• Yu-Chieh Tzeng and Braid A MacRae.
• Cardiovascular Systems Laboratory, Centre for Translational Physiology, University of Otago, Wellington, New Zealand. shieak.tzeng@otago.ac.nz
• J. Appl. Physiol. 2013 Apr 1; 114 (7): 888-95.

AbstractThe relationships between blood pressure variability (BPV) and cerebral blood flow variability (CFV) across individuals in the presence of intact and blunted cerebrovascular control are poorly understood. This study sought to characterize the interindividual associations between spontaneous BPV and CFV under conditions of normal and blunted [calcium channel blockade (CCB)] cerebrovascular control in healthy humans. We analyzed blood pressure and flow velocity data from 12 subjects treated with CCB (60 mg oral nimodipine) and 11 subjects treated with a placebo pill. Spontaneously occurring fluctuations in mean arterial blood pressure (MAP) and middle cerebral artery flow velocity (MCAv(mean); transcranial Doppler) were characterized using power spectral and transfer function analysis in the very-low- (0.02-0.07 Hz), low- (0.07-0.20 Hz), and high-frequency (0.20-0.40 Hz) ranges. Across our study sample, MAP and MCAv(mean) power were positively correlated in all three frequency ranges, both before (R(2) = 0.34-0.67, all P < 0.01) and after CCB (R(2) = 0.53-0.61, all P < 0.02). Compared with placebo, CCB reduced very-low-frequency MAP (P < 0.05) and MCAv(mean) power (P < 0.01) and the low-frequency cross-spectral phase angle (P < 0.05). The magnitude of change in MAP and MCAv(mean) power with CCB (i.e., change scores) was positively related in the very-low-frequency range. Collectively, these findings indicate that CFV may be an explanatory factor in the association between elevated BPV and adverse cerebrovascular outcomes and support the possibility of using CCB to improve hemodynamic stability under resting conditions.

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