The small intestine in experimental peritonitis : An experimental study focusing om intestinal energy metabolism, bacterial translocation and mucosal immunology

Sammanfattning: The gut is highly susceptible to injury during sepsis. An impaired mucosal barrier permitstranslocation of enteric microorganisms to blood or other organs. In a porcine model sepsiswas induced by faecal peritonitis. Temporary occlusion of the superior mesenteric arterycaused a reduction in intramucosal pH (pHi) and increased concentrations of lactate in bloodand intestinal fluid. In peritonitis a similar reduction in pHii was seen but without an increasein lactate. To increase gut oxygen delivery (DO2) in peritonitis, animals received a colloid(dextran 70) alone or together with dobutamine. The reduction in gut DO2 and pHi wasattenuated, and the mucosal-arterial pCO2 difference (pCO2-gap) remained unchanged. Inperitonitis, the intestinal energy charge decreased and the lactate concentration increasedmoderately, but first after the reduction in pHi.In conclusion, in peritonitis intramucosal acidosis cannot be explained by a reduction in gutDO2 alone. Despite increased gut blood flow, pHi was somewhat decreased. This indicatesthat pHi does not solely reflect tissue hypoxia. Instead, pHi and the pCO2-gap may beinfluenced by other factors.Instillation of microorganisms into the intestinal lumen demonstrated that only bacteria witha known ability to translocate were found in the blood and mesenteric lymph nodes (MLNs),i.e., translocation is dependent on bacterial characteristics and not on mucosal injury per se.The distribution of immune cells in the intestinal mucosa and MLNs was evaluated (monoclonal antibodies against CD2, IgM, and CD11a/CD18), and interleukin-6 (IL-6) wasmeasured in systemic and mesenteric venous blood. Peritonitis was shown to induce aninflammatory response with changes in the distribution of immune cells and release of IL-6.