| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Department of Surgery, University of Florida College of Medicine and Malcom Randall VAMC, Gainesville, FL, USA
* To whom correspondence should be addressed. E-mail: Bercesa{at}mail.surgery.ufl.edu.
Accelerated intimal hyperplasia in response to an altered flow environment is critical to the process of vein bypass graft failure. Lack of a reproducible animal model for dissecting the mechanisms of vein graft (VG) remodeling has limited progress toward solving this clinically significant problem. Combining a cuffed anastomotic technique with other surgical manipulations, a well defined, more robust method for studying hemodynamic factors in vein graft arterialization was developed. METHODS Vein grafting in combination with fistula placement, complete occlusion, or partial distal branch ligation (DBL) was performed in the carotid artery of 56 rabbits. Extensive hemodynamic and physiologic analyses were performed to define the hemodynamic forces and histologic adaptations of the wall at times ranging from 1 to 28 days. RESULTS Anastomotic time averaged 12 minutes, with 100% patency of bilateral grafts and unilateral grafts plus no adjunct or delayed fistula. Bilateral VG/DBL resulted in an immediate disparity in wall shear (0.8 ± 0.1 vs. 12.4 ± 1.1 dynes/cm2 , ligated vs. contralateral graft). Grafts exposed to low shear stress responded primarily through enhanced intimal thickening (231 ± 35 µm vs. 36 ± 18, low vs. high shear). High shear stress grafts adapted through enhanced outward remodeling, with a 24% increase in lumen diameter at 28-days (3.0 ± 0.1 vs. 3.7 ± 0.2 mm, low vs. high shear). CONCLUSIONS We have taken advantage of the cuffed anastomotic technique, and combined it with a bilateral VG/DBL model to dissect the impact NOVEL VEIN GRAFT MODEL 3 of hemodynamic forces on vein graft arterialization. This novel model offers a robust, clinically relevant, and statistically powerful small animal model for the evaluation of high and low shear-regulated vein graft remodeling.
This article has been cited by other articles:
|
|
 |
|
  Z. Jiang, M. Tao, K. A. Omalley, D. Wang, C. K. Ozaki, and S. A. Berceli Established neointimal hyperplasia in vein grafts expands via TGF-{beta}-mediated progressive fibrosis Am J Physiol Heart Circ Physiol, October 1, 2009; 297(4): H1200 - H1207. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Z. Jiang, P. Yu, M. Tao, C. Fernandez, C. Ifantides, O. Moloye, G. S. Schultz, C. K. Ozaki, and S. A. Berceli TGF-beta- and CTGF-mediated fibroblast recruitment influences early outward vein graft remodeling Am J Physiol Heart Circ Physiol, July 1, 2007; 293(1): H482 - H488. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Schachner, G. Laufer, and J. Bonatti In vivo (animal) models of vein graft disease. Eur. J. Cardiothorac. Surg., September 1, 2006; 30(3): 451 - 463. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Schachner Pharmacologic inhibition of vein graft neointimal hyperplasia J. Thorac. Cardiovasc. Surg., May 1, 2006; 131(5): 1065 - 1072. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. J. Wang, X. X. Sui, H. F. Simosa, M. K. Jain, D. C. Altieri, and M. S. Conte Regulation of Vein Graft Hyperplasia by Survivin, an Inhibitor of Apoptosis Protein Arterioscler Thromb Vasc Biol, October 1, 2005; 25(10): 2081 - 2087. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. L. Unthank, K. M. Sheridan, and M. C. Dalsing Collateral Growth in the Peripheral Circulation: A Review Vascular and Endovascular Surgery, July 1, 2004; 38(4): 291 - 313. [Abstract] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
