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1 Cardiorespiratory and Vascular Dynamics Laboratory, University of Waterloo, Waterloo, Ontario, Canada
* To whom correspondence should be addressed. E-mail: hughson{at}uwaterloo.ca.
The new two-breath CO2 method was employed to test the hypotheses that small alterations in arterial PCO2 had an impact on both the magnitude and dynamic response time of the CO2 effect on cerebrovascular resistance (CVRi) and the dynamic autoregulatory response to fluctuations in arterial pressure. During a 10-min protocol, 8 subjects inspired two-breaths from a bag with elevated PCO2, four different times, while end-tidal PCO2 was maintained at three levels: hypocapnia (LoCO2; -8 mmHg from resting values), normocapnia, and hypercapnia (HiCO2; +8 mmHg). Continuous measurements were made of mean blood pressure corrected to the level of the middle cerebral artery (BPMCA), PCO2 (estimated from expired CO2) and mean flow velocity (MFV, of the MCA by Doppler ultrasound), with CVRi=BPMCA/MFV. Data were processed by a system identification technique (autoregressive moving average analysis) with gain and dynamic response time of adaptation estimated from the theoretical step responses. Consistent with our hypotheses the magnitude of the PCO2-CVRi response was reduced from LoCO2 to HiCO2 (-0.04±0.02 to -0.01±0.01 [(mmHg / cm/s) / mmHg PCO2, mean±SD] and the time to reach 95% of the step plateau increased from 12.0±4.9s to 20.5±10.6s. Dynamic autoregulation was impaired with elevated PCO2 as indicated by a reduction in gain from LoCO2 to HiCO2 (0.021±0.012 to 0.007±0.004 [(mmHg / cm/s) / mmHg BPMCA] and time to reach 95% increased from 3.7±2.8s to 20.0±9.6s. The two-breath technique detected dependence of the cerebrovascular CO2 response on PCO2 and changes in dynamic autoregulation with only small deviations in estimated arterial PCO2.
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