Effect of calcitonin gene-related peptide on anastomotic healing in the presence of endotoxin

Background:  Intestinal anastomotic healing is a complex procedure in which several mediators, cytokines and other substances play roles, as well as calcitonin gene‐related peptide (CGRP). CGRP is capable of stimulating DNA synthesis and cell proliferation in endothelial cells by increasing vasodila...

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Published in:ANZ journal of surgery Vol. 75; no. 12; pp. 1106 - 1110
Main Authors: Dogmuş, Mehmet, Ersoy, Emin, Anadol, A. Ziya, Özel, Ümmühani, Bilgehan, Ayse
Format: Journal Article
Language:English
Published: Oxford, UK Blackwell Science Pty 01-12-2005
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Summary:Background:  Intestinal anastomotic healing is a complex procedure in which several mediators, cytokines and other substances play roles, as well as calcitonin gene‐related peptide (CGRP). CGRP is capable of stimulating DNA synthesis and cell proliferation in endothelial cells by increasing vasodilatation and inflammatory response and promoting epithelial, vascular and mesothelial cell proliferation. This study was undertaken to investigate whether CGRP has a beneficial effect on intestinal anastomotic healing, even in septic conditions. Methods:  Four groups of 10 rats were administered normal saline (0.5 mL), lipopolysaccharide (LPS) (0.5 mg/kg), CGRP (0.5 mL 6.5 × 10−10 mol/L) and LPS + CGRP (0.5 mg/kg + 0.5 mL 6.5 × 10−10 mol/L) via intraperitoneal route, respectively, 24 h prior to operation and postoperatively. All rats underwent ileo−ileal end‐to‐end anastomosis. Anastomotic bursting pressure and tissue hydroxyproline levels were measured on postoperative day 7. Results:  Calcitonin gene‐related peptide was found to have positive effects on both parameters of healing. The LPS‐injected group showed intestinal anastomotic healing disorder suggesting impaired collagen production, which showed improvement after CGRP administration. Conclusions:  Calcitonin gene‐related peptide increases anastomotic wound healing in experimental intestinal anastomosis in the presence of endotoxin.
Bibliography:ArticleID:ANS3616
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istex:6AC8AC0B561DE1560AE7D46209691ECDBCF128C6
A. Z. Anadol
M. Dogmuş
E. Ersoy
Ü. Özel
MD.
MD
A. Bilgehan
PhD
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:1445-1433
1445-2197
DOI:10.1111/j.1445-2197.2005.03616.x