Abstract
Objective: To test the hypothesis that terminal arteriolar remodeling that is stimulated by elevated levels of circumferential wall stress (σθ) 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 (τij) and σθij, a stimulus was provided by dilating the arterioles and raising input pressure. Wall shear stresses and σθij were then recomputed. The diameters of transverse arteriolar segments with σθij greater than a σθ threshold were increased by an amount that was dependent on the original diameter and the difference between σθ and the σθ 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 τij were also performed for comparison.
Results: Arterialization patterns from simulations of σθij 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 τij yielded arterio-venous shunts, which are rarely seen in vivo, but no arcade arterioles.
Conclusion: 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.
SUMMARY
A network model of two consecutive skeletal muscle TA—CV units was used to test the hypothesis that terminal arteriolar growth in response to elevated levels of σθij could give rise to new arcade arterioles. Capillaries experiencing an intraluminal pressure greater than a chosen pressure threshold were arterialized and the diameters of existing arterioles experiencing a σθij greater than a chosen σθ threshold were increased. The network pattern of arterialization produced a new arcade arteriole, whereas simulations in which growth was stimulated by elevated levels of wall shear stress (τij) produced AV shunts only. These results are consistent with the hypothesis that circumferential wall stress (σθij) is a stimulus for terminal arteriolar growth and that arcade arteriole formation is a consequence of terminal arteriolar growth.