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The etiology, and hence most effective treatment, of cerebral vasospasm remains unknown, thus this devastating sequela to
subarachnoid hemorrhage continues to be responsible for significant morbidity and mortality. Based on abundant and diverse
clinical and laboratory observations, we hypothesize that vasospasm and its subsequent resolution result from a short-term
chemo-dominated turnover of cells and matrix in evolving vasoconstricted states that produces a narrowed lumen and thicker
wall, which is stiffer and largely unresponsive to exogenous vasodilators, and a subsequent mechano-dominated turnover of
cells and matrix in evolving vasodilated states that restores the vessel toward normal. There is, however, a pressing need
for a mathematical model of arterial growth and remodeling that can guide the design and interpretation of experiments to
test this and competing hypotheses. Toward this end, we present a new biochemomechanical framework that couples a 2-D model
of the evolving geometry, structure, and properties of the affected arterial wall, a 1-D model of the blood flow within the
affected segment, and a 0-D model of the biochemical insult to the segment. We submit that such a framework can capture salient
features of the time-course of vasospasm and its potential resolution, as illustrated numerically in part II of this paper.
Address correspondence to J. D. Humphrey, Department of Biomedical Engineering, Texas A&M University, 337 Zachry Engineering
Center, 3120 TAMU, College Station, TX 77843-3120, USA. Electronic mail: jhumphrey@tamu.edu 相似文献
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