摘要
目的探讨肝门阻断对肠黏膜屏障的影响及其意义。方法采用雄性Wistar大鼠,随机分为2组:假手术组(Ⅰ组)和实验组(Ⅱ组)。采用Pringle’s法进行肝门阻断,持续35分钟。分别于肝门阻断前及再灌注后2、4、24小时每组各选取10只大鼠,分别测定肠组织谷胱甘肽(GSH)、超氧化物歧化酶(SOD)、丙二醛(MDA)的含量,检测门静脉血浆内毒素水平。光镜观察组织形态学变化,测定肠粘膜厚度,肠绒毛高度。结果与Ⅰ组相比,再灌注后Ⅱ组肠组织中MDA含量增高(P<0.05),而GSH及SOD水平下降(P<0.05),门静脉内毒素水平明显增高(P<0.05)。再灌注后,Ⅱ组肠粘膜厚度、肠绒毛高度明显低于Ⅰ组(P<0.05)。结论肝门阻断可造成肠道过氧化损伤,导致肠粘膜屏障的破坏,促进内毒素移位。
Objective To explore the effects of total hepatic inflow occlusion on gut mucosal barrier. Methods Male Wistar rats were assigned randomly to 2 groups ( n = 40 ) : Group Ⅰ served as sham-operation group. The rats of the group Ⅱ underwent total hepatic inflow occlusion for 35min through the Pringle' s manoeuvre. Ten rats from each group were randomly chosen and killed before the initiation of occlusion and 2,4,24h after reperfusion respectively. The levels of MDA, SOD, GSH in intestinal tissue were measured. The levels of portal vein endotoxin were detected. Pathomorphological changes of intestine were oberserved under light microscope. Villus height and mucosal thickness were measured. Results Compared with the group Ⅰ,the levels of GSH and SOD in intestine of group Ⅱ decreased after reperfusion ( P 〈 0.05 ) , MDA of intestine increased ( P 〈 0.05 ), and endotoxin increased ( P 〈 0.05 ). After reperfusion mucosal thickness and villus height decreased significantly in the group Ⅱ as compared with that of the group Ⅰ ( P 〈 0.05 ). Conclusion Total hepatic inflow occlusion might result in lipid peroxidation-mediated injury of gut and disruption of the structure in intestine mucosa, thus promote the translocation of gut-derived endotoxin.
出处
《创伤外科杂志》
2007年第5期458-461,共4页
Journal of Traumatic Surgery
关键词
肝门阻断
肠黏膜屏障
内毒素
hepatic inflow occlusion
gut mucosal barrier
endotoxin