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. 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. 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. 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.