Guy E Meadows

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PURPOSE To compare the quantification of cerebral blood flow (CBF) at 1.5 and 3.0 Tesla, under normo- and hypercapnia, and to determine the cerebral vascular response (CVR) of gray matter (GM) to hypercapnia, a pulsed arterial spin labeling technique was used. Additionally, to improve GM CBF quantification a high-resolution GM-mask was applied. MATERIALS(More)
During wakefulness, cerebral blood flow (CBF) is closely coupled to regional cerebral metabolism; however CBF is also strongly modulated by breathing, increasing in response to both hypercapnia and hypoxia. During stage III/IV non-rapid eye (NREM) sleep, cerebral metabolism and CBF decrease whilst the partial pressure of arterial CO2 increases due to a(More)
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(More)
During wakefulness, increases in the partial pressure of arterial CO(2) result in marked rises in cortical blood flow. However, during stage III-IV, non-rapid eye movement (NREM) sleep, and despite a relative state of hypercapnia, cortical blood flow is reduced compared with wakefulness. In the present study, we tested the hypothesis that, in normal(More)
Cerebral blood flow (CBF) is typically reduced during stable non-rapid eye movement (non-REM) sleep compared with the waking level. It is not known when in the sleep cycle these changes occur. However, spontaneous fluctuations in alpha and theta rhythm during sleep onset are associated with marked changes in cardio-respiratory control. The aim of this study(More)
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