Modulation of Cerebral Arteriolar Diameter by Intraluminal Flow and Pressure

Ngai, Al C.; Winn, H. Richard

doi:10.1161/01.res.77.4.832

Cited by 139 publications

(104 citation statements)

References 40 publications

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“…The magnitude of the dilatation elicited by flow in these preconstricted control arteries (13.4 %) was comparable to that observed in non-preconstricted rat cerebral arteries [21] and mesenteric arteries from pregnant rats [14]. The response to flow was biphasic, vessels dilated at low flow rates but at higher flow rates there was a tendency for vessel diameter to decrease.…”

Section: Discussionsupporting

confidence: 73%

Flow-induced dilatation in isolated resistance arteries from control and streptozotocin-diabetic rats

1998

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Section: Discussionsupporting

confidence: 73%

Flow-induced dilatation in isolated resistance arteries from control and streptozotocin-diabetic rats

1998

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“…However, the response to wall shear stress was based on one study (33), giving information corresponding to the large arteriole in the present model. The effects of flow and pressure on vessel diameter were examined in two other studies (17,26). In one (17), the shear-dependent vasodilatory response was fully saturated at a level of wall shear stress below typical physiological levels, whereas in the other (26), the variation in diameter was recorded as a function of flow for only one intraluminal pressure.…”

Section: Discussionmentioning

confidence: 99%

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

148

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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“…Moreover, alterations of sympathetic and parasympathetic cholinergic mechanisms by superior cervical ganglionectomy, atropine application, and lesioning of cholinergic input did not affect the pial dilator response to sciatic nerve stimulation (7). Pial arterioles may also dilate by a shear stress-dependent mechanism (4,14). Synaptic activity evoked by somatosensory stimulation may initially cause the dilation of parenchymal arterioles, leading to an increase in blood flow.…”

Section: Discussionmentioning

confidence: 99%

“…Synaptic activity evoked by somatosensory stimulation may initially cause the dilation of parenchymal arterioles, leading to an increase in blood flow. This could then induce an increase in shear stress in pial arterioles, resulting in "flow-mediated dilation" (4,14). However, the simultaneous measurement of flow velocity and pial arteriole diameter (15) revealed no significant change in wall shear rate during sciatic nerve stimulation.…”

Section: Discussionmentioning

confidence: 99%

Pial arteriole dilation during somatosensory stimulation is not mediated by an increase in CSF metabolites

Ngai

Winn

2002

American Journal of Physiology-Heart and Circulatory Physiology

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Ngai, Al C., and H. Richard Winn. Pial arteriole dilation during somatosensory stimulation is not mediated by an increase in CSF metabolites. Am J Physiol Heart Circ Physiol 282: H902-H907, 2002; 10.1152/ajpheart.00128.2001.-Pial arterioles supplying the hindlimb somatosensory cortex dilate in response to contralateral sciatic nerve stimulation. The mechanism of this pial vasodilation is not well understood. One possibility is that vasoactive metabolites released during brain activation may diffuse to subarachnoid cerebrospinal fluid (CSF) to dilate pial vessels. To test this hypothesis, we implanted closed cranial windows in rats and measured pial arteriolar dilation to sciatic nerve stimulation during constant rate superfusion of the pial surface with artificial CSF. We reason that flushing the pial surface with CSF should quickly dissipate vasoactive substances and prevent these substances from dilating pial arterioles. CSF flow (1 and 1.5 ml/min) significantly reduced pial arteriole dilation induced by 5% CO 2 inhalation, but the same flow rates did not affect dilator responses to sciatic nerve stimulation. We conclude that brain-to-CSF diffusion of vasoactive metabolites does not play a significant role in the dilation of pial arterioles during somatosensory activity. cerebral blood flow; coupling; hypercapnia CEREBRAL ACTIVATION by sensory stimulation is accompanied by adjustments of vascular resistance and blood flow in the activated region. For example, we (13) have shown that pial arterioles supplying the hindlimb somatosensory cortex dilate in response to contralateral sciatic nerve stimulation. The mechanism of this pial vasodilation remains unclear. One possibility is that neuronal activity evoked by sensory stimulation causes the release of metabolites, which may diffuse to subarachnoid cerebrospinal fluid (CSF) to dilate pial arterioles. Putative vasoactive metabolites released during cortical synaptic activity include adenosine, H ϩ , K ϩ , and nitric oxide (1, 6). A variation of this diffusion mechanism is an arteriolar-venular countercurrent scheme (5) involving 1) the release of a vasodilator substance in the brain parenchyma and 2) the transport of the vasoactive substance by the draining venules to the pial surface.The present study tested this diffusion hypothesis. We reasoned that flushing the pial surface with CSF should quickly dissipate vasoactive substances and prevent these substances from dilating pial arterioles. We also studied the effect of CSF superfusion on dilation induced by hypercapnia. Moving CSF has previously been shown to attenuate hypercapnic vasodilation of pial arterioles, presumably by washing away perivascular CO 2 released locally from the vascular compartment (9). METHODSExperimental protocols in the present study were approved by the Animal Care Committee of the University of Washington. Adult male Sprague-Dawley rats weighing between 350 and 400 g were initially anesthetized with 2% halothane. The right femoral artery was exposed and cannulated for arterial blood ...

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Modulation of Cerebral Arteriolar Diameter by Intraluminal Flow and Pressure

Cited by 139 publications

References 40 publications

Flow-induced dilatation in isolated resistance arteries from control and streptozotocin-diabetic rats

Flow-induced dilatation in isolated resistance arteries from control and streptozotocin-diabetic rats

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

Pial arteriole dilation during somatosensory stimulation is not mediated by an increase in CSF metabolites

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