Article
The role of pyrrolidine dithiocarbamate (PDTC) as a viability factor on an epigastric adipocutaneus flap (EAF) in a rat model
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Authors
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Stefan Lyutenski
- Department of Otolaryngology, Head and Neck Surgery, University of Leipzig, Germany
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Andreas Dacho
- Department of Plastic and Aesthetic Surgery, Catholic Hospitals Ruhr Peninsula, St. Josef Medical Center, Essen, Germany
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Gabriela Aust
- Department of Surgery II (Intestinal-, Transplant-, Thoracic- and Vascular Surgery), University of Leipzig, Germany
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Andreas Dietz
- Department of Otolaryngology, Head and Neck Surgery, University of Leipzig, Germany
| Published: | July 6, 2010 |
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Outline
Text
Introduction: The iNOS plays a key role in the signal transduction cascade of the pharmacologic preconditioning. PDTC is a chemical substance with various effects as a chelator and as an inhibitor of the NF-kappaB’s DNA binding. Thus PDTC blocks the transcription and expression of the iNOS and the inflammatory citokines (TNF-alpha, IL-6 und ICAM-1). Our objective is to assess the effect of PDTC on an EAF in a rat model using a planimetric and hitopathologic approach.
Methods and materials: Fifty-six male Wisar rats (about 350 g) were divided into four experimental groups (n=14). After the induction of anesthesia with ketamine, xylazine and atropine, a central venous catheter was inserted and a pedicled EAF was raised. In the control groups flap was either raised (K-I) or clamped for two hours (K+I). After intravenous application of 51 μg/g PDTC two other groups were subjected to a 15 min ischemia and 30 min of reperfusion without (PDTC-I) or followed by another two hours of induced ischemia (PDTC+I). Planimetric measurement of the mean flap necrosis area and histopathologic evaluation in all groups followed on the 5th postoperative day.
Results: The average necrosis in the control groups was: K-I: 36.1%±13.6%, K+I: 48.6%±14.6%, PDTC-I: 30.5%±13.5%, PDTC+I: 38.1%±13.2%. The difference between the groups K-I and PDTC-I (p<0.5) as well as between K+I and PDTC+I (p<0.5) was not significant. There weren’t any histopathologic group differences of the inflammatory response to detect.
Conclusion: The application of PDTC caused no significant extension of the necrosis on EAF in a rat model. Furthermore no inhibition of the inflammatory respose was detected. PDTC seems to have no survival effect on the EAF.
