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目的:建立大鼠肠淤血再灌注动物模型,探讨淤血再灌注肠神经组织损伤的机制,为临床相关疾病的诊断、治疗提供理论依据。方法:成年Wistar大鼠60只,雌雄不限,随机分为正常组、对照组和实验组,每组20只。实验组采用阻断门静脉1h后开放的方法建立大鼠小肠淤血再灌注模型,对照组只进行同样腹部手术操作但不夹闭门静脉,正常组不手术。6小时后取各组下腔静脉血,测定血清中超氧化物歧化酶(SOD)活性和丙二醛(MDA)的含量,然后处死动物,取距回盲部15厘米处肠管1厘米,采用伊红-苏木素(HE)染色观察肠粘膜组织形态学变化;用免疫组织化学方法观察正常组、对照组和实验组小肠壁肠神经组织中微管相关蛋白2(MAP-2)的表达情况。结果:HE染色可见,正常组、对照组为正常肠道管壁结构,实验组肠壁各层有比较明显的淤血、出血,小肠绒毛固有层水肿,黏膜上皮有脱落、坏死;实验组MAP-2的表达明显低于正常组及对照组(P<0.05);与正常组及对照组相比较,实验组SOD活性明显降低(P<0.05),MDA的含量则明显升高(P<0.05)。结论:肠淤血再灌注可能导致肠道神经元数量减少,其机制可能与肠淤血再灌注造成的自由基损伤和脂质过氧化有关。
OBJECTIVE: To establish animal models of intestinal congestion and reperfusion in rats and explore the mechanism of intestinal nerve injury induced by congestion and reperfusion, so as to provide a theoretical basis for the diagnosis and treatment of clinically relevant diseases. Methods: Sixty adult Wistar rats were randomly divided into normal group, control group and experimental group with 20 rats in each group. In the experimental group, the model of small intestine congestion and reperfusion was established by blocking the portal vein 1h after opening, while the control group only performed the same abdominal operation but did not clamp the portal vein. The normal group was not operated. Six hours later, the inferior vena cava blood of each group was taken for determination of the activity of superoxide dismutase (SOD) and the content of malondialdehyde (MDA) in the serum, and then the animals were sacrificed and the intestine at 15 cm away from the ileocecal part was 1 cm. The morphological changes of intestinal mucosa were observed by HE staining. The expression of microtubule-associated protein 2 (MAP-2) in intestinal mucosa of small intestine in normal group, control group and experimental group was observed by immunohistochemistry. Results: The HE staining showed that the normal group and the control group were normal intestinal wall structure. The intestinal wall of the experimental group had obvious congestion, hemorrhage, edema of the lamina propria of the intestinal villus and shedding and necrosis of mucosal epithelium. The MAP- (P <0.05). Compared with normal group and control group, the activity of SOD in experimental group was significantly decreased (P <0.05) and the content of MDA was significantly increased (P <0.05) . Conclusion: Intestinal congestion reperfusion may result in the decrease of intestinal neurons. The mechanism may be related to free radical damage and lipid peroxidation induced by intestinal congestion reperfusion.