Oral prostaglandin E2 prevents gut atrophy during intravenous feeding but not bacterial translocation
W. S. Helton and R. Garcia
Department of Surgery, University of Washington Medical School, Seattle 98195.
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.