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1 National Heart and Lung Institute, Department of Respiratory Medicine, Imperial College, London, United Kingdom
2 National Heart and Lung Institute, Department of Respiratory Medicine, Imperial College, London, United Kingdom; Sleep & Ventilation Unit, Royal Brompton Hospital, London, United Kingdom
3 National Heart and Lung Institute, Department of Respiratory Medicine, Imperial College, London, United Kingdom; School of Life Sciences, Keele University, Keele, United Kingdom
* To whom correspondence should be addressed. E-mail: guy.meadows{at}ic.ac.uk.
During wakefulness, increases in the partial pressure of arterial carbon dioxide (PaCO2) result in marked rises in cortical blood flow. However, during stage III/IV, non-REM (NREM) sleep, and despite a relative state of hypercapnia, cortical blood flow is reduced compared to wakefulness. In the present study we have tested the hypothesis that, in normal subjects, hypercapnic cerebral vascular reactivity is decreased during stage III/IV, NREM sleep compared to wakefulness. A 2MHz pulsed Doppler ultrasound system was used to measure the left middle cerebral artery velocity (MCAV; cm/sec) in 12 healthy individuals whilst awake and during stage III-IV NREM sleep. The end-tidal PCO2 (PETCO2) was elevated awake and during sleep by regulating the inspired CO2 load. The cerebral vascular reactivity to CO2 was calculated from the relationship between PETCO2 and MCAV using linear regression. From wakefulness to sleep, the PETCO2 increased by 3.4 mmHg (P < 0.001) and the MCAV fell by 11.7 % (P < 0.001). A marked decrease in cerebral vascular reactivity was noted in all subjects, with an average fall of 70.1% (P = 0.001). This decrease in hypercapnic cerebral vascular reactivity may, at least in part, explain the stage III/IV, NREM sleep related reduction in cortical blood flow.
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