Hypercapnic cerebral vascular reactivity is decreased,  in humans, during sleep compared with wakefulness

Meadows, Guy E.; Dunroy, Helen M. A.; Morrell, Mary J.; Corfield, Douglas R.

doi:10.1152/japplphysiol.00606.2002

Cited by 44 publications

(53 citation statements)

References 29 publications

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“…However, in 3 individuals, CBF increased in response to hypoxia during the evening but decreased in response to the same stimulus in the morning ( Figure 3B); these reductions are similar to those reported during sleep 7 and may indicate individual variation in the rate of recovery of the response on waking. In common with hypoxia, the cerebral vascular response to hypercapnia is also reduced during NREM sleep 6 ; because this response to hypercapnia remains low in the morning, it appears that its recovery after sleep is slower than that of hypoxia. These findings, therefore, suggest that substantial differences exist in the regulation of CBF between waking and sleep and between hypoxia and hypercapnia.…”

Section: Discussionmentioning

confidence: 99%

“…6,7 The hypercapnic cerebral vascular reactivity was characterized by the slope of the linear regression fitted to the mean measurements of MCAV and P ET CO 2 . 6 The cerebral vascular response to IH in each individual was determined as the percentage change in MCAV from baseline isocapnic normoxia to IH (Ϫ5 and Ϫ10% SaO 2 ). 7…”

Section: Discussionmentioning

confidence: 99%

“…The MCA was identified by an insonation pathway through the left temporal window, just above the zygomatic arch, using search techniques previously described. 6,7,11 In brief, optimization of the Doppler signals from the MCA was performed by varying the sample volume depth in incremental steps and at each depth, varying the angle of insonance to obtain the best-quality signals from the Doppler frequency. A headband (modification of the Welder TCD Fixation; Nicolet EME GmbH) was used to hold the ultrasound probe ensuring optimal insonation position and angle for the duration of the experiment.…”

Section: Protocolmentioning

confidence: 99%

“…(B) Original traces from 1 subject highlighting the cerebral vascular response to isocapnic hypoxia using the clamping circuit to regulate the fraction of inspired oxygen (FiO 2 ) and to maintain the P ET CO 2 . 6,14 As the SaO 2 is reduced, the P ET CO 2 remains constant and the MCAV and V E increase.…”

Section: Reproducibilitymentioning

confidence: 99%

“…However, during nonrapid eye movement (NREM) sleep, cerebral metabolism, blood flow, and the cerebral vascular response to CO 2 are all reported to be reduced. 5,6 It is therefore possible that the reduction in cerebral vascular reactivity is determined by changes in cerebral vascular regulation during the proceeding sleep period and that this phenomenon may reflect a "carryover" from the sleeping state.…”

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confidence: 99%

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Overnight Changes in the Cerebral Vascular Response to Isocapnic Hypoxia and Hypercapnia in Healthy Humans

Meadows

Kotajima

Vazir

et al. 2005

Stroke

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Background and Purpose-The reduction in hypercapnic cerebral vascular reactivity that occurs in the morning after sleep is associated with an increased risk of cerebral ischemia and stroke. It is not known if the cerebral vascular response to hypoxia is similarly reduced in the morning, but such a reduction could be considered a further risk factor for cerebral vascular disease. Methods-To test if the cerebral vascular response to hypoxia is reduced in the morning, the overnight changes in the left middle cerebral artery velocity (MCAV) in response to isocapnic hypoxia (IH) and hypercapnia before and after a normal night sleep were determined in 18 individuals. Results-From evening to morning, hypercapnic cerebral vascular reactivity decreased significantly (evening 2.0Ϯ0.4, morning 1.3Ϯ0.2 cm/sec/mm Hg; PϽ0.05); in contrast, the increase in MCAV in response to IH (Ϫ10% SaO 2 ) was unchanged (evening 9.0Ϯ1.4, morning 8.7Ϯ2.2%; PϾ0.05). Conclusions-Our findings indicate that substantial differences exist in the regulation of the cerebral circulation in response to hypoxia and hypercapnia on waking from sleep. An intact cerebral vascular response to IH, during this time period, could be interpreted as a protective mechanism against cerebral ischemia and stroke; this is of particular relevance to patients with obstructive sleep apnea who arouse from sleep during hypoxia.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Protocolmentioning

confidence: 99%

Section: Reproducibilitymentioning

confidence: 99%

mentioning

confidence: 99%

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Overnight Changes in the Cerebral Vascular Response to Isocapnic Hypoxia and Hypercapnia in Healthy Humans

Meadows

Kotajima

Vazir

et al. 2005

Stroke

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Central Chemoreceptors: Locations and Functions

Nattie¹,

Li²

2012

Comprehensive Physiology

204

139

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Central chemoreception traditionally refers to a change in ventilation attributable to changes in CO2/H+ detected within the brain. Interest in central chemoreception has grown substantially since the previous Handbook of Physiology published in 1986. Initially, central chemoreception was localized to areas on the ventral medullary surface, a hypothesis complemented by the recent identification of neurons with specific phenotypes near one of these areas as putative chemoreceptor cells. However, there is substantial evidence that many sites participate in central chemoreception some located at a distance from the ventral medulla. Functionally, central chemoreception, via the sensing of brain interstitial fluid H+, serves to detect and integrate information on 1) alveolar ventilation (arterial PCO2), 2) brain blood flow and metabolism and 3) acid-base balance, and, in response, can affect breathing, airway resistance, blood pressure (sympathetic tone) and arousal. In addition, central chemoreception provides a tonic ‘drive’ (source of excitation) at the normal, baseline PCO2 level that maintains a degree of functional connectivity among brainstem respiratory neurons necessary to produce eupneic breathing. Central chemoreception responds to small variations in PCO2 to regulate normal gas exchange and to large changes in PCO2 to minimize acid-base changes. Central chemoreceptor sites vary in function with sex and with development. From an evolutionary perspective, central chemoreception grew out of the demands posed by air vs. water breathing, homeothermy, sleep, optimization of the work of breathing with the ‘ideal’ arterial PCO2, and the maintenance of the appropriate pH at 37°C for optimal protein structure and function.

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Regulation of the Cerebral Circulation by Arterial Carbon Dioxide

Hoiland

Fisher

Ainslie

2019

Comprehensive Physiology

178

189

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Intact, coordinated, and precisely regulated cerebrovascular responses are required for the maintenance of cerebral metabolic homeostasis, adequate perfusion, oxygen delivery, and acid‐base balance during deviations from homeostasis. Increases and decreases in the partial pressure of arterial carbon dioxide (PaCO 2 ) lead to robust and rapid increases and decreases in cerebral blood flow (CBF). In awake and healthy humans, PaCO 2 is the most potent regulator of CBF, and even small fluctuations can result in large changes in CBF. Alterations in the responsiveness of the cerebral vasculature can be detected with carefully controlled stimulus‐response paradigms and hold relevance for cerebrovascular risk in steno‐occlusive disease. As changes in PaCO 2 do not typically occur in isolation, the integrative influence of physiological factors such as intracranial pressure, arterial oxygen content, cerebral perfusion pressure, and sympathetic nervous activity must be considered. Further, age and sex, as well as vascular pathologies are also important to consider. Following a brief summary of key historical events in the development of our understanding of cerebrovascular physiology and an overview of the measurement techniques to index CBF this review provides an in‐depth description of CBF regulation in response to alterations in PaCO 2 . Cerebrovascular reactivity and regional flow distribution are described, with further consideration of how differences in reactivity of parallel networks can lead to the “steal” phenomenon. Factors that influence cerebrovascular reactivity are discussed and the mechanisms and regulatory pathways mediating the exquisite sensitivity of the cerebral vasculature to changes in PaCO 2 are outlined. Finally, topical avenues for future research are proposed. © 2019 American Physiological Society. Compr Physiol 9:1101‐1154, 2019.

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Hypercapnic cerebral vascular reactivity is decreased, in humans, during sleep compared with wakefulness

Cited by 44 publications

References 29 publications

Overnight Changes in the Cerebral Vascular Response to Isocapnic Hypoxia and Hypercapnia in Healthy Humans

Overnight Changes in the Cerebral Vascular Response to Isocapnic Hypoxia and Hypercapnia in Healthy Humans

Central Chemoreceptors: Locations and Functions

Regulation of the Cerebral Circulation by Arterial Carbon Dioxide

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