A circumferential stress-growth rule predicts arcade arteriole formation in a network model.
OBJECTIVE
To test the hypothesis that terminal arteriolar remodeling that is stimulated by elevated levels of circumferential wall stress (sigma theta) will proceed in a network pattern that gives rise to new arcade arterioles.


METHODS
A network model of two interconnected skeletal muscle arterio-capillary-venous units that incorporated diameter- and hematocrit-dependent blood viscosity was constructed. After computing the control values for wall shear stresses (tau ij) and sigma theta ij, a stimulus was provided by dilating the arterioles and raising input pressure. Wall shear stresses and sigma theta ij were then recomputed. The diameters of transverse arteriolar segments with sigma theta ij greater than a sigma theta threshold were increased by an amount that was dependent on the original diameter and the difference between sigma theta ij and the sigma theta threshold. Capillaries with an intraluminal pressure greater than a specified threshold were converted to terminal arterioles. Separate simulations in which remodeling was stimulated by elevated levels of tau ij were also performed for comparison.


RESULTS
Arterialization patterns from simulations of sigma theta ij stimulated arteriolar remodeling were representative of those seen in vivo with arterialization of back-connection capillaries leading to arcade arteriole formation. Simulations based on similar rules for tau ij yielded arterio-venous shunts, which are rarely seen in vivo, but no arcade arterioles.


CONCLUSIONS
The simulations presented here are consistent with the hypothesis that arteriolar remodeling is stimulated by increased levels of circumferential wall stress and that new arcade arteriole formation is a consequence of terminal arteriolar growth.
Price
R J
RJ
Department of Biomedical Engineering, University of Virginia, Charlottesville 22908, USA.
Skalak
T C
TC
D000818:Animals; D001160:Arterioles / Q000648:ultrastructure*; D006439:Hemodynamics / Q000502:physiology*; D008955:Models, Cardiovascular; D018482:Muscle, Skeletal / Q000098:blood supply*; D018919:Neovascularization, Physiologic; D051381:Rats; D013314:Stress, Mechanical; D014699:Venules / Q000648:ultrastructure