Reduktion der erhöhten bakteriellen Translokation bei simultaner Leberresektion und Kolonanastomose durch Probiotika im Rattenmodell

2004 
One important cause of postoperative nosocomial infections is bacterial translocation. Enterai administration of probiotics is thought to reduce translocation. Methods: 68 rats were randomized to 7 groups: 5 groups received standard rat chow and were subjected to either sham-operation, 70% liver resection, colonie anastomosis or a combination of 30%- or 70% liver resection with synchronous colonie anastomosis. Two additional groups with synchronous operation received a combination of four different lactic acid bacteria twice daily 48 h pre- and postoperatively. Bacterial concentrations in coecum, mesenteric lymph nodes (MLN), liver and spleen were analyzed 48 hours after operation. Furthermore, histological changes in the intestine, intestinal paracellular permeability (Ussing-chamber) and mitosis rate of the remnant liver were analyzed. Results: Bacterial translocation occurred in all rats, except in the sham group. Following liver resection, the highest bacterial concentration was found in liver and spleen, after colonie anastomosis in the MLN. Translocation was potentiated after combined operation, parallel to the extent of liver resection. Application of probiotics significantly reduced bacterial concentration in the MLN, especially in animals with a high coecal lactobacillus concentration. No histological changes were observed. Colonie paracellular permeability for ions, but not for larger molecules was increased after colonie anastomosis. 70% liver resection led to a high rate of hepatocyte mitosis, whereas combination with colon anastomosis impaired this regeneration process. Conclusion: Synchronous liver resection and colonie anastomosis induce increased bacterial translocation compared to the single operations. Translocation is diminished by oral probiotics in the rat model. Coecal bacterial overgrowth and impaired hepatic regeneration, but not histological changes or alterations of paracellular permeability are potential pathogenic mechanisms in this setting.
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