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.
Keywords: cerebral blood flow; cerebral hemodynamics; mathematical modeling; receptors; sympathetic nervous system.
Copyright © 2016 the American Physiological Society.