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Right Ventricular Dysfunction in Pulmonary Arterial Hypertension: Cellular and Hemodynamic Changes in a Mouse Model

[+] Author Affiliations
Zhijie Wang, Jitandrakumar R. Patel, David A. Schreier, Richard Moss, Timothy A. Hacker, Naomi C. Chesler

University of Wisconsin – Madison, Madison, WI

Paper No. SBC2013-14687, pp. V01AT11A004; 2 pages
doi:10.1115/SBC2013-14687
From:
  • ASME 2013 Summer Bioengineering Conference
  • Volume 1A: Abdominal Aortic Aneurysms; Active and Reactive Soft Matter; Atherosclerosis; BioFluid Mechanics; Education; Biotransport Phenomena; Bone, Joint and Spine Mechanics; Brain Injury; Cardiac Mechanics; Cardiovascular Devices, Fluids and Imaging; Cartilage and Disc Mechanics; Cell and Tissue Engineering; Cerebral Aneurysms; Computational Biofluid Dynamics; Device Design, Human Dynamics, and Rehabilitation; Drug Delivery and Disease Treatment; Engineered Cellular Environments
  • Sunriver, Oregon, USA, June 26–29, 2013
  • Conference Sponsors: Bioengineering Division
  • ISBN: 978-0-7918-5560-7
  • Copyright © 2013 by ASME

abstract

Pulmonary arterial hypertension (PAH) is the most severe form of pulmonary hypertension due to its rapid progression to right ventricular (RV) failure. Until the recent combination of chronic hypoxia with VEGF receptor blockage by SU5416 [1], there was no mouse model for severe PAH. This new model (HySu) recapitulates hallmarks of human PAH, especially distal arteriolar neointima formation and obliteration [1]. However, the changes in RV function in this model have not been examined. Here we investigate the hypothesis that the HySu mouse model mimics the progression of RV dysfunction found in PAH clinically from compensatory to maladaptive RV remodeling.

Copyright © 2013 by ASME
Topics: Hemodynamics , Failure

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