Theoretical model of blood flow autoregulation: roles of myogenic, shear-dependent, and metabolic responses

Abstract

Carlson BE, Arciero JC, Secomb TW. Theoretical model of blood flow autoregulation: roles of myogenic, shear-dependent, and metabolic responses. Am J Physiol Heart Circ Physiol 295: H1572-H1579, 2008. First published August 22, 2008; doi:10.1152/ajpheart.00262.2008The autoregulation of blood flow, the maintenance of almost constant blood flow in the face of variations in arterial pressure, is characteristic of many tissue types. Here, contributions to the autoregulation of pressure-dependent, shear stress-dependent, and metabolic vasoactive responses are analyzed using a theoretical model. Seven segments, connected in series, represent classes of vessels: arteries, large arterioles, small arterioles, capillaries, small venules, large venules, and veins. The large and small arterioles respond actively to local changes in pressure and wall shear stress and to the downstream metabolic state communicated via conducted responses. All other segments are considered fixed resistances. The myogenic, shear-dependent, and metabolic responses of the arteriolar segments are represented by a theoretical model based on experimental data from isolated vessels. To assess autoregulation, the predicted flow at an arterial pressure of 130 mmHg is compared with that at 80 mmHg. If the degree of vascular smooth muscle activation is held constant at 0.5, there is a fivefold increase in blood flow. When myogenic variation of tone is included, flow increases by a factor of 1.66 over the same pressure range, indicating weak autoregulation. The inclusion of both myogenic and shear-dependent responses results in an increase in flow by a factor of 2.43. A further addition of the metabolic response produces strong autoregulation with flow increasing by a factor of 1.18 and gives results consistent with experimental observation. The model results indicate that the combined effects of myogenic and metabolic regulation overcome the vasodilatory effect of the shear response and lead to the autoregulation of blood flow. conducted response; microcirculation; blood flow regulation; vascular smooth muscle; vascular tone THE ABILITY OF VASCULAR BEDS to maintain a relatively constant blood flow over a large range of arterial pressures is known as vascular autoregulation. With increasing arterial pressure, the degree of vascular smooth muscle (VSM) activation, VSM tone, increases in arterioles, resulting in decreased vessel diameter and increased flow resistance. Several mechanisms contribute to changes in vascular tone, including responses to intraluminal pressure (myogenic response), shear stress on the endothelial lining of vessels (shear-dependent response), metabolite concentrations in vessels and/or tissue (metabolic response), and neural stimuli. The cerebral and renal vasculature show the most stable flow over a wide range of arterial pressures (2, 25), whereas in other beds, such as those in the mesentery, autoregulation is less effective.Several theoretical models for the autoregulation of blood flow have been developed using a multicompartmen...

Spontaneous oscillations in a model for active control of microvessel diameters

“…The present study is based on a previous theoretical model for the regulation of blood flow in the circulation Carlson et al, 2008) in which the degree of activation (tone) of smooth muscle is assumed to depend on responses to several factors. An increase in intravascular pressure, and thus wall tension, results in arteriolar constriction (myogenic response).…”

“…The theoretical model is based on a description of the length-tension characteristics of vessel walls containing VSM Carlson et al, 2008;Carlson & Secomb, 2005). Tension, T total , generated in the wall is represented as the sum of a passive component, T pass , and an active component, expressed as the product of the maximal active tension generated by the VSM cells, T max act , and the degree of VSM activation or tone, A:…”

“…As defined in Carlson & Secomb (2005) and Carlson et al (2008), the passive tension is assumed to be an exponential function of diameter since tension increases rapidly with increasing circumferential stretch. D 0 is the passive diameter of the vessel at an intraluminal pressure of 100 mmHg (13.33 kPa), C pass is the passive tension at D 0 and C pass determines the steepness of the curve and was fit to experimental data.…”

“…The parameter values in (2.6) were fit to pressure and flow data as described in Arciero et al (2008), Carlson et al (2008), and the numerical values are restated in Table 1. Under non-steady conditions, the activation A is assumed to approach A total according to a first-order equation with a time constant τ a , which reflects the dynamics of force generation within the VSM:…”

Passive Pressure–Diameter Relationship and Structural Composition of Rat Mesenteric Lymphangions

“…Numerous models have been developed for arterial microcirculatory networks and the roles of myogenic, shear, and metabolic responses in the autoregulation of blood flow. [12][13][14] However, none of these models have been adapted to describe the regulation of lymph flow.…”