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ISSN: 2168-9873

Journal of Applied Mechanical Engineering
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Research Article

Strain-Induced Tissue Growth Laws: Applications to Embryonic Cardiovascular Development

Sandra Rugonyi*
Oregon Health & Science University, Biomedical Engineering, 3303 SW Bond Ave, Mail Code: CH13B, Portland, USA
Corresponding Author : Sandra Rugonyi
Associate Professor, Oregon Health & Science University
Biomedical Engineering, 3303 SW Bond Ave
Mail Code: CH13B, Portland, USA
E-mail: [email protected]
Received January 28, 2013; Accepted February 21, 2013; Published February 28, 2013
Citation: Rugonyi S (2013) Strain-Induced Tissue Growth Laws: Applications to Embryonic Cardiovascular Development. J Appl Mech Eng S11:001 doi:10.4172/2168-9873.S11-001
Copyright: © 2013 Rugonyi S. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

      leading to growth and remodeling of cardiovascular walls. During embryonic development, altered hemodynamic conditions lead to congenital heart disease, which affects about 1% of newborn babies in developed countries. However, the mechanisms by which hemodynamic conditions affect cardiovascular development have not been fully elucidated. In this paper, we propose a model of cardiac growth in response to hemodynamic conditions, in which growth is modulated by a combination of wall strains and wall shear stresses. This is in contrast to previous models that proposed stress-induced growth laws. Because during embryonic development blood pressure increases over time, and this increase in blood pressure produces an increase in wall stresses, stress-induced growth laws would require time-dependent parameters. Instead, we postulate that strains experienced by cells remain approximately the same during development. This assumption motivated our cardioavascular model of strain-induced growth in response to hemodynamic conditions, which we implemented using finite element methods. Model simulations show that the proposed model results in tissue growth that is physiologically reasonable. Further, our analyses demonstrate that mechanical coupling–that results from residual stresses originating from differential tissue growth -may play a more important role in the modulation of cardiovascular tissue growth and remodeling than currently.    

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