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Immediate and delayed surgical repair of duodenal defects in rats with small intestinal submucosa patch.

TitleImmediate and delayed surgical repair of duodenal defects in rats with small intestinal submucosa patch.
Publication TypeJournal Article
Year of Publication2014
AuthorsMiliaras, D., Miliaras S., Meditskou S., & Papamitsou T.
JournalPol Przegl Chir
Volume86
Issue3
Pagination116-21
Date Published2014 Mar
ISSN0032-373X
KeywordsAnimals, Duodenum, Intestinal Mucosa, Peritonitis, Rats, Rats, Wistar, Time Factors, Transforming Growth Factor beta, Wound Healing, Wounds, Penetrating
Abstract

UNLABELLED: Duodenal injuries, though rare, carry high rates of morbidity and mortality. The aim of the study was to evaluate the healing of the duodenal wall with the use of a Small Intestinal Submucosa (SIS) patch.MATERIAL AND METHODS: We studied 40 Wistar-Albino rats divided into two groups. In group A, we created a small defect in the duodenal wall, which was immediately covered with a SIS patch. In group B, the SIS patch was sutured over the defect after 6-8 hours, in order to induce peritonitis. The animals of both groups were sacrificed after 2, 6, 12 and 16 weeks respectively. In addition, we studied the immunohistochemical expression of TGF-β, which is a major constituent of SIS, and plays a central role in the healing process.RESULTS: Histology showed progressive development of the layers of the duodenal wall over the patch as early as the 2nd week in some of the animals of group A. Mucosa developed later on in the animals of group B, presumably due to the more intense inflammation elicited by peritonitis. Expression of TGF-β was initially more pronounced in the epithelial cells of the regenerating mucosa of animals of group A, but it was maintained in higher levels in the animals of group B, which showed delayed mucosa degeneration.CONCLUSIONS: SIS appears to be both efficient and safe for the management of duodenal trauma. TGF-β seems to play an important role in the healing process, inducing regeneration of the stroma, and controlling epithelial growth.

DOI10.2478/pjs-2014-0022
Alternate JournalPol Przegl Chir
PubMed ID24791813

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