Contribution of arterial blood pressure and PaCO2 to the cerebrovascular responses to motor stimulation

Abstract

Motor stimulation induces a neurovascular response that can be detected by continuous measurement of cerebral blood flow (CBF). Simultaneous changes in arterial blood pressure (ABP) and PaCO2 have been reported, but their influence on the CBF response has not been quantified. Continuous bilateral recordings of CBF velocity (CBFV), ABP, and end-tidal CO2 (ETCO2) were obtained in 10 healthy middle-aged subjects at rest and during 60 s of repetitive, metronome-controlled (1 Hz) elbow flexion. A multivariate autoregressive-moving average model was adopted to quantify the relationship between beat-to-beat changes in ABP, breath-by-breath ETCO2, and the motor stimulus, represented by the metronome on-off signal (inputs), and the CBFV response to stimulation (output). All three inputs contributed to explain CBFV variance following stimulation. For the ipsi- and contralateral hemispheres, ABP explained 20.3 ± 17.3% ( P = 0.0007) and 19.5 ± 17.2% ( P = 0.01) of CBFV variance, respectively. Corresponding values for ETCO2 and metronome signals were 22.0 ± 24.2% ( P = 0.008), 24.0 ± 24.1% ( P = 0.037), 32.7 ± 22.5% ( P = 0.0015), and 43.2 ± 25.1% ( P = 0.013), respectively. Synchronized population averages suggest that the initial sudden change in CBFV was largely due to ABP, while the influence of ETCO2 was more erratic. The component due to elbow flexion showed a well-defined pattern, with rise time slower than the main CBFV change but reaching a stable plateau after 15 s of stimulation. Identifying and removing the influences of ABP and PaCO2 to motor-induced changes in CBF should lead to more robust estimates of neurovascular coupling and better understanding of its physiological covariates.