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Showing papers by "James B. Skatrud published in 2008"


Journal ArticleDOI
01 Mar 2008-Sleep
TL;DR: Arousals from NREM sleep transiently reduce CBFV, whereas arousals from REMSleep transiently increase CBFv, despite qualitatively and quantitatively similar increases in MAP, HR, and VE in the two sleep states.
Abstract: SLEEP DISORDERED BREATHING IS ASSOCIATED WITH ELEVATED ARTERIAL PRESSURE AND AN INCREASED RISK OF STROKE1,2; THIS INCREASED RISK MAY be related to changes in the regulation of cerebral blood flow. Numerous factors contribute to cerebral blood flow regulation, among them cerebral metabolism, arterial carbon dioxide tension, and cerebral perfusion pressure.3–5 Sleep state has profound direct and indirect effects on cerebral hemodynamics. Several studies using a variety of methods (transcranial Doppler ultrasonography,133 Xe inhalation, and single-photon emission computerized tomography) have shown a reduction in cerebral blood flow during NREM sleep and an increase during REM sleep as compared to the awake state in healthy persons.1,6–13 Arousal from sleep, per se, causes abrupt hemodynamic and respiratory changes characterized by increases in sympathetic nervous system activity, blood pressure, heart rate,14 and ventilation.15,16 Moreover, arousal from sleep accentuates the hemodynamic changes produced by upper airway obstruction.17 Although changes in cerebral blood flow associated with arousal12 and with spontaneous theta-alpha transitions during the sleep onset period18 have been characterized, the interaction of hemodynamic, ventilatory, and cerebrovascular responses to arousal from stable sleep has not been rigorously studied thus far. In this study we investigated arousal-induced changes in cerebral blood flow velocity (CBFV) in healthy young adults. In addition, we investigated the temporal relationships among the cerebrovascular, ventilatory, and systemic hemodynamic perturbations associated with arousal from NREM and REM sleep.

36 citations