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Published in: Journal of Hepato-Biliary-Pancreatic Sciences 4/2009

01-07-2009 | Original article

The effect of calcitonin gene-related peptide on healing of intestinal anastomosis in rats with experimental obstructive jaundice

Authors: Sezai Leventoglu, Hande Koksal, Banu Sancak, Ferit Taneri, Erhan Onuk

Published in: Journal of Hepato-Biliary-Pancreatic Sciences | Issue 4/2009

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Abstract

Purpose

Intestinal anastomotic healing is a complex procedure in which several mediators and cytokines play roles. Calcitonin gene-related peptide is an important neuropeptide in inflammation. In this study we aimed to investigate the effect of calcitonin gene-related peptide on healing of intestinal anastomosis in rats with obstructive jaundice.

Materials and methods

Obstructive jaundice was induced in rats by the ligation and division of the common bile duct. Four days after the operation, intestinal anastomosis was performed, and either calcitonin gene-related peptide or 0.9% NaCl was administered intraperitoneally to these jaundiced rats and controls. The concentrations of serum tumor necrosis factor-α (TNF-α) and triglyceride levels of all rats were measured, and healing of the anastomosis was evaluated by measuring the bursting pressure and hydroxyproline content on the 7th postoperative day.

Results

Calcitonin gene-related peptide was found to have positive effects on healing of the anastomosis by inhibiting the effects of TNF-α and increasing the bursting pressure and hydroxyproline content of the anastomosis.

Conclusion

Calcitonin gene-related peptide increases anastomotic wound healing in experimental anastomosis in the presence of obstructive jaundice in rats.
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Metadata
Title
The effect of calcitonin gene-related peptide on healing of intestinal anastomosis in rats with experimental obstructive jaundice
Authors
Sezai Leventoglu
Hande Koksal
Banu Sancak
Ferit Taneri
Erhan Onuk
Publication date
01-07-2009
Publisher
Springer Japan
Published in
Journal of Hepato-Biliary-Pancreatic Sciences / Issue 4/2009
Print ISSN: 1868-6974
Electronic ISSN: 1868-6982
DOI
https://doi.org/10.1007/s00534-009-0098-2

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