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Intimal and medial contributions to the hydraulic resistance of the arterial wall at different pressures: a combined computational and experimental study
The hydraulic resistances of the intima and media determine water flux and the advection of macromolecules into and across the arterial wall. Despite several experimental and computational studies, these transport processes and their dependence on transmural pressure remain incompletely understood....
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Royal Society
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4938088/ https://www.ncbi.nlm.nih.gov/pubmed/27307514 http://dx.doi.org/10.1098/rsif.2016.0234 |
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author | Chooi, K. Y. Comerford, A. Sherwin, S. J. Weinberg, P. D. |
author_facet | Chooi, K. Y. Comerford, A. Sherwin, S. J. Weinberg, P. D. |
author_sort | Chooi, K. Y. |
collection | PubMed |
description | The hydraulic resistances of the intima and media determine water flux and the advection of macromolecules into and across the arterial wall. Despite several experimental and computational studies, these transport processes and their dependence on transmural pressure remain incompletely understood. Here, we use a combination of experimental and computational methods to ascertain how the hydraulic permeability of the rat abdominal aorta depends on these two layers and how it is affected by structural rearrangement of the media under pressure. Ex vivo experiments determined the conductance of the whole wall, the thickness of the media and the geometry of medial smooth muscle cells (SMCs) and extracellular matrix (ECM). Numerical methods were used to compute water flux through the media. Intimal values were obtained by subtraction. A mechanism was identified that modulates pressure-induced changes in medial transport properties: compaction of the ECM leading to spatial reorganization of SMCs. This is summarized in an empirical constitutive law for permeability and volumetric strain. It led to the physiologically interesting observation that, as a consequence of the changes in medial microstructure, the relative contributions of the intima and media to the hydraulic resistance of the wall depend on the applied pressure; medial resistance dominated at pressures above approximately 93 mmHg in this vessel. |
format | Online Article Text |
id | pubmed-4938088 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | The Royal Society |
record_format | MEDLINE/PubMed |
spelling | pubmed-49380882016-07-15 Intimal and medial contributions to the hydraulic resistance of the arterial wall at different pressures: a combined computational and experimental study Chooi, K. Y. Comerford, A. Sherwin, S. J. Weinberg, P. D. J R Soc Interface Life Sciences–Engineering interface The hydraulic resistances of the intima and media determine water flux and the advection of macromolecules into and across the arterial wall. Despite several experimental and computational studies, these transport processes and their dependence on transmural pressure remain incompletely understood. Here, we use a combination of experimental and computational methods to ascertain how the hydraulic permeability of the rat abdominal aorta depends on these two layers and how it is affected by structural rearrangement of the media under pressure. Ex vivo experiments determined the conductance of the whole wall, the thickness of the media and the geometry of medial smooth muscle cells (SMCs) and extracellular matrix (ECM). Numerical methods were used to compute water flux through the media. Intimal values were obtained by subtraction. A mechanism was identified that modulates pressure-induced changes in medial transport properties: compaction of the ECM leading to spatial reorganization of SMCs. This is summarized in an empirical constitutive law for permeability and volumetric strain. It led to the physiologically interesting observation that, as a consequence of the changes in medial microstructure, the relative contributions of the intima and media to the hydraulic resistance of the wall depend on the applied pressure; medial resistance dominated at pressures above approximately 93 mmHg in this vessel. The Royal Society 2016-06 /pmc/articles/PMC4938088/ /pubmed/27307514 http://dx.doi.org/10.1098/rsif.2016.0234 Text en © 2016 The Authors. http://creativecommons.org/licenses/by/4.0/ Published by the Royal Society under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/4.0/, which permits unrestricted use, provided the original author and source are credited. |
spellingShingle | Life Sciences–Engineering interface Chooi, K. Y. Comerford, A. Sherwin, S. J. Weinberg, P. D. Intimal and medial contributions to the hydraulic resistance of the arterial wall at different pressures: a combined computational and experimental study |
title | Intimal and medial contributions to the hydraulic resistance of the arterial wall at different pressures: a combined computational and experimental study |
title_full | Intimal and medial contributions to the hydraulic resistance of the arterial wall at different pressures: a combined computational and experimental study |
title_fullStr | Intimal and medial contributions to the hydraulic resistance of the arterial wall at different pressures: a combined computational and experimental study |
title_full_unstemmed | Intimal and medial contributions to the hydraulic resistance of the arterial wall at different pressures: a combined computational and experimental study |
title_short | Intimal and medial contributions to the hydraulic resistance of the arterial wall at different pressures: a combined computational and experimental study |
title_sort | intimal and medial contributions to the hydraulic resistance of the arterial wall at different pressures: a combined computational and experimental study |
topic | Life Sciences–Engineering interface |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4938088/ https://www.ncbi.nlm.nih.gov/pubmed/27307514 http://dx.doi.org/10.1098/rsif.2016.0234 |
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