Abstract
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 1.52×10-9, 1.01×10-8, and 1.07×10-8 mm4/μN.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.