P <0 0 5 ) ,并持续至再灌流后 6h ;血浆二胺氧化酶活性在肠缺血 1h和再灌流后 2h升高 (P<0 0 5 ) ,血浆D 乳酸浓度在肠缺血 1 5h时开始增加 ,再灌流后 0 5h和 1h时大幅度升高 (P <0 0 1,P <0 0 5 )。结论 肠缺血 再灌流时肠血管内皮细胞ICAM 1表达增加 ,由此介导的中性粒细胞在局部聚集、活化可能是造成肠粘膜上皮损伤和肠通透性增加的病理生理学基础
Objective To investigate the relationship between changes in mRNA and protein expression of intercellular adhesion molecule-1 (ICAM-1) and neutrophils in intestinal endothelium during intestinal ischemia-reperfusion and its relationship with intestinal injury effect. Methods The rat model of intestinal ischemia-reperfusion was established by clipping the superior mesenteric artery. The changes of ICAM-1 expression in the small intestine were observed by reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemistry. The myeloperoxidase D-lactate, a diamine oxidase activity index reflecting intestinal function. Results The expression of ICAM 1 mRNA in small intestine increased from 0 to 15 h after intestinal ischemia. The protein expression of ICAM 1 increased in intestinal ischemia 1 h and 1 h after reperfusion. The activity of myeloperoxidase in intestinal tissue increased at the same time (P <0. 0 5) for 6 h after reperfusion. Plasma diamine oxidase activity increased 1 h after ischemia and 2 h after reperfusion (P <0 05), and plasma D lactic acid concentration started at 15 h after ischemia (P <0.01, P <0 05) at 0 5 h and 1 h after reperfusion. Conclusion The expression of ICAM-1 in intestinal vascular endothelial cells increases after intestinal ischemia-reperfusion, and the neutrophils are locally aggregated and activated, which may be the pathophysiological basis of intestinal mucosal injury and intestinal permeability increase