Is there an active mechanism limiting the influence of the sympathetic system on the cerebral vascular bed? Evidence for vasomotor escape from sympathetic stimulation in the rabbit

Sercombe, Richard; Lacombe, Pierre; Aubineau, P.; Hamo, H.; Pinard, Elisabeth; Reynier-Rebuffel, A. M.; Seylaz, Jacques

doi:10.1016/0006-8993(79)90008-8

Cited by 61 publications

(27 citation statements)

References 44 publications

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“…31 However, with sustained sympathetic activation, a "vasomotor escape" phenomenon may occur, suggesting that neural control of the cerebral circulation may be more effective under dynamic than under steady-state conditions. 32 In the present study, CBF velocity variability at the very low frequencies persisted while pressure variability was reduced after ganglion blockade. Thus, transfer function gain, which reflects the magnitude of the relationship between these variables, increased substantially, while the phase lead of CBF velocity to pressure was diminished.…”

Section: Dynamic Autoregulationsupporting

confidence: 55%

Autonomic Neural Control of Dynamic Cerebral Autoregulation in Humans

et al. 2002

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Background-The purpose of the present study was to determine the role of autonomic neural control of dynamic cerebral autoregulation in humans. Methods and Results-We measured arterial pressure and cerebral blood flow (CBF) velocity in 12 healthy subjects (aged 29Ϯ6 years) before and after ganglion blockade with trimethaphan. CBF velocity was measured in the middle cerebral artery using transcranial Doppler. The magnitude of spontaneous changes in mean blood pressure and CBF velocity were quantified by spectral analysis. The transfer function gain, phase, and coherence between these variables were estimated to quantify dynamic cerebral autoregulation. After ganglion blockade, systolic and pulse pressure decreased significantly by 13% and 26%, respectively. CBF velocity decreased by 6% (PϽ0.05). In the very low frequency range (0.02 to 0.07 Hz), mean blood pressure variability decreased significantly (by 82%), while CBF velocity variability persisted. Thus, transfer function gain increased by 81%. In addition, the phase lead of CBF velocity to arterial pressure diminished. These changes in transfer function gain and phase persisted despite restoration of arterial pressure by infusion of phenylephrine and normalization of mean blood pressure variability by oscillatory lower body negative pressure. Conclusions-These data suggest that dynamic cerebral autoregulation is altered by ganglion blockade. We speculate that autonomic neural control of the cerebral circulation is tonically active and likely plays a significant role in the regulation of beat-to

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Section: Dynamic Autoregulationsupporting

confidence: 55%

Autonomic Neural Control of Dynamic Cerebral Autoregulation in Humans

et al. 2002

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“…It is unknown whether the cerebral autoregulation is preserved in patients with CHF. Theoretically, CHF-induced activation of physiological neurohormonal counterregulatory mechanisms, such as the sympathetic nervous system and the renin-angiotensin system, may result in a rightward shift of the lower limit of autoregulation, 11,12 whereby a decrease in CBF may result from the low MAP values found in the CHF patients. On the other hand, since adaptive mechanisms for rightward shift of the lower limit of autoregulation are known to occur in arterial hypertension, 13 the converse phenomenon is likely to happen in chronic hypotension.…”

Section: Discussionmentioning

confidence: 99%

Cerebral Blood Flow in Patients With Chronic Heart Failure Before and After Heart Transplantation

Gruhn¹,

Larsen²,

Boesgaard³

et al. 2001

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259

215

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Section: Autonomic Regulation Of Cbfmentioning

confidence: 99%

“…15,16 This lack of effect of sympathetic activation on CBF under steady-state conditions has been referred to as "sympathetic vasomotor escape." 16 Thus, although ganglionic blockade did not prevent reductions in steady-state CBF velocity during LBNP, the possibility of sympathetic regulation of transient changes in CBF cannot be excluded. 10 Finally, it should be noted that besides the extrinsic autonomic nerves, cerebral vessels are innervated by the central intrinsic nerves that arise directly from within the brain parenchyma.…”

Section: Autonomic Regulation Of Cbfmentioning

confidence: 99%

Autonomic Ganglionic Blockade Does Not Prevent Reduction in Cerebral Blood Flow Velocity During Orthostasis in Humans

Zhang

Levine

2007

Stroke

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Background and Purpose-The underlying mechanisms for reductions in cerebral blood flow (CBF) during orthostasis are not completely understood. This study tested the hypothesis that sympathetic activation causes cerebral vasoconstriction leading to reductions in CBF during lower body negative pressure (LBNP). Methods-CBF velocity, arterial pressure, and end-tidal CO 2 were measured during LBNP (Ϫ30 to Ϫ50 mm Hg) in 11 healthy subjects before and after autonomic ganglionic blockade with trimethaphan. Arterial partial pressure of CO 2 also was measured in a subgroup of 5 subjects. Mean arterial pressure during LBNP after blockade was maintained by infusion of phenylephrine. Results-Before blockade, mean arterial pressure did not change during LBNP. However, CBF velocity was reduced in all subjects by 14% (PϽ0.05). Systolic and pulsatile (systolic-diastolic) CBF velocity were reduced by 18% and 28%, respectively, associated with significant reductions in pulse arterial pressure and end-tidal CO 2 (all PϽ0.05). After blockade, mean arterial pressure during LBNP was well-maintained and even increased slightly with infusion of phenylephrine. However, reductions in mean, systolic, and pulsatile CBF velocity, pulse arterial pressure, and ETCO 2 were similar to those before blockade. In contrast to reductions in end-tidal CO 2 , arterial partial pressure of CO 2 did not change during LBNP. Conclusions-These data, contrary to our hypothesis, demonstrate that sympathetic vasoconstriction is not the primary mechanism underlying reductions in CBF during moderate LBNP. We speculate that diminished pulse arterial pressure or pulsatile blood flow may reduce cerebral vessel wall shear stress and contribute to reductions in CBF during orthostasis through flow mediated regulatory mechanisms.

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Is there an active mechanism limiting the influence of the sympathetic system on the cerebral vascular bed? Evidence for vasomotor escape from sympathetic stimulation in the rabbit

Cited by 61 publications

References 44 publications

Autonomic Neural Control of Dynamic Cerebral Autoregulation in Humans

Autonomic Neural Control of Dynamic Cerebral Autoregulation in Humans

Cerebral Blood Flow in Patients With Chronic Heart Failure Before and After Heart Transplantation

Autonomic Ganglionic Blockade Does Not Prevent Reduction in Cerebral Blood Flow Velocity During Orthostasis in Humans

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