Abstract
INTRODUCTION: Animal studies have shown that cerebral arteries are richly innervated with sympathetic nerve fibers. However, the role of autonomic neural control of the cerebral circulation remains controversial. Until recently it has been thought that changes in sympathetic tone have a limited effect on cerebral blood flow (CBF) at normal PaCO2 levels. PURPOSE: This investigation tested the hypothesis that sympathetic activation via the carotid baroreflex directly influences cerebral vasomotion at rest and during exercise. METHODS: In five healthy human volunteers (mean ± SE: age 25 ± 2 yr; height 166 ± 5 cm; weight 71 ± 7 kg) we examined the effects of pulsatile neck pressure (NP) and neck suction (NS) during rest and steady-state cycling exercise. Pulsatile (5-seconds on 5 seconds off; 0.1 Hz) neck pressure (NP, +40 Torr) was applied for 6 minutes at rest and during exercise. Changes in heart rate (HR), mean arterial arterial pressure (MAP) and mean middle cerebral arterial velocity (MCA V mean), were measured at rest in the seated position and during leg cycling exercise with and without NP and NS. RESULTS: The power spectral density (PSD) of MAP at 0. 1Hz increased during pulsatile NP and NS. Importantly, the PSD of MCA V mean at 0. 1Hz was much greater during NP than that of NS at rest (4237 ± 1628 v 92 ± 101 cm2/s2/Hz, P = 0.015). Similar responses of PSD of MAP and MCA V mean to NP and NS was observed during dynamic exercise. There were no significant differences between end-tidal CO2 between each condition. CONCLUSION: These findings suggest that cerebral vasoconstriction during NP was a result of the autoregulatory response to the NP mediated pulsatile changes in arterial pressure and the NP induced sympathetically mediated vasoconstriction.
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