Monday, 11 October 2004 - 9:40 AM

This presentation is part of : Rajagopal Symposium

Biomechanics of Arterial Growth and Remodeling

Jay D Humphrey and Rudy Gleason. Texas A&M University, Department of Biomedical Engineering, College Station, TX 77843-3120

Research over the last three decades has revealed a ubiquitous cell-mediated growth and remodeling in arterial development, adaptation, and response to disease/injury, and demonstrated that these processes are controlled in large part by mechanical stimuli. Although the response of an artery to disease/injury versus perturbed blood pressures, flows, and axial loads may be manifested differently, the basic underlying processes appear to be the same. Arterial adaptation results from changes in cellular activity that include changes in the rates of mitosis (cell division) or apoptosis (programmed cell death), rates of cell migration and differentiation (change of phenotype), hypertrophy and atrophy, and rates of synthesis, degradation, or cross-linking of extracellular matrix. Overall, therefore, what appears to be most important mechanically are the separate rates of turnover of individual constituents and the configurations in which such turnover occurs. The goal of this work is to formulate a simple theoretical framework to model basic features of the biomechanics of arterial growth and remodeling. The framework is motivated by the hypothesis that growth and remodeling occurs via the heightened replacement of previously existing constituents with new constituents that have new ‘natural configurations’ but otherwise similar mechanical properties.

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