A standardised and reproducible model of intraabdominal infection and abscess formation in rats.

OBJECTIVE: To develop a standardised and reproducible model of intra-abdominal infection and abscess formation in rats. DESIGN: Experimental study. SETTING: University hospital, The Netherlands. SUBJECTS: 36 adult male Wistar rats. INTERVENTIONS: In 32 rats, peritonitis was produced using two different concentrations of Escherichia coli (E. coli) and Bacteroides fragilis (B. fragilis) incorporated in fibrin clots (E. coii 1 x 10(5) colony forming units (CFU)/ml or 1 x 10(8) CFU/ml, B. fragilis: 1 x 10(8) CFU/ml). Four rats with fibrin clots without bacteria served as uninfected controls. MAIN OUTCOME MEASUREMENTS: Macroscopy and bacterial counts in peritoneal fluid, blood, and fibrin clots after 24 hours, 4 days, 7 days, and 4 weeks. RESULTS: Macroscopically, there were signs of intra-abdominal infection and abscesses. With the higher starting concentration of E. coli, macroscopic signs were more pronounced and in nearly all rats bacterial counts in peritoneal fluid and fibrin clots showed persistently high numbers of E. coli and B. fragilis for at least 7 days (E. coli = 2 x 10(3) to 1 x 10(6) CFU/ml and 5 x 10(7) to 9 x 10(8) CFU/clot; B. fragilis = 1 x 10(3) to 1 x 10(6) CFU/ml and 5 x 10(7) to 6 x 10(8) CFU/clot). CONCLUSION: This standardised and reproducible model of intra-abdominal infection and abscess formation seems well suited for further use and development in experiments on the pathophysiology of intra-abdominal infection and abscesses.

The effects of ABT-229 and octreotide on interdigestive small bowel motility, bacterial overgrowth and bacterial translocation in rats.

BACKGROUND: Interdigestive small bowel motility has a regulatory function on the microflora of the upper small bowel. Here we investigate the effects of ABT-229 and octreotide on morphine-induced dysmotility, the accompanying bacterial overgrowth and bacterial translocation. METHODS: Rats were fitted with jejunal myoelectrodes and a subcutaneous cannula for continuous infusion of saline or morphine. Fasting motility was measured for 6 h on four occasions: one control measurement (day 0) and three measurements on consecutive days (days 1-3) while receiving saline alone (group A), morphine alone (group B), saline + ABT-229 (group C), morphine + ABT-229 (group D), saline + octreotide (group E) or morphine + octreotide (group F). Samples from the mesenteric lymph node complex (MLN), liver, spleen, duodenum and ileum were taken for quantitative microbial culturing on day 4. RESULTS: Neither ABT-229 nor octreotide increased the number of propagated activity fronts during saline infusion. During morphine-induced dysmotility, ABT-229 induced more propagated activity fronts in group D (13.4, 9.8 and 8.8 per 6 h) than in group B (7.0, 4.5, 3.8 per 6 h) on days 1, 2 and 3 (P < 0.05 for all days) Octreotide did not induce more propagated activity fronts. Disruption of small bowel motility by morphine led to bacterial overgrowth in the duodenum. ABT-229 and octreotide did not reduce the bacterial growth levels. The total incidence of bacterial translocation was significantly higher in the morphine-treated animals than in the saline-treated animals. Neither ABT-229 nor octreotide reduced the bacterial translocation incidence. The number of propagated activity fronts on day 3 and duodenal bacterial growth correlated significantly in groups A, E and F. CONCLUSIONS: ABT-229, but not octreotide, reduced morphine induced dysmotility. Small bowel bacterial overgrowth and bacterial translocation were not prevented. Fasting small bowel motility has a regulatory function on the intestinal microflora of the upper small bowel.

The role of interdigestive small bowel motility in the regulation of gut microflora, bacterial overgrowth, and bacterial translocation in rats.

OBJECTIVE: To clarify the role of the migrating motor complex (MMC) in the regulation of small intestinal microflora and bacterial translocation. SUMMARY BACKGROUND DATA: The intestinal microflora may serve as a source of infectious microorganisms. Failure of regulatory mechanisms of the intestinal flora could therefore play an important role in the pathogenesis of gut-derived infections. METHODS: Rats were fitted with small intestinal myoelectrodes. MMCs were measured on a control day and 3 consecutive days during continuous administration of morphine or placebo. Mesenteric lymph nodes, liver, spleen, peripheral blood, duodenum, and ileum samples were cultured quantitatively. RESULTS: The mean MMC cycle length in placebo-treated animals was 15.1+/-0.5 minutes. MMCs were completely disrupted after morphine treatment. Total bacterial growth in the duodenum was 7.27+/-0.34 10log colony-forming units (CFU)/g with placebo and 8.28+/-0.27 CFU/g with morphine. In placebo-treated animals, the mean MMC cycle length the day before culturing correlated with total bacterial growth in the duodenum. Translocation incidences to the mesenteric lymph nodes, liver, spleen, and blood were 0/8, 1/8, 0/8, and 0/8 with placebo and 7/8, 6/8, 5/8, and 0/8 with morphine. The overall translocation incidence was 1/8 in placebo-treated animals and 8/8 in morphine-treated animals. CONCLUSIONS: The MMC is an important mechanism controlling bacterial growth in the upper small bowel. Its disruption with morphine promotes duodenal bacterial overgrowth and bacterial translocation.