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This Article Full Text Full Text (PDF) All Versions of this Article: 295/4/H1562    most recent 00261.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Google Scholar Articles by Arciero, J. C. Articles by Secomb, T. W. PubMed PubMed Citation Articles by Arciero, J. C. Articles by Secomb, T. W.

Theoretical model of metabolic blood flow regulation: roles of ATP release by red blood cells and conducted responses

¹Program in Applied Mathematics, University of Arizona, Tucson, Arizona; ²Biotechnology and Bioengineering Center, Medical College of Wisconsin, Milwaukee, Wisconsin; and ³Department of Physiology, University of Arizona, Tucson, Arizona

Submitted 11 March 2008 ; accepted in final form 6 August 2008

A proposed mechanism for metabolic flow regulation involves the saturation-dependent release of ATP by red blood cells, which triggers an upstream conducted response signal and arteriolar vasodilation. To analyze this mechanism, a theoretical model is used to simulate the variation of oxygen and ATP levels along a flow pathway of seven representative segments, including two vasoactive arteriolar segments. The conducted response signal is defined by integrating the ATP concentration along the vascular pathway, assuming exponential decay of the signal in the upstream direction with a length constant of 1 cm. Arteriolar tone depends on the conducted metabolic signal and on local wall shear stress and wall tension. Arteriolar diameters are calculated based on vascular smooth muscle mechanics. The model predicts that conducted responses stimulated by ATP release in venules and propagated to arterioles can account for increases in perfusion in response to increased oxygen demand that are consistent with experimental findings at low to moderate oxygen consumption rates. Myogenic and shear-dependent responses are found to act in opposition to this mechanism of metabolic flow regulation.

microcirculation; myogenic response; shear-dependent response

This article has been cited by other articles:

				B. E. Carlson, J. C. Arciero, and T. W. Secomb Theoretical model of blood flow autoregulation: roles of myogenic, shear-dependent, and metabolic responses Am J Physiol Heart Circ Physiol, October 1, 2008; 295(4): H1572 - H1579. [Abstract] [Full Text] [PDF]