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Mucosal changes in interposed colon segment as gastric substitute following gastrectomy in rats.

AbstractBACKGROUND:
An interposed colon segment has been clinically reconstructed as a gastric substitute. The purpose of this study is to establish a rat model of colonic interposition and to investigate serial mucosal changes and adaptation of interposed colon mucosa under prolonged exposure to bile and pancreatic juice reflux.
METHODS:
About 80% of the glandular stomach was resected, and a 3-cm segment of the transverse colon interposed isoperistaltically between the remnant stomach and duodenum. Epithelial proliferation, aberrant crypt foci (ACF), and tumors in the interposed colon segment were investigated after 4 months of administration of N-ethyl-N'-nitro-N-nitrosoguanidine (ENNG) to rats (ENNG-treated rats).
RESULTS:
In the interposed colon, crypt lengths increased significantly, and the number of goblet cells per crypt per 1 mm decreased significantly compared to those in the remnant colon, whether ENNG was administered or not. Both crypt lengths and the number of goblet cells in the interposed colon of controls and ENNG-treated rats showed no significant difference. A proliferating cell nuclear antigen (PCNA) labeling index (LI) of the remnant colon was almost 30% in both controls and ENNG-treated rats. In controls, the PCNA LI in the interposed colon at 4, 8, and 12 months after surgery was 30.8, 31.8, and 47.8%. In ENNG-treated rats, the PCNA LI in the nontumorous mucosa of the interposed colon was 44.9, 55.4, and 61.5% at the above postsurgical intervals. ACF and carcinoma were observed only in the interposed colon of ENNG-treated rats. ACF was observed as early as 4 months after surgery, and its incidence increased serially. Both the incidence of carcinogenesis and the number of tumors had increased 8 months after surgery.
CONCLUSIONS:
We established a rat model of colonic interposition following gastrectomy. The adaptation of interposed colon mucosa was well conducted. A malignant condition, however, was induced in the interposed colon segment serving as a gastric substitute because of both carcinogen predisposition and prolonged exposure to bile and pancreatic juice reflux.
AuthorsY Sato, S Ohwada, T Ogawa
JournalThe Journal of surgical research (J Surg Res) Vol. 73 Issue 1 Pg. 66-72 (Nov 1997) ISSN: 0022-4804 [Print] United States
PMID9441795 (Publication Type: Journal Article)
CopyrightCopyright 1997 Academic Press.
Chemical References
  • Carcinogens
  • Proliferating Cell Nuclear Antigen
  • Methylnitronitrosoguanidine
  • ENNG
Topics
  • Adaptation, Physiological
  • Animals
  • Bile (physiology)
  • Carcinogens
  • Colon (pathology, transplantation)
  • Colonic Neoplasms (chemically induced, pathology)
  • Epithelium (pathology)
  • Gastrectomy
  • Intestinal Mucosa (pathology, physiology)
  • Male
  • Methylnitronitrosoguanidine (analogs & derivatives)
  • Pancreatic Juice (physiology)
  • Proliferating Cell Nuclear Antigen (analysis)
  • Rats
  • Rats, Wistar
  • Time Factors

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