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Sympathetic escape in a theoretical model of microvascular flow regulation (1079.18)

A mathematical simulation of flow regulation is used to investigate the hypothesis that vasoconstriction due to sympathetic nerve activity (SNA) in smaller arterioles is inhibited by functional vasodilation at higher values of oxygen demand, termed functional sympatholysis. A network with 13 vessel compartments in series is used, each compartment representing different size ranges of arterioles and venules. The model includes 5 actively regulating arteriolar segments with diameters influenced by shear stress, wall tension, metabolic regulation, and SNA. Metabolic signals are assumed to be propagated upstream along vessel walls via a conducted response. We show that for appropriately chosen parameter values, the vasoconstriction due to SNA in feed arterioles overcomes metabolic vasodilation at higher oxygen demand, resulting in persistent vasoconstriction throughout the period of SNA. In smaller arterioles under similar conditions, however, the initial vasoconstriction with SNA is followed by partial relaxation, consistent with the experimentally observed phenomenon of sympathetic escape. This implies that metabolic responses can account for observed characteristics of functional sympatholysis, including the different responses of large and small arterioles.