title: Effects of a sustained extension on arterial growth and remodeling: a theoretical study.
abstract: Three recent studies reveal that the unloaded length of a carotid artery increases significantly and rapidly in response to sustained increases in axial extension. Moreover, such lengthening involves an "unprecedented" increase in the rate of turnover of cells and matrix. Although current data are not sufficient for detailed biomechanical analyses, we present general numerical simulations that are consistent with the reported observations and support the hypothesis that rates of turnover correlate with the extent that stresses are perturbed from normal. In particular, a 3-D analysis of wall stress suggests that moderate (15%) increases in axial extension can increase the axial stress to a much greater extent than marked (50%) increases in blood pressure increase the circumferential stress. Furthermore, such increases in axial stress can occur without inducing significant gradients in stress within the wall. Consequently, we use a new, 2-D constrained mixture model to study evolving changes in the geometry, structure, and properties of carotid arteries in response to a sustained increase in axial extension. These simulations are qualitatively similar to the reports in the literature and support the notion that the stress-free lengths of individual constituents evolve during growth and remodeling.
authors.affiliation: Department of Biomedical Engineering, M.E. DeBakey Institute, Texas A&M University, 233 Zachry Engineering Center, College Station, TX 77843-3120, USA.
authors.forename: R L
authors.initials: RL
authors.lastname: Gleason
authors.forename: J D
authors.initials: JD
authors.lastname: Humphrey
mesh_terms: D000222:Adaptation, Physiological / Q000502:physiology; D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D002339:Carotid Arteries / Q000254:growth & development* / Q000502:physiology*; D003198:Computer Simulation; D004548:Elasticity; D005109:Extracellular Matrix / Q000502:physiology*; D006801:Humans; D040542:Mechanotransduction, Cellular / Q000502:physiology*; D008955:Models, Cardiovascular; D009131:Muscle, Smooth, Vascular / Q000503:physiopathology*; D010812:Physical Stimulation / Q000379:methods; D013314:Stress, Mechanical