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Oral Prostaglandin E2 Prevents Gut Atrophy During Intravenous Feeding but Not Bacterial Translocation
W. Scott Helton, MD;
Richard Garcia
Arch Surg. 1993;128(2):178-184.
Abstract
• 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 µg/kg twice a day). Rats were fed their 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.
(Arch Surg. 1993;128:178-184)
Author Affiliations
From the Department of Surgery, University of Washington Medical School, Seattle.
Footnotes
Accepted for publication August 23, 1992.
Presented at the 12th Annual Meeting of the Surgical Infection Society, Los Angeles, Calif, April 11, 1992.
Reprint requests to Department of Surgery, RF-25, University of Washington Medical Center, Seattle, WA 98195 (Dr Helton).
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