对淤血再灌注肠神经组织损伤机制的探讨  

Investigation on the Mechanism of Congestion-Reperfusion Injury in Intestinal Nervous Tissue

作　　者：孔滨[1] 丛丽 沈若武[3] 

机构地区：[1]青岛大学医学院附属医院普外科,山东青岛266021 [2]青岛市立医院麻醉科,山东青岛266021 [3]青岛大学医学院解剖教研室,山东青岛266021

出　　处：《现代生物医学进展》2009年第10期1852-1853,1860,F0002,共4页Progress in Modern Biomedicine

基　　金：青岛市科技局(No.Kzd-80)

摘　　要：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 the rat model of intestinal congestion-reperfusion injury, and to investigate the mechanism of congestion-reperfusion injury in intestinal nervous tissue, in order to provide theoretical basis for clinical diagnose and treatment. Methods： A total of 60 adult Wistar rats were randomly divided into three groups： normal group （NG）, control group （CG） and experimental group （EG）, 20 respectively. The model of congestion-reperfusion of intestine was established by means of the occlusion of portal vein for one hour and then was reflowed in EG. The same operation on abdominal region was carried out, but except for the occlusion of the portal vein in CG, NG. After six hours, hemocuprein （SOD） and malondialdehyde （MDA） were detected in serum. Then the rats were executed, the lcm intestine tissue was obtained distance between ileocecal junction 15cm. Eosin-hematoxylin （HE） staining was adopted to observe the injury in the tissue, and the expression of MAP-2 in nerve tissue of small-intestine wall in the normal, control and experimental group was detected by immunohistochemistry. Results： The results of HE stain demonstrated that intestine wall were normal in NG and CG, and was congestion, hemorrhage and edema in EG. Compared with NG and CG, the positive expression of MAP-2 was significantly lower （P〈0.05）, and the positive expression of SOD was also significantly lower （P〈0.05）, but the MDA was significantly higher （P〈0.05） in EG. Conclusions： The results demonstrate that intestinal congestion-reperfusion may induce decrease of amount of neuron, and the mechanism may be related with free radical injury and lipid peroxidation.

关 键 词：肠淤血再灌注 MAP-2 SOD MDA 

分 类 号：Q95-3[生物学—动物学] R322.451[医药卫生—人体解剖和组织胚胎学]