Sandostatin Impairs Post-Resection Intestinal Adaptation in a Rat – מתוך כנס גאסטרו ילדים, 9 ביולי 2002


Model of Short Bowel Syndrome

Igor Sukhotnik1,2, Leonardo, Siplovich, 2 Michael M. Krausz, 3 Arnold G.Coran,4 Eitan Shiloni,1.

Rappaport Faculty of Medicine, Technion, Carmel Medical Center1, Ha-Emek Medical center 2, Rambam Medical Center 3 and University of Michigan, Section of Pediatric Surgery, Mott Children's Hospital, Ann Arbor, MI4

Background: Because of its antisecretory properties, somatostatin has been advocated for the treatment of patients with short bowel syndrome. However its use has been limited because of concern about a potential negative effect on intestinal adaptation. This study was conducted to determine the effect of sandostatin (SND) on structural intestinal adaptation, cell proliferation and apoptosis in a rat model of short bowel syndrome (SBS).

Methods: Forty five male Sprague-Dawley rats were divided into three experimental groups: Sham rats underwent bowel transection and re-anastomosis, SBS- rats underwent 75% small bowel resection and SBS-sandostatin rats underwent bowel resection and were treated with sandostatin (200 µg/kg/day) (SBS-SND). Parameters of intestinal adaptation, enterocyte proliferation and enterocyte apoptosis were determined on day 14 following operation.

Results: SBS-rats demonstrated a significant increase (vs Sham) in jejunal and ileal bowel and mucosal weight, mucosal DNA and protein, villus height and crypt depth. SBS-SND animals demonstrated lower (vs SBS-rats) duodenal and jejunal bowel weights, jejunal and ileal mucosal weight, jejunal and ileal mucosal DNA and protein, and jejunal and ileal villus height. A significant decrease in enterocyte apoptosis in jejunum and ileum and a decrease in cell proliferation in ileum was seen also in SBS-SND rats compared to SBS- animals.

Conclusions: In a rat model of SBS sandostatin inhibits structural intestinal adaptation. Possible mechanism for this effect may be decreased cell proliferation. Decreased enterocyte loss via apoptosis, found in this study, may reflect a reduced number of enterocytes.

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