title: Structural remodeling of mouse gracilis artery after chronic alteration in blood supply.
abstract: 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 approximately 7 days was included. The results suggest that delayed stimuli significantly influence the dynamic characteristics of vascular remodeling resulting from reduced blood supply.
authors.affiliation: Biomedical Engineering Program, University of Arizona, Tucson, Arizona 85724-5051, USA.
authors.forename: Gabriel
authors.initials: G
authors.lastname: Gruionu
authors.forename: James B
authors.initials: JB
authors.lastname: Hoying
authors.forename: Axel R
authors.initials: AR
authors.lastname: Pries
authors.forename: Timothy W
authors.initials: TW
authors.lastname: Secomb
mesh_terms: D000222:Adaptation, Physiological / Q000502:physiology*; D000818:Animals; D001158:Arteries / Q000502:physiology*; D006614:Hindlimb / Q000098:blood supply; D007511:Ischemia / Q000503:physiopathology*; D008026:Ligation; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D008955:Models, Cardiovascular; D018482:Muscle, Skeletal / Q000098:blood supply*; D012039:Regional Blood Flow / Q000502:physiology; D014664:Vasodilation / Q000502:physiology