TY - JOUR
T1 - Impact of mild orthostatic stress on aortic-cerebral hemodynamic transmission
T2 - Insight from the frequency domain
AU - Sugawara, Jun
AU - Tomoto, Tsubasa
AU - Imai, Tomoko
AU - Maeda, Seiji
AU - Ogoh, Shigehiko
N1 - Funding Information:
This study was supported by Japan Society for the Promotion of Science Grants-in Aid for Scientific Research (KAKENHI) grants (nos. 25702045 and 26670116 to J. Sugawara).
Publisher Copyright:
© 2017 the American Physiological Society.
PY - 2017/5/15
Y1 - 2017/5/15
N2 - High cerebral pressure and flow fluctuations could be a risk for future cerebrovascular disease. This study aims to determine whether acute systemic vasoconstriction affects the dynamic pulsatile hemodynamic transmission from the aorta to the brain. We applied a stepwise lower body negative pressure (LBNP) (–10, –20, and –30 mmHg) in 15 young men to induce systemic vasoconstriction. To elucidate the dynamic relationship between the changes in aortic pressure (AoP; estimated from the radial arterial pressure waveforms) and the cerebral blood flow velocity (CBFV) at the middle cerebral artery (via a transcranial Doppler), frequency-domain analysis characterized the beat-to-beat slow oscillation (0.02–0.30 Hz) and the intra-beat rapid change (0.78–9.69 Hz). The systemic vascular resistance gradually and significantly increased throughout the LBNP protocol. In the low-frequency range (LF: 0.07–0.20 Hz) of a slow oscillation, the normalized transfer function gain of the steady-state component (between mean AoP and mean CBFV) remained unchanged, whereas that of the pulsatile component (between pulsatile AoP and pulsatile CBFV) was significantly augmented during –20 and –30 mmHg of LBNP (+28.8% and +32.4% vs. baseline). Furthermore, the relative change in the normalized transfer function gain of the pulsatile component at the LF range correlated with the corresponding change in systemic vascular resistance (r = 0.41, P = 0.005). Regarding the intra-beat analysis, the normalized transfer function gain from AoP to CBFV was not significantly affected by the LBNP stimulation (P = 0.77). Our findings suggest that systemic vasoconstriction deteriorates the dampening effect on the pulsatile hemodynamics toward the brain, particularly in slow oscillations (e.g., 0.07–0.20 Hz). NEW & NOTEWORTHY We characterized the pulsatile hemodynamic transmission from the heart to the brain by frequency-domain analysis. The low-frequency transmission was augmented with a mild LBNP stimulation partly due to the elevated systemic vascular resistance. A systemic vasoconstriction deteriorates the dampening effect on slow oscillations of pulsatile hemodynamics toward the brain.
AB - High cerebral pressure and flow fluctuations could be a risk for future cerebrovascular disease. This study aims to determine whether acute systemic vasoconstriction affects the dynamic pulsatile hemodynamic transmission from the aorta to the brain. We applied a stepwise lower body negative pressure (LBNP) (–10, –20, and –30 mmHg) in 15 young men to induce systemic vasoconstriction. To elucidate the dynamic relationship between the changes in aortic pressure (AoP; estimated from the radial arterial pressure waveforms) and the cerebral blood flow velocity (CBFV) at the middle cerebral artery (via a transcranial Doppler), frequency-domain analysis characterized the beat-to-beat slow oscillation (0.02–0.30 Hz) and the intra-beat rapid change (0.78–9.69 Hz). The systemic vascular resistance gradually and significantly increased throughout the LBNP protocol. In the low-frequency range (LF: 0.07–0.20 Hz) of a slow oscillation, the normalized transfer function gain of the steady-state component (between mean AoP and mean CBFV) remained unchanged, whereas that of the pulsatile component (between pulsatile AoP and pulsatile CBFV) was significantly augmented during –20 and –30 mmHg of LBNP (+28.8% and +32.4% vs. baseline). Furthermore, the relative change in the normalized transfer function gain of the pulsatile component at the LF range correlated with the corresponding change in systemic vascular resistance (r = 0.41, P = 0.005). Regarding the intra-beat analysis, the normalized transfer function gain from AoP to CBFV was not significantly affected by the LBNP stimulation (P = 0.77). Our findings suggest that systemic vasoconstriction deteriorates the dampening effect on the pulsatile hemodynamics toward the brain, particularly in slow oscillations (e.g., 0.07–0.20 Hz). NEW & NOTEWORTHY We characterized the pulsatile hemodynamic transmission from the heart to the brain by frequency-domain analysis. The low-frequency transmission was augmented with a mild LBNP stimulation partly due to the elevated systemic vascular resistance. A systemic vasoconstriction deteriorates the dampening effect on slow oscillations of pulsatile hemodynamics toward the brain.
KW - Lower body negative pressure
KW - Power spectral analysis
KW - Transcranial Doppler method
KW - Windkessel function
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U2 - 10.1152/ajpheart.00802.2016
DO - 10.1152/ajpheart.00802.2016
M3 - Article
C2 - 28258058
AN - SCOPUS:85019639804
SN - 0363-6135
VL - 312
SP - H1076-H1084
JO - American Journal of Physiology - Heart and Circulatory Physiology
JF - American Journal of Physiology - Heart and Circulatory Physiology
IS - 5
ER -