Identification of human sympathetic neurovascular control using multivariate wavelet decomposition analysis.
The dynamic regulation of cerebral blood flow (CBF) is thought to involve myogenic and chemoreflex mechanisms, but the extent to which the sympathetic nervous system also plays a role remains debated. Here we sought to identify the role of human sympathetic neurovascular control by examining cerebral pressure-flow relations using linear transfer function analysis and multivariate wavelet decomposition analysis that explicitly accounts for the confounding effects of dynamic end-tidal Pco2 (PetCO2 ) fluctuations. In 18 healthy participants randomly assigned to the α1-adrenergic blockade group (n = 9; oral Prazosin, 0.05 mg/kg) or the placebo group (n = 9), we recorded blood pressure, middle cerebral blood flow velocity, and breath-to-breath PetCO2 Analyses showed that the placebo administration did not alter wavelet phase synchronization index (PSI) values, whereas sympathetic blockade increased PSI for frequency components ≤0.03 Hz. Additionally, three-way interaction effects were found for PSI change scores, indicating that the treatment response varied as a function of frequency and whether PSI values were PetCO2 corrected. In contrast, sympathetic blockade did not affect any linear transfer function parameters. These data show that very-low-frequency CBF dynamics have a composite origin involving, not only nonlinear and nonstationary interactions between BP and PetCO2 , but also frequency-dependent interplay with the sympathetic nervous system.
School of Engineering and Computer Science, Victoria University of Wellington, Wellington, New Zealand; Interdisciplinary Neuroprotection Research Group, Centre for Translational Physiology, University of Otago, Wellington, New Zealand.
Saqib
S
Saleem
School of Engineering and Computer Science, Victoria University of Wellington, Wellington, New Zealand;
Paul D
PD
Teal
School of Engineering and Computer Science, Victoria University of Wellington, Wellington, New Zealand;
W Bastiaan
WB
Kleijn
Centre for Heart Lung and Vascular Health, School of Health and Exercise Science, University of British Columbia Okanagan, Kelowna, British Columbia, Canada;
Philip N
PN
Ainslie
Interdisciplinary Neuroprotection Research Group, Centre for Translational Physiology, University of Otago, Wellington, New Zealand shieak.tzeng@otago.ac.nz.
Yu-Chieh
YC
Tzeng
D058668:Adrenergic alpha-1 Receptor Antagonists / Q000494:pharmacology*; D000328:Adult; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002245:Carbon Dioxide / Q000378:metabolism; D002560:Cerebrovascular Circulation / Q000187:drug effects* / Q000502:physiology; D004562:Electrocardiography; D005260:Female; D064368:Healthy Volunteers; D006801:Humans; D016014:Linear Models; D008297:Male; D020768:Middle Cerebral Artery / Q000187:drug effects* / Q000502:physiology; D015999:Multivariate Analysis; D000069336:Neurovascular Coupling / Q000187:drug effects* / Q000502:physiology; D010991:Plethysmography; D011224:Prazosin / Q000494:pharmacology*; D013564:Sympathetic Nervous System / Q000187:drug effects* / Q000502:physiology; D017585:Ultrasonography, Doppler, Transcranial; D058067:Wavelet Analysis; D055815:Young Adult
D058668:Adrenergic alpha-1 Receptor Antagonists; D002245:Carbon Dioxide; D011224:Prazosin
cerebral blood flow; cerebral hemodynamics; mathematical modeling; receptors; sympathetic nervous system