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Pulmonary hypertension is a cardiovascular disorder manifested by elevatedarterial blood pressure together with vessel wall stiffening and thickening dueto alterations in collagen, elastin and smooth muscle cells. Hypoxia-induced(type 3) pulmonary hypertension can be studied in animals exposed to a lowoxygen environment for prolonged time periods leading to biomechanicalalterations in vessel wall structure. This study formulates and systematicallyreduces a nonlinear elastic structural wall model for a large pulmonary artery,generating a novel pressure-area relation capturing remodeling in type 3pulmonary hypertension. The model is calibrated using {\em ex vivo}measurements of vessel diameter and wall thickness changes, under controlledflow conditions, in left pulmonary arteries isolated from control andhypertensive mice. A two-layer, hyperelastic, anisotropic model incorporatingresidual stresses is formulated using the Holzapfel-Gasser-Ogden model. Complexrelations predicting vessel area and wall thickness with increasing bloodpressure are derived and calibrated using the data. Sensitivity analysis,parameter estimation and subset selection are used to systematically reduce the16-parameter model to one in which a much smaller subset of identifiableparameters is estimated via solution of an inverse problem. Our final reducedmodel includes a single set of three elastic moduli. Estimated ranges of theseparameters demonstrate that nonlinear stiffening is dominated by elastin in thecontrol animals and by collagen in the hypertensive group. The novelpressure-area relation developed in this study has potential impact onone-dimensional fluids network models of vessel wall remodeling in the presenceof cardiovascular disease.

Application and reduction of a nonlinear hyperelastic wall model  capturing ex vivo relationships between fluid pressure, area and wall  thickness in normal and hypertensive murine left pulmonary arteries