Effective total parenteral nutrition plus morphine on bacterial translocation in rats.

Abstract

The gut atrophy associated with total parenteral nutrition (TPN) may lead to a breakdown in the normal mucosal barrier and cause bacterial translocation. It has been hypothesized that a component of this breakdown involves stasis with bacterial overgrowth of more pathogenic organisms.1 Postoperative, critically ill surgical patients may be maintained with both TPN and morphine for analgesia. The effect of morphine on the gastrointestinal tract includes inhibition of intestinal transit with the potential for increased bacterial overgrowth. The objective of this study was to determine whether gut stasis induced by parenteral morphine led to enhanced bacterial translocation during TPN. Male Sprague‐Dawley rats were allowed a period of time to adapt to their environment and then underwent a double‐lumen cannulation. A line was placed in the internal jugular vein for the infusion of TPN, and a second subcutaneous line was tunneled in the back for the continuous infusion of morphine, similar to the infusion of repeated injections. These lines were maintained on a free swivel using standard procedures. Rats were randomized to a control group that had lines placed and infused with saline, and this group was allowed free access to food. A second group received TPN alone. A third group received TPN plus continuous morphine sulfate, and a fourth received TPN supplemented with glutamine plus morphine. All groups on TPN received nothing by mouth. After 4 days, a subgroup of animals was given L‐fluorescein isothiocyanate‐dextran (FTTC) through a duodenal catheter. Intestinal motility was measured by distribution of the fluorescent label in sequential intestinal segments throughout the GI tract over time. Other subgroups underwent harvesting of mesenteric lymph nodes, spleen, liver, and lung to assess bacterial translocation. Small‐intestine transit time was significantly slower in the morphine groups. TPN alone had no effect on motility but did result in significant increases of anaerobic and facultative bacteria in the ileum. The addition of morphine to the TPN solution induced overgrowth throughout the small bowel and cecum. Bacterial translocation to lymph nodes occurred in 14% of the control animals and in 50% of the TPN animals. The mean number of colony‐forming units per node was quite low, averaging 13 and 33, respectively. Of the animals receiving TPN plus morphine, 100% had bacteria recovered from lymph nodes with the highest number of bacteria being in the group that was also deficient in glutamine (2079 ± 811 vs 1009 ± 404). The majority of recovered organisms was of gut origin, such as Escherichia coli and enterococcus. When more invasive forms of translocation were examined, as noted by recovery of bacteria from spleen, blood, and lung, there was a significant increase in bacteria in the TPN plus morphine group. The addition of glutamine to the TPN solution decreased translocation to the blood and lung to levels seen in the TPN‐alone group and in controls.