ALTERATIONS IN MUCOSAL MORPHOLOGY AND PERMEABILITY, BUT NO BACTERIAL OR ENDOTOXIN TRANSLOCATION TAKES PLACE AFTER INTESTINAL ISCHEMIA AND EARLY REPERFUSION IN PIGS

Ischemia and reperfusion of the gut may be an important etiological fa ctor in the development of multiple organ failure. We have used a hemo rrhagic and a superior mesenteric artery (SMA) occlusion shock model i n pigs to estimate the effect of ischemia and reperfusion on intestina l morphology, mucosal permeability, and the occurrence of bacterial or endotoxin translocation. Mucosal ulceration and necrosis were found i n the SMA shock model, while the morphological changes were less prono unced in the hemorrhagic shock model. Scanning electron microscopy sho wed shrinkage of the villi and plugging of the colonic crypts in both shock models. Enterocyte cell kinetics was investigated using 5-bromo- 2'-deoksyuridine (BrdU) incorporation and immunovisualization by anti- BrdU antibodies. Cell renewal was almost completely lost from the jeju num to the rectum in both shock models. Intramucosal pH was measured u sing a tonometer placed in the terminal ileum. Segments of intestinal mucosa were mounted in Ussing chambers, and permeability was measured using radioloabeled probe molecules of differing molecular weights, Au gmented molecular flux of inulin (M(r) 5.000) and mannitol (M(r) 182) and loss of short circuit current (I-sc) and transepithelial potential difference (PD) were found in mucosae from both shock models. Endotox in was demonstrated in the ascitic fluid in both shock models; 9.5 (2. 7-14.3) (median and 95% confidence interval) EU/mL in the SMA occlusio n model and 16.0 (4.9-29.4) EU/mL in the hemorrhagic shock model), but the levels were not significantly higher than in the control model 6. 5 (4.3-34.0) EU/mL. In agreement with this, no pathogenic bacteria or endotoxin could be detected in the systemic circulation, portal blood, lymph, or in homogenates of mesenterial lymph nodes, liver, or lung. These findings suggest that there is no translocation of bacteria and endotoxin to the systemic circulation during intestinal ischemia and e arly reperfusion even though the mucosa morphology is highly aberrated and its permeability increased.