Cerebral Circulation in Sleep: Vasodilatory Response to Cerebral Hypotension

Grant, Daniel; Franzini, Carlo; Wild, Jennene; Walker, Adrian M.

doi:10.1097/00004647-199806000-00006

Cited by 15 publications

(29 citation statements)

References 16 publications

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“…We chose the upper limit to be 0.1 Hz because autonomic vascular control and cerebral autoregulatory processes occur well below this frequency. 19 For each 20-minute segment, the Coh and G values were averaged over the frequency bands of 0.003-0.020 Hz (ultralow frequency [ULF]), 0.020 -0.050 Hz (very low frequency [VLF]), and 0.050 -0.100 Hz (low frequency [LF]). Where more than one 20-minute segment was analyzed in an infant, the maximum Coh and G values were selected for further analysis.…”

Section: Discussionmentioning

confidence: 99%

Impaired Autoregulation in Preterm Infants Identified by Using Spatially Resolved Spectroscopy

et al. 2008

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High coherence between mean arterial blood pressure and tissue-oxygenation index indicates impaired cerebral autoregulation in clinically sick preterm infants and is strongly associated with subsequent mortality. Cross-spectral analysis of mean arterial blood pressure and tissue-oxygenation index has the potential to provide continuous bedside assessment of cerebral autoregulation and to guide therapeutic interventions.

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Section: Discussionmentioning

confidence: 99%

Impaired Autoregulation in Preterm Infants Identified by Using Spatially Resolved Spectroscopy

et al. 2008

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“…The upper limit was chosen to be 0.02 Hz as autonomic vascular control of cerebral autoregulatory processes occur at frequencies below this level [16]. The lower limit of 0.003 Hz was chosen to be above the lower frequency limit which was determined by the data segment length of 20 minutes.…”

Section: Methodsmentioning

confidence: 99%

Cerebral Oxygenation Is Highly Sensitive to Blood Pressure Variability in Sick Preterm Infants

et al. 2012

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ObjectivesThe significance of blood pressure variability (BPV) for cerebral oxygenation in extremely preterm infants has not been explored, though BPV may well be associated with end organ injury. We hypothesized that increased BPV in sick preterm infants, by exceeding the cerebral autoregulatory capacity, is associated with cerebral oxygenation changes which closely follow the blood pressure fluctuations. We assessed the autoregulatory capacity in the early postnatal period, by determining the correlation between BPV (mmHg2) and coherence of mean arterial blood pressure (MABP mmHg) and cerebral oxygenation (tissue oxygenation index, TOI %).Study DesignThirty-two preterm infants of mean gestational age of 26.3 (±1.5) weeks were studied on the first 3 postnatal days. Spectral analysis (Coherence and transfer-function gain analysis) was used to calculate coherence of MABP and TOI; BPV was quantified using power spectral density of MABP.ResultsOverall, maximum Coherence showed a trend for positive correlation with BPV (n = 32, p = 0.06). Infants identified as clinically unstable with documented brain injury (n = 7) had high Coherence values at low BPV. Separate analysis of stable infants (excluding the 7 critically ill infants) revealed a significant association between maximum Coherence and BPV (n = 25, p = 0.006).ConclusionsFluctuation in cerebral oxygenation is closely associated with increased BPV in preterm infants undergoing intensive care. Moreover, in the critically sick preterm infant, blood pressure-dependent variations in cerebral oxygenation occur even with relatively lower BPV, suggesting they have severely impaired autoregulation, and placing them at greater vulnerability to cerebral injury arising from blood pressure fluctuations.

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“…Cortical blood flow is usually independent of variations in arterial blood pressure, over a wide range, because of autoregulatory mechanisms. Although the presence of autoregulation has not been tested in humans during sleep, it is preserved in lambs (13). Assuming that cerebral autoregulation is present during sleep, a reduction in blood pressure will be met by a reduction in cerebral vascular tone and the maintenance of cerebral blood flow (15).…”

Section: Validity Of Transcranial Doppler (Tcd) Techniquementioning

confidence: 99%

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

Meadows¹,

O'Driscoll²,

Simonds³

et al. 2004

Journal of Applied Physiology

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. 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...

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Cerebral Circulation in Sleep: Vasodilatory Response to Cerebral Hypotension

Cited by 15 publications

References 16 publications

Impaired Autoregulation in Preterm Infants Identified by Using Spatially Resolved Spectroscopy

Impaired Autoregulation in Preterm Infants Identified by Using Spatially Resolved Spectroscopy

Cerebral Oxygenation Is Highly Sensitive to Blood Pressure Variability in Sick Preterm Infants

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

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