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Cerebral blood flow response to isocapnic hypoxia during slow-wave sleep and wakefulness

¹Clinical and Academic Unit of Sleep and Breathing, National Heart and Lung Institute, Imperial College, London SW3 6LY; ²MacKay Institute of Communication and Neuroscience, School of Life Sciences, Keele University, Keele ST5 5BG; and ³Sleep and Ventilation Unit, Royal Brompton Hospital, London SW3 6NP, United Kingdom

Submitted 10 October 2003 ; accepted in final form 7 June 2004

Nocturnal hypoxia is a major pathological factor associated with cardiorespiratory disease. During wakefulness, a decrease in arterial O₂ tension results in a decrease in cerebral vascular tone and a consequent increase in cerebral blood flow; however, the cerebral vascular response to hypoxia during sleep is unknown. In the present study, we determined the cerebral vascular reactivity to isocapnic hypoxia during wakefulness and during stage 3/4 non-rapid eye movement (NREM) sleep. In 13 healthy individuals, left middle cerebral artery velocity (MCAV) was measured with the use of transcranial Doppler ultrasound as an index of cerebral blood flow. During wakefulness, in response to isocapnic hypoxia (arterial O₂ saturation –10%), the mean (±SE) MCAV increased by 12.9 ± 2.2% (P < 0.001); during NREM sleep, isocapnic hypoxia was associated with a –7.4 ± 1.6% reduction in MCAV (P < 0.001). Mean arterial blood pressure was unaffected by isocapnic hypoxia (P > 0.05); R-R interval decreased similarly in response to isocapnic hypoxia during wakefulness (–21.9 ± 10.4%; P < 0.001) and sleep (–20.5 ± 8.5%; P < 0.001). The failure of the cerebral vasculature to react to hypoxia during sleep suggests a major state-dependent vulnerability associated with the control of the cerebral circulation and may contribute to the pathophysiologies of stroke and sleep apnea.

transcranial Doppler ultrasound; middle cerebral artery velocity; cortical blood flow

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