Functional sympatholysis and sympathetic escape in a theoretical model for blood flow regulation

Abstract

A mathematical simulation of flow regulation in vascular networks is used to investigate the interaction between arteriolar vasoconstriction due to sympathetic nerve activity (SNA) and vasodilation due to increased oxygen demand. A network with 13 vessel segments in series is used, each segment representing a different size range of arterioles or venules. The network includes five actively regulating arteriolar segments with time-dependent 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. The model exhibits functional sympatholysis, in which sympathetic vasoconstriction is partially abrogated by increases in metabolic demand, and sympathetic escape, in which SNA elicits an initial vasoconstriction followed by vasodilation. In accordance with experimental observations, these phenomena are more prominent in small arterioles than in larger arterioles when SNA is assumed to act equally on arterioles of all sizes. The results imply that a mechanism based on the competing effects on arteriolar tone of SNA and conducted metabolic signals can account for several observed characteristics of functional sympatholysis, including the different responses of large and small arterioles.

Regulation of Increased Blood Flow (Hyperemia) to Muscles During Exercise: A Hierarchy of Competing Physiological Needs

“…Consistent with this hypothesis, it is interesting to note that infusions of vasodilating substances into the limbs of humans performing heavy exercise do not improve oxygen consumption. In fact, vasodilator infusions during heavy exercise seem to disrupt the matching of blood flow and metabolism that might result from the interactions of metabolic vasodilation and sympathetic vasoconstriction described above (69,288,401). Our interpretation of these observations is that when total limb flow is already very high and parts of the muscle are maximally dilated, infusions of exogenous vasodilators would dilate regions with little demand for oxygen and blood flow.…”

The Gastrointestinal Circulation: Physiology and Pathophysiology

“…Moreover, autoregulatory escape is attenuated by blockade of adenosine bioavailability (103). Finally, a computer modeling approach predicts that vasodilatory mechanisms linked to O 2 utilization would override sympathetic-mediated vasoconstriction and that smaller resistance arteries would be more prone to metabolic override than upstream arteries (411).…”

Radial artery spasm: Should we worry?

“…18 Il est intéressant de noter que le SAR ne semble pas être contre-régulé par un échappement sympathique, une sympatholyse fonctionnelle que l'on peut observer dans différents réseaux vasculaires au cours d'une stimulation sympathique prolongée. 19 Bien que le bloc du nerf radial, tel que décrit par Bhakta et Zaheer, 1 constitue une solution relativement simple au SAR liée au cathétérisme radial, un traitement efficace peut également être obtenu par l'injection intra-artérielle de vasodilatateurs. 20 …”

“…18 Of interest, RAS does not seem to be counter-regulated by sympathetic escape -a functional sympatholysis that may be observed in a variety of vascular networks during prolonged sympathetic stimulation. 19 Although radial nerve blockade, as described by Bhakta and Zaheer, 1 is a relatively simple solution to arterial linerelated RAS, an effective treatment may also be achieved with intra-arterial injection of vasodilators. 20 Not surprisingly, neither of these strategies has been subjected to rigorous scientific scrutiny as to their effectiveness, duration of action, etc.…”