摘要
目的:探讨肠缺血再灌注损伤大鼠肠黏膜结构和通透性的变化及其与细菌移位的相关性。方法:雄性SD大鼠随机分为模型1组、模型2组、手术组和对照组。模型1组和手术组通过夹闭肠系膜上动脉造成肠缺血再灌注损伤,模型2组和对照组分离肠系膜上动脉但不夹闭。模型1组大鼠于再灌注后30min处死,模型2组暴露肠系膜上动脉相同时间后处死,留取小肠标本行病理检查。余两组术后第3、7天收集尿液,检测肠黏膜通透性,第8天留取胰腺及淋巴组织作培养,并抽取门静脉血作16srRNA检测(PCR)。结果:模型1组再灌注30min后小肠绒毛肿胀破坏,固有层炎性细胞浸润;术后第3、7天手术组肠黏膜通透性较对照组明显增大(P<0.05,P<0.01);手术组组织培养阳性率明显高于对照组(P<0.005),手术组门静脉血16srRNA阳性率高于对照组(P<0.01);肠黏膜通透性与门静脉血16srRNA阳性率具有明显的相关性(P<0.01),而与组织培养阳性率无相关性。结论:肠缺血再灌注损伤使大鼠肠黏膜结构破坏、通透性增加,肠黏膜通透性增加与循环细菌移位有关,门静脉系统可能是重要的细菌移位途径。
Objective: To investigate the changes of morphology and intestinal permeability of rats with intestinal ischemia reperfusion injury, and its relation with bacterial translocation. Methods: Male SD rats were divided into model group 1, model group 2, control and operation group randomly. The intestinal ischemia/reperfusion (I/R) model of group 1 and operation group were established by clip occluding superior mesenteric artery (SMA). SMA was isolated but not occluded in model group 2 and control group. Rats in model group 1 and 2 were sacrificed 30 minutes after reperfusion or isolation of SMA, specimens of small intestinal were taken for pathological examination. In the other 2 groups, 24 h of urine was collected on day 3 and 7 after the operation for detection of permeability of intestinal mucosa via L/M determination. Portal venous blood was collected on day 8 for 16s rRNA gene expression, pancreatic and lymphoid tissue were taken for culture. Results: Villi of small intestine were engorged and destroyed, proper layer was infiltrated by inflammatory cells in model group 1 thirty minutes after reperfusion;permeability of intestinal mucosa was significantly higher in operation group compared with that of control group on day 3 and 7 after the operation(P〈0. 05, P〈0. 01 ) ; positive rate of culture in operation group was significantly higher than that of control group (P〈0. 005), positive rate of 16s rRNA gene in control group was lower than that of operation group(P〈0. 01);there was obvious corelation between L/M and the positive rate of 16s rRNA gene(P〈0. 01), but not with the positive rate of culture. Conclusion; The intestinal I/R injury can impair mucosa structure of small intestine, increases the intesital permeability and facilitates bacterial translocation. There was obvious relationship between the intesital permeability and bacterial translocation in the portal system. Portal system may be an important way of bacterial translocation from the intestine.
出处
《内科急危重症杂志》
2007年第4期122-124,共3页
Journal of Critical Care In Internal Medicine
关键词
缺血再灌注
细菌移位
16s
RRNA基因
Intestinal ischemia reperfusion Bacterial translocotion 16s rRNA gene