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1 Clinical and Academic Unit of Sleep and Breathing, Imperial College, London, United Kingdom; Sleep and Ventilation Unit, Royal Brompton Hospital, London, United Kingdom
2 Clinical and Academic Unit of Sleep and Breathing, Imperial College, London, United Kingdom; MacKay Institute of Communication and Neuroscience, School of Life Sciences, Keele University, Keele, United Kingdom
* To whom correspondence should be addressed. E-mail: d.corfield{at}keele.ac.uk.
Nocturnal hypoxia is a major pathological factor associated with cardio-respiratory disease. During wakefulness, a decrease in arterial oxygen tension results in a decrease in cerebral vascular tone and a consequent increase in cerebral blood flow; however, the cerebrovascular 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 III/IV, NREM sleep. In 13 healthy individuals, left middle cerebral artery velocity (MCAV) was measured using transcranial Doppler ultrasound, as an index of cerebral blood flow. During wakefulness, in response to isocapnic hypoxia (arterial oxygen saturation -10%), the mean (± sem) MCAV increased by 12.9 ± 2.16% (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 ± 8.54%, 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.
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