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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 subjects, hypercapnic cerebral vascular reactivity is decreased during stage III-IV NREM sleep compared with wakefulness. A 2-MHz pulsed Doppler ultrasound system was used to measure the left middle cerebral artery velocity (MCAV; cm/s) in 12 healthy individuals while awake and during stage III-IV NREM sleep. The end-tidal Pco(2) (Pet(CO(2))) was elevated during the awake and sleep states by regulating the inspired CO(2) load. The cerebral vascular reactivity to CO(2) was calculated from the relationship between Pet(CO(2)) and MCAV by using linear regression. From wakefulness to sleep, the Pet(CO(2)) increased by 3.4 Torr (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.

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 and Methods:CBF was determined with the QUIPSS II with thin slice TI1 periodic saturation (Q2TIPS) sequence at 1.5 and 3.0 Tesla in the same group of eight subjects, both under normocapnia and hypercapnia. Absolute GM-CBF maps were calculated using a GM-mask obtained from a high-resolution structural scan by segmentation. The CVR to hypercapnia was derived from the quantitative GM-CBF maps.Results: For both field strengths, the GM-CBF was significantly higher under hypercapnia compared to normocapnia. For both conditions, there was no significant difference of GM-CBF for 1.5 and 3.0 Tesla; the same applies to the CVR, which was 4.3 and 4.5%/mmHg at 1.5 and 3.0 Tesla, respectively. Conclusion:The method presented allows for the quantification of CBF and CVR in GM at the common clinical field strengths of 1.5 and 3.0 Tesla and could therefore be a useful tool to study these parameters under physiological and pathophysiological conditions.

. Cerebral blood flow response to isocapnic hypoxia during slow-wave sleep and wakefulness. J Appl Physiol 97: 1343-1348, 2004. First published June 11, 2004 10.1152/japplphysiol.01101.2003.-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 Ϫ10%), the mean (ϮSE) MCAV increased by 12.9 Ϯ 2.2% (P Ͻ 0.001); during NREM sleep, isocapnic hypoxia was associated with a Ϫ7.4 Ϯ 1.6% reduction in MCAV (P Ͻ 0.001). Mean arterial blood pressure was unaffected by isocapnic hypoxia (P Ͼ 0.05); R-R interval decreased similarly in response to isocapnic hypoxia during wakefulness (Ϫ21.9 Ϯ 10.4%; P Ͻ 0.001) and sleep (Ϫ20.5 Ϯ 8.5%; P Ͻ 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 NOCTURNAL HYPOXIA IS A MAJOR pathological factor associated with cardiorespiratory diseases, including obstructive sleep apnea (OSA) (14) and congestive heart failure (16). Reductions in arterial blood O 2 levels will impose stress on all organ systems; however, the brain is particularly vulnerable to the effects of hypoxia (3). Recently, OSA, a condition in which cognitive function can be substantially impaired, has been associated with pathological loss of cortical gray matter (19,22), suggesting that the nocturnal hypoxia associated with OSA may be sufficient to damage brain tissue directly.During any hypoxic insult, protection of the brain will depend on an adequate cerebral vascular response. Normally, perfusion of the brain is dependent on a tight coupling between its O 2 supply and the metabolic demand (31). During wakefulness, a decrease in O 2 supply results in a decrease in cerebral vascular tone and a consequent increase in cerebral blood flow that will mitigate the effects of the systemic hypoxia. Although the cerebral vascular response to hypoxia is not linearly related to the fall in arterial PO 2 , like the ventilatory response to hypoxia, it is linearly related to the fall in arterial O 2 saturation (Sa O 2 ) (15).The transition from wakefulness to stage 3/4 non-rapid eye movement (NREM) sleep is accompanied by marked alterations in the control of the cerebral vascular system. Du...

The cardiovascular response to an arousal occurring at the termination of an obstructive apnea is almost double that to a spontaneous arousal. We investigated the hypothesis that central plus peripheral chemoreceptor stimulation, induced by hypercapnic hypoxia (HH), augments the cardiovascular response to arousal from sleep. Auditory-induced arousals during normoxia and HH (>10-s duration) were analyzed in 13 healthy men [age 24 +/- 1 (SE) yr]. Subjects breathed on a respiratory circuit that held arterial blood gases constant, despite the increased ventilation associated with arousal. Arousals were associated with a significant increase in mean arterial blood pressure at 5 s (P < 0.001) and with a significant decrease in the R-R interval at 3 s (P < 0.001); however, the magnitude of the changes was not significantly different during normoxia compared with HH (mean arterial blood pressure: normoxia, 91 +/- 4 to 106 +/- 4 mmHg; HH, 91 +/- 4 to 109 +/- 5 mmHg; P = 0.32; R-R interval: normoxia, 1.12 +/- 0.04 to 0.90 +/- 0.05 s; HH, 1.09 +/- 0.05 to 0.82 +/- 0.03 [corrected] s; P = 0.78). Mean ventilation increased significantly at the second breath postarousal for both conditions (P < 0.001), but the increase was not significantly different between the two conditions (normoxia, 5.35 +/- 0.40 to 9.57 +/- 1.69 l/min; HH, 8.57 +/- 0.63 to 11.98 +/- 0.70 l/min; P = 0.71). We conclude that combined central and peripheral chemoreceptor stimulation with the use of HH does not interact with the autonomic outflow associated with arousal from sleep to augment the cardiovascular response.