Disruption of the Small-Intestine Mucosal Barrier After Intestinal Occlusion: A Study with Light and Electron Microscopy

Abstract

It is known that the gut may serve as a reservoir for various microorganisms, which under specific circumstances may intrude into the systemic circulation, causing systemic infections. The aim of the present study was to estimate the "critical time" of disruption of the small-intestine mucosal barrier in conditions of experimentally induced intestinal occlusion, based on the histopathological alterations observed under light and electron microscopy. Forty rabbits underwent small-intestine obstruction through ligation with a nonabsorbable suture. Blood cultures from portal vein and inferior vena cava, as well as cultures from the peritoneal fluid, a hepatic fragment, and a mesenteric lymph node, were obtained before the ligation (0 h). The same cultures were repeated at 4 and 8 h (group A, 20 rabbits) and at 6 and 12 h after the ligation (group B, 20 rabbits). Small-intestine specimens proximal to the occlusion were taken for examination under the optic and electronic microscope in the same time intervals. Five of 20 rabbits of group A died within 4 h and 6 of 20 rabbits of group B died within 6 h after the operation. All anaerobic cultures were negative. All aerobic cultures that became positive developed Escherichia coli colonies. Intestinal epithelium of dead animals was transformed to cuboid with destruction of goblet cells and alteration in secretion of acid polysaccharides. The mucosal appearance of all rabbits that survived 12 hours after ligation was the same. The disruption of the mucosal barrier begins 4 h after complete intestinal occlusion. At 12 h after complete intestinal occlusion, the disruption is total with different degrees of severity.

Role of myosin light chain kinase in intestinal epithelial barrier defects in a rat model of bowel obstruction

“…The histological damage in our IO rats was similar to other models of mechanical obstruction showing swollen and edematous villous structure [8,24]. The continuity of epithelial layer on the villi was not disrupted in IO rats, in comparison to models with mesenteric ischemia/reperfusion injury that display severe villous denudation and tissue necrosis [9,23].…”

Review article: bacterial translocation in the critically ill – evidence and methods of prevention

“…Increased bacterial loads and breakdown of tight junctions associated with intestinal obstruction are thought to promote bacterial translocation. First proposed by Deitch et al , 47, 58 intestinal obstruction has been shown to promote bacterial overgrowth, 58 and disruption of the intestinal epithelium in animal models, 48, 59, 60 resulting in an increased prevalence of bacterial translocation on univariate analysis 61 . These observations have also been substantiated by some human studies 23, 24, 46 …”

“…Factors that influence bacterial translocation are believed to act on the delicate homeostatic equilibrium between luminal organisms and the gut barrier, promoting ingress of antigens across the intestinal barrier 44, 45 . These factors are thought to include intestinal obstruction, 23, 24, 46–48 jaundice, 23, 24, 49–52 inflammatory bowel disease, 24, 53, 54 malignancy, 55–57 pre‐operative total perenteral nutrition (TPN), 23 emergency surgery, 23 and gastric colonization with microrganisms 23, 40 . Much of the evidence to substantiate these claims is available from animal studies.…”

Bacterial translocation in colorectal cancer patients

“…The composition of normal intestinal microbiota is affected by various factors: diet, gastric and intestinal secretions, bile salts, lysozyme, secretory IgA, antibacterial drugs, endotoxic shock, parenteral nutrition, bowel obstruction, and much more [34]. All these factors can lead to microbiota imbalance and bacterial overgrowth, which in its turn, contributes to BT, as it is been proven in animal models [35] and in humans [36].…”