大鼠失血性休克肠粘膜形态学与功能变化

目的 探讨失血性休克肠缺血/再灌注损伤后,粘膜屏障功能与形态学的变化。方法 制作大鼠失血性休克模型,以休克复苏后0h、1h、3h、6h、12h、24h时间段取回肠组织标本,通过光镜和电镜下进行肠粘膜的形态学改变的观察,包括组织学检查、肠粘膜及绒毛厚度测量、粘膜损伤指数评定;同时在肝门静脉血作内毒素测定及复苏后1h、3h、6h的尿液作乳果糖/甘露醇比值检测以分析肠粘膜屏障功能的改变。结果 肠粘膜损伤主要表现出凋亡、坏死的两种细胞死亡形式。复苏0h组粘膜上皮就发生明显损伤改变,1h进一步加重,3h组出现修复现象,6h部分空肠及回肠绒毛已修复,12h时大部分肠粘膜结构基本恢复正常;内毒素和乳果糖/甘露醇比值在6h组达到高峰,仅24h组才恢复正常。结论 失血性休克缺血-再灌注后,肠粘膜屏障早期受累,表现为回肠粘膜细胞凋亡及坏死的两种损伤形式;肠粘膜具有强大的修复潜能;肠屏障功能的恢复滞后于形态学修复。

Study on Relationship between Functional,Morphological Changes and Reconstitution in Intestinal mucosal Barrier after Hemorrhagic Shock in rats

Objective To study on relationship between functional, morphological changes and resuscitation in small intestinal mucosal barrier after traumatic-hemorrhagic shock. Methods Specimen of ileum tissues were taken in the 0h, 1h, 3h, 6h, 12h and 24h after resuscitation. The morphological changes of intestinal mucosa were observated through light and electronic microscope, including histologic examination of intestinal mucosa and determination of villous thickness and evaluation of mucosa damage index. At the same time, hepato-portal vein blood was drawn in every rat for assaying endotoxin and lactulose/mannitol ratio of urine was detected to analyze the change of intestinal mucosal barrier function after resuscitation Oh, 3h, 6h respectively. Results The apoptosis and necrosis were main manifestation in the intestinal mucosal injury after hemorrhagic shock. The lesions were even obvious in Oh group and were on the increase in Ih group, the tissue reconstitution began within 3h group, but its damage is still serious. In 6h group, partial damage mucosa almost was near to entire reconstitution and finished in 12h group. Urine lactulose/mannitol ratio and endotoxin content in the experimental groups were raised notably, in which the peaks were in 6h group, and they were recovered to normal status in 24h group. Conclusion In the early stage of ischemia-reperfusion injury after hemorrhagic shock, intestinal mucosal barrier were subjected to serious damage, which showed as mucosal cell apoptosis and necrosis. Intestinal mucosa possesses stronger repair potential, but the recovery of intestinal barrier function was obviously slower than that of intestinal mucosal morphological changes.