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.

溶质跨动脉壁的运输是由对流和扩散驱动的过程。在疾病中，动脉壁中的弹性纤维被破坏并导致流体和质量输送动力学改变。使用计算混合模型在数值上匹配先前发表的具有弹性纤维遗传（敲除fibulin-5）或化学（用弹性蛋白酶处理）破坏的小鼠动脉组中的流体和溶质渗透实验的数据。流体渗透的双相模型表明控制特性是水力渗透率，估计为 1.52 × 10 ^–9、1.01 × 10 ^–8和 1.07 × 10 ^–8 mm ⁴/µN.s 分别用于对照、敲除和弹性蛋白酶组。结合溶质转运的多相模型用于估计依赖于分子量的有效扩散率，这与多相生物组织中的预期转运行为一致。4 kDA FITC-葡聚糖溶质而不是 70 或 150 kDa FITC-葡聚糖溶质的有效扩散率取决于弹性纤维结构，从对照到敲除再到弹性蛋白酶组的值增加，这表明弹性纤维破坏会影响分子量较低的溶质。这里使用的模型为未来研究通过动脉壁的运输奠定了基础。