Oral prostaglandin E2 prevents gut atrophy during intravenous feeding but not bacterial translocation.

The pathophysiologic changes in gut physiology that result in bacterial translocation during intravenous feeding are poorly defined, though believed to be related in part to intestinal atrophy, decreased mesenteric blood flow, and lack of intestinal secretions. This study investigated the hypothesis that pharmacologic preservation of intestinal structure and function by orally administered 16,16-dimethyl-prostaglandin E2 would prevent bacterial translocation in intravenously fed rats. Thirty-five rats were randomized to three groups: group 1 was fed rat chow ad libitum, group 2 received standard parenteral nutrition, and group 3 received parenteral nutrition plus oral 16,16-dimethyl-prostaglandin E2 (150 micrograms/kg twice a day). Rats were fed there respective diets for 5 days and killed. Mesenteric lymph nodes were procured for culture, and the intestine was assessed for weight, DNA, protein values, and histologic character. Results demonstrate that orally administered 16,16-dimethyl-prostaglandin E2 potently attenuates the intestinal atrophy associated with parenteral feeding but does not prevent bacterial translocation. Intestinal barrier dysfunction and bacterial translocation during intravenous feeding is related to factors other than the development of gut atrophy.