Dynamic cerebral autoregulation is preserved during acute head-down tilt
- 1 October 2003
- journal article
- clinical trial
- Published by American Physiological Society in Journal of Applied Physiology
- Vol. 95 (4) , 1439-1445
- https://doi.org/10.1152/japplphysiol.00524.2003
Abstract
Complete ganglion blockade alters dynamic cerebral autoregulation, suggesting links between systemic autonomic traffic and regulation of cerebral blood flow velocity. We tested the hypothesis that acute head-down tilt, a physiological maneuver that decreases systemic sympathetic activity, would similarly disrupt normal dynamic cerebral autoregulation. We studied 10 healthy young subjects (5 men and 5 women; age 21 ± 0.88 yr, height 169 ± 3.1 cm, and weight 76 ± 6.1 kg). ECG, beat-by-beat arterial pressure, respiratory rate, end-tidal CO2 concentration, and middle cerebral blood flow velocity were recorded continuously while subjects breathed to a metronome. We recorded data during 5-min periods and averaged responses from three Valsalva maneuvers with subjects in both the supine and -10° head-down tilt positions (randomized). Controlled-breathing data were analyzed in the frequency domain with power spectral analysis. The magnitude of input-output relations were determined with cross-spectral techniques. Head-down tilt significantly reduced Valsalva phase IV systolic pressure overshoot from 36 ± 4.0 (supine position) to 25 ± 4.0 mmHg (head down) ( P = 0.03). Systolic arterial pressure spectral power at the low frequency decreased from 5.7 ± 1.6 (supine) to 4.4 ± 1.6 mmHg2 (head down) ( P = 0.02), and mean arterial pressure spectral power at the low frequency decreased from 3.3 ± 0.79 (supine) to 2.0 ± 0.38 mmHg2 (head down) ( P = 0.05). Head-down tilt did not affect cerebral blood flow velocity or the transfer function magnitude and phase angle between arterial pressure and cerebral blood flow velocity. Our results show that in healthy humans, mild physiological manipulation of autonomic activity with acute head-down tilt has no effect on the ability of the cerebral vasculature to regulate flow velocity.Keywords
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