Contributions of pressure and flow sensitivity to autoregulation in mesenteric arterioles

Pc, Johnson; Intaglietta, Marcos

doi:10.1152/ajplegacy.1976.231.6.1686

Cited by 113 publications

(39 citation statements)

References 2 publications

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“…The contribution of the metabolic response to autoregulation has not been previously evaluated. Including the metabolic response with both the myogenic and shear-dependent responses produces a level of autoregulation close to that which is observed in cerebral (7,12,21), mesenteric (14), and renal (30,31) tissue. The current model shows that the combined effects of the myogenic and metabolic responses are necessary and sufficient to generate autoregulatory behavior, despite the contrary effect of the shear-dependent response.…”

Section: Discussionmentioning

confidence: 57%

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

Carlson¹,

Arciero²,

Secomb³

2008

American Journal of Physiology-Heart and Circulatory Physiology

146

160

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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...

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Section: Discussionmentioning

confidence: 57%

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

Carlson¹,

Arciero²,

Secomb³

2008

American Journal of Physiology-Heart and Circulatory Physiology

146

160

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“…Because detailed descriptions of both systems used in this study have been presented previously (20,43), only brief descriptions are given here.…”

Section: System Descriptionmentioning

confidence: 99%

“…In both sets of studies arterial pressure was recorded in the left femoral artery via a catheter that led to a model TNF-R Viggo Spectramed pressure transducer connected to a strip-chart recorder (Gould, 3400). RBC velocity measurements utilized a dual-slit RBC velocity-video microscope system described previously (20). In the present studies a Leitz UM ϫ10 objective (numerical aperture ϭ 0.32) was used.…”

Section: System Descriptionmentioning

confidence: 99%

Contribution of anaerobic metabolism to reactive hyperemia in skeletal muscle

Tóth

Pál

Intaglietta

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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Tó th A, Pal M, Intaglietta M, Johnson PC. Contribution of anaerobic metabolism to reactive hyperemia in skeletal muscle. Am J Physiol Heart Circ Physiol 292: H2643-H2653, 2007. First published February 16, 2007 doi:10.1152/ajpheart.00207.2006.-Elevated blood flow (reactive hyperemia) is seen in many organs after a period of blood flow stoppage. This hyperemia is often considered to be due in part to a shift to anaerobic metabolism during tissue hypoxia. The aim of our study was to test this hypothesis in skeletal muscle. For this purpose we measured NADH fluorescence at localized tissue areas in cat sartorius muscle during and after arterial occlusions of 5-300 s. In parallel studies, red blood cell (RBC) velocity was measured in venules. Tissue NADH fluorescence rose significantly with occlusions of 45 s or greater, reaching a maximum of 44% above control at 180 s. Peak RBC velocity rose to four times control as occlusion duration was increased from 5 to 45 s, but hyperemia duration was stable at ϳ70 s. With occlusions of 45-240 s, hyperemia duration increased progressively to 210 s while peak flow was unchanged. However, after 300-s occlusions, peak flow rose to six times above control and hyperemia duration fell to 140 s. With occlusions of 45-300 s the time integral both of increased NADH fluorescence and of reduced fluorescence following occlusion release showed a high degree of correlation with the additional hyperemia. We conclude that in this muscle anaerobic vasodilator metabolites are responsible for the increase in reactive hyperemia with arterial occlusions longer than 45 s. Since the durations of reactive hyperemia and reduced fluorescence are substantially different, vasodilator metabolite removal may be due to washout by the bloodstream rather than metabolic uptake. anoxia; vasodilator metabolites; metabolic feedback; NADH fluorescence; red blood cell velocity; microcirculation; blood flow regulation REACTIVE HYPEREMIA is the increase in blood flow above resting levels that occurs after a period of blood flow stoppage, usually induced by arterial occlusion. This phenomenon has been demonstrated in a wide variety of vascular beds including skeletal muscle (4), myocardium (9), liver (14), kidney (16), intestine (36), and skin (27). The hyperemia is often attributed to accumulation of vasodilator metabolites produced by anaerobic metabolism during tissue hypoxia (1,13,28,47). However, occlusions of a few seconds' duration also elicit a hyperemic response, although this is too brief to deplete oxygen stores as noted initially by Bayliss in 1902 (3). This finding suggests that other mechanisms such as the myogenic response may contribute, since a fall in intravascular pressure during arterial occlusion would lead to arteriolar relaxation and a subsequent hyperemia when the pressure is restored. Studies on skeletal muscle (21, 25) supported the suggestion that the response following short-term (5-30 s) occlusions in resting skeletal muscle is primarily myogenic. However, with reports of additional flo...

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“…Myogenic mechanisms 48 - 49 have been proposed to explain autoregulation of blood flow. This mechanism, however, has not yet been proven, and the contribution of metabolic factors may be more important.…”

Section: Role Of Adenosine In Autoregulation Of Coronary Blood Flowmentioning

confidence: 99%

Adenosine, the heart, and coronary circulation.

1991

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Adenosine is known to regulate myocardial and coronary circulatory functions. Adenosine not only dilates coronary vessels, but attenuates 0-adrenergic receptor-mediated increases in myocardial contractility and depresses both sinoatrial and atrioventricular node activities. The effects of adenosine are mediated by two distinct receptors (i.e., A, and A 2 receptors). A, adenosine receptors, located in atrial and ventricular myocardium and sinoatrial/atrioventricular nodes, are responsible for inhibition of adenylyl cyclase activity. A 2 adenosine receptors, located in coronary endothelial and smooth muscle cells, are responsible for stimulation of this enzyme activity. During increased myocardial oxygen demand due to rapid pacing and exercise, although both coronary blood flow and adenosine concentrations in the myocardium and coronary efflux increased, there is no clear consensus explaining its cause and effect relation at present However, ischemia/reperfusion-induced coronary hyperemia is believed to be mostly attributed to released adenosine, and it has been proven that adenosine attenuates the severity of ischemia due to its coronary vasodilatory action. The beneficial effects of adenosine during ischemia/reperfusion processes do not seem simple. This is because myocardial ischemia and reperfusion injury is caused by 1) activated leukocytes and platelets, 2) ATP depletion and calcium overload of myocardium, and 3) catecholamine release from the presynaptic nerves as well as 4) the impaired coronary circulation. Intriguingly adenosine attenuates all of these deleterious actions and thereby attenuates ischemia/reperfusion injury. Indeed, adenosine attenuates the severity of contractile dysfunction (myocardial stunning) and limits the infarct size. Thus, administration of adenosine or potentiators of adenosine production in the ischemic myocardium may be beneficial for the attenuation of ischemic and reperfusion injuries, although further clinical investigations are necessary. (Hypertension 1991;18:565-574)

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Contributions of pressure and flow sensitivity to autoregulation in mesenteric arterioles

Cited by 113 publications

References 2 publications

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

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

Contribution of anaerobic metabolism to reactive hyperemia in skeletal muscle

Adenosine, the heart, and coronary circulation.

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