Arterial wall morphology depends strongly on the hemodynamic environment experienced in vivo. The mammalian heart pumps blood through rhythmic contractions forcing blood vessels to undergo cyclic, mechanical stimulation in the form of pulsatile blood pressure and flow. While it has been shown that stepwise, chronic increases in blood pressure and flow modify arterial wall thickness and diameter respectively, few studies on arterial remodeling have examined the influences that pulsatility (i.e., the range of cyclic stimuli) may have on biaxial wall morphology. We experimentally studied the biaxial behavior of carotid arteries from 8 control (CCA), 15 transgenic, and 21 mechanically altered mice using a custom designed mechanical testing device and correlated those results with hemodynamic measurements using pulsed Doppler. In this dissertation, we establish that increased pulsatile stimulation in the right carotid artery after banding (RCCA-B) has a strong affect on wall morphological parameters that peak at 2 weeks and include thickness (CCA=24.8±0.878, RCCA-B=99.0±8.43 μ m), inner diameter (CCA=530±7.36, RCCA-B=680±32.0μ m), and in vivo axial stretch (CCA=1.7±0.029, RCCAB= 1.19±0.067). These modifications entail stress and the change in stress across the cardiac cycle from an arterial wall macro-structural point of view (i.e., cellular and extracellular matrix) citing increases in collagen mass fraction (CCA=0.223±0.056, RCCA-B=0.314±0.011), collagen to elastin ratio (CCA=0.708±0.152, RCCA-B=1.487±0.26), and cross-sectional cellular nuclei counts (CCA=298±58.9, RCCA-B=578±28.3 cells) at 0, 7, 10, 14, and 42 post-banding surgery. Furthermore, we study the biomechanical properties of carotid arteries from a transgenic mouse of Marfan Syndrome. This arterial disease experiences increased pulse transmission and our findings indicate that alterations occur primarily in the axial direction. The above results are all applied to a predictive biaxial model of Cauchy stress vs. strain.

The purpose of this manuscript is to establish a unified theory of porohyperelasticity with transport and growth and to demonstrate the capability of this theory using a finite element model developed in MATLAB. We combine the theories of volumetric growth and mixed porohyperelasticity with transport and swelling (MPHETS) to derive a new method that models growth of biological soft tissues. The conservation equations and constitutive equations are developed for both solid-only growth and solid/fluid growth. An axisymmetric finite element framework is introduced for the new theory of growing MPHETS (GMPHETS). To illustrate the capabilities of this model, several example finite element test problems are considered using model geometry and material parameters based on experimental data from a porcine coronary artery. Multiple growth laws are considered, including time-driven, concentrationdriven, and stress-driven growth. Time-driven growth is compared against an exact analytical solution to validate the model. For concentration-dependent growth, changing the diffusivity (representing a change in drug) fundamentally changes growth behavior. We further demonstrate that for stress-dependent, solid-only growth of an artery, growth of an MPHETS model results in a more uniform hoop stress than growth in a hyperelastic model for the same amount of growth time using the same growth law. This may have implications in the context of developing residual stresses in soft tissues under intraluminal pressure. To our knowledge, this manuscript provides the first full description of an MPHETS model with growth. The developed computational framework can be used in concert with novel in-vitro and in-vivo experimental approaches to identify the governing growth laws for various soft tissues.