| Literature DB >> 26863177 |
Chun Yu Wong1, Margreet R de Vries2, Yang Wang3, Joost R van der Vorst4, Alexander L Vahrmeijer4, Anton-Jan van Zonneveld5, Jaap F Hamming4, Prabir Roy-Chaudhury3, Ton J Rabelink5, Paul H A Quax2, Joris I Rotmans6.
Abstract
The arteriovenous fistula (AVF) still suffers from a high number of failures caused by insufficient remodeling and intimal hyperplasia from which the exact pathophysiology remains unknown. In order to unravel the pathophysiology a murine model of AVF-failure was developed in which the configuration of the anastomosis resembles the preferred situation in the clinical setting. A model was described in which an AVF is created by connecting the venous end of the branch of the external jugular vein to the side of the common carotid artery using interrupted sutures. At a histological level, we observed progressive stenotic intimal lesions in the venous outflow tract that is also seen in failed human AVFs. Although this procedure can be technically challenging due to the small dimensions of the animal, we were able to achieve a surgical success rate of 97% after sufficient training. The key advantage of a murine model is the availability of transgenic animals. In view of the different proposed mechanisms that are responsible for AVF failure, disabling genes that might play a role in vascular remodeling can help us to unravel the complex pathophysiology of AVF failure.Entities:
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Year: 2016 PMID： 26863177 PMCID： PMC4781715 DOI： 10.3791/53294
Source DB: PubMed Journal: J Vis Exp ISSN： 1940-087X Impact factor: 1.355