4.5 Article

A multiphasic model for determination of water and solute transport across the arterial wall: effects of elastic fiber defects

期刊

ARCHIVE OF APPLIED MECHANICS
卷 92, 期 2, 页码 447-459

出版社

SPRINGER
DOI: 10.1007/s00419-021-01985-3

关键词

Biphasic; Febio; Permeation; Dextran; Mouse model; Elastin; Elastase; Finite element

资金

  1. American Heart Association [19TPA-34910047]
  2. National Institute of Arthritis and Musculoskeletal and Skin Diseases of the NIH [R01AR070975]
  3. NIH
  4. Washington University School of Medicine
  5. Children's Discovery Institute of Washington University, St. Louis Children's Hospital [CDI-CORE-2015-505, CDI-CORE-2019-813]
  6. Foundation for Barnes-Jewish Hospital [3770, 4642]

向作者/读者索取更多资源

Transport of solute across the arterial wall is influenced by convection, diffusion, and disruption of elastic fibers. A computational mixture model was used to study these changes, with results showing that elastic fiber structure affects the transport of lower molecular weight solutes.
Transport of solute across the arterial wall is a process driven by both convection and diffusion. In disease, the elastic fibers in the arterial wall are disrupted and lead to altered fluid and mass transport kinetics. A computational mixture model was used to numerically match previously published data of fluid and solute permeation experiments in groups of mouse arteries with genetic (knockout of fibulin-5) or chemical (treatment with elastase) disruption of elastic fibers. A biphasic model of fluid permeation indicated the governing property to be the hydraulic permeability, which was estimated to be 1.52 x 10(-9), 1.01 x 10(-8), and 1.07 x 10(-8) mm(4)/mu N.s for control, knockout, and elastase groups, respectively. A multiphasic model incorporating solute transport was used to estimate effective diffusivities that were dependent on molecular weight, consistent with expected transport behaviors in multiphasic biological tissues. The effective diffusivity for the 4 kDA FITC-dextran solute, but not the 70 or 150 kDa FITC-dextran solutes, was dependent on elastic fiber structure, with increasing values from control to knockout to elastase groups, suggesting that elastic fiber disruption affects transport of lower molecular weight solutes. The model used here sets the groundwork for future work investigating transport through the arterial wall.

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