Alterations in rat intestinal transit by morphine promote bacterial translocation

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Abstract
Translocation of enteric microorganisms from the intestinal tract to extraintestinal sites has been proposed as an early step in the development of gram-negative sepsis. This study examined the role of altered bowel transit in influencing intestinal bacteriostasis and bacterial translocation using morphine as a pharmacologic inhibitor of such transit. In the first experiment, either normal saline (N=8) or morphine sulfate (20 mg/kg;N=8) was injected subcutaneously. Two hours later, morphine (7.5 mg/kg) was infused subcutaneously for an additional 22 hr; control animals received saline alone. After completion of this regimen, a volume of 0.2 ml of 2.5 mM FITC dextrans (10,000 daltons) were injected intraduodenally in each group. The bowel was removed 25 min later, divided into 5-cm segments, and the content of dextrans measured. Small bowel propulsion was expressed as the geometric center of the distribution of dextrans throughout the intestine (in percentage length of small bowel). Gut propulsion was significantly reduced after morphine treatment as compared to controls (32.8±8.2% vs 55.8±4.0%;PP<0.05); no translocation to distant sites occurred in control animals. We conclude that the morphine-induced prolongation in bowel transit promotes bacterial translocation secondary to an overgrowth of enteric bacteria in the intestinal lumen.