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Am J Physiol Heart Circ Physiol 288: H2047-H2054, 2005. First published December 16, 2004; doi:10.1152/ajpheart.00496.2004
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Structural remodeling of mouse gracilis artery after chronic alteration in blood supply

Gabriel Gruionu,1,2 James B. Hoying,1,2,4 Axel R. Pries,3 and Timothy W. Secomb1,4

1Biomedical Engineering Program, 2Vascular Research Group, University of Arizona, Tucson, Arizona; 3Department of Physiology, Charité-Universitätsmedizin Berlin, Campus Benjamin Franklin, Berlin, Germany; and 4Department of Physiology, University of Arizona, Tucson, Arizona

Submitted 7 June 2004 ; accepted in final form 9 December 2004

The goals of this study were to determine the time course and spatial dependence of structural diameter changes in the mouse gracilis artery after a redistribution of blood flow and to compare the observations with predictions of computational models for structural adaptation. Diameters were measured 1, 2, 7, 14, 21, 28, and 56 days after resection of one of the two blood supplies to the artery. Overall average diameter, normalized with respect to diameters in untreated vessels, increased slightly during the first 7 days, then increased more rapidly, reaching a peak around day 21, and then decreased. This transient increase in diameter was spatially nonuniform, being largest toward the point of resection. A previously developed theoretical model, in which diameter varies in response to stimuli derived from local metabolic and hemodynamic conditions, was extended to include effects of time-delayed remodeling stimuli in regions of reduced perfusion. Predictions of this model were consistent with observed diameter changes, including the transient increase in diameters near the point of resection, when a remodeling stimulus with a time delay of ~7 days was included. The results suggest that delayed stimuli significantly influence the dynamic characteristics of vascular remodeling resulting from reduced blood supply.

metabolic response; shear stress; vessel wall conduction; adaptation; computational model



Address for reprint requests and other correspondence: T. W. Secomb, Dept. of Physiology, Univ. of Arizona, Tucson, AZ 85724-5051 (E-mail: secomb{at}u.arizona.edu)




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