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Journal article
Origin of axial prestretch and residual stress in arteries
Biomechanics and modeling in mechanobiology, v 8(6), pp 431-446
01 Dec 2009
PMID: 19123012
Abstract
The structural protein elastin endows large arteries with unique biological functionality and mechanical integrity, hence its disorganization, fragmentation, or degradation can have important consequences on the progression and treatment of vascular diseases. There is, therefore, a need in arterial mechanics to move from materially uniform, phenomenological, constitutive relations for the wall to those that account for separate contributions of the primary structural constituents: elastin, fibrillar collagens, smooth muscle, and amorphous matrix. In this paper, we employ a recently proposed constrained mixture model of the arterial wall and show that prestretched elastin contributes significantly to both the retraction of arteries that is observed upon transection and the opening angle that follows the introduction of a radial cut in an unloaded segment. We also show that the transmural distributions of elastin and collagen, compressive stiffness of collagen, and smooth muscle tone play complementary roles. Axial prestresses and residual stresses in arteries contribute to the homeostatic state of stress in vivo as well as adaptations to perturbed loads, disease, or injury. Understanding better the development of and changes in wall stress due to individual extracellular matrix constituents thus promises to provide considerable clinically important insight into arterial health and disease.
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Details
- Title
- Origin of axial prestretch and residual stress in arteries
- Creators
- L. Cardamone - University of SalernoA. Valentin - Texas A&M Univ, Dept Biomed Engn, College Stn, TX 77843 USAJ. F. Eberth - Texas A&M Univ, Dept Biomed Engn, College Stn, TX 77843 USAJ. D. Humphrey - Texas A&M Univ, Dept Biomed Engn, College Stn, TX 77843 USA
- Publication Details
- Biomechanics and modeling in mechanobiology, v 8(6), pp 431-446
- Publisher
- Springer Nature
- Number of pages
- 16
- Grant note
- R01HL086418 / NATIONAL HEART, LUNG, AND BLOOD INSTITUTE; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Heart Lung & Blood Institute (NHLBI) HL-64372; HL-80415; HL-86418 / NIH; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA
- Resource Type
- Journal article
- Language
- English
- Academic Unit
- School of Biomedical Engineering, Science, and Health Systems
- Web of Science ID
- WOS:000272072100001
- Scopus ID
- 2-s2.0-69849098361
- Other Identifier
- 991021902500904721
InCites Highlights
Data related to this publication, from InCites Benchmarking & Analytics tool:
- Collaboration types
- Domestic collaboration
- International collaboration
- Web of Science research areas
- Biophysics
- Engineering, Biomedical