Cerebral blood flow response to acute hypoxic hypoxia

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dc.contributor.authorHarris, Ashley D.
dc.contributor.authorMurphy, Kevin
dc.contributor.authorDiaz, Claris M.
dc.contributor.authorSaxena, Neeraj
dc.contributor.authorHall, Judith E.
dc.contributor.authorLiu, Thomas T.
dc.contributor.authorWise, Richard G.
dc.date.accessioned2021-01-06T20:50:53Z
dc.date.available2021-01-06T20:50:53Z
dc.date.issued2013-10-07
dc.description.abstractHypoxic hypoxia (inspiratory hypoxia) stimulates an increase in cerebral blood flow (CBF) maintaining oxygen delivery to the brain. However, this response, particularly at the tissue level, is not well characterised. This study quantifies the CBF response to acute hypoxic hypoxia in healthy subjects. A 20-min hypoxic (mean P(ET)o(2)=52 mmHg) challenge was induced and controlled by dynamic end-tidal forcing whilst CBF was measured using pulsed arterial spin labelling perfusion MRI. The rate constant, temporal delay and magnitude of the CBF response were characterised using an exponential model for whole-brain and regional grey matter. Grey matter CBF increased from 76.1 mL/100 g/min (95% confidence interval (CI) of fitting: 75.5 mL/100 g/min, 76.7 mL/100 g/min) to 87.8 mL/100 g/min (95% CI: 86.7 mL/100 g/min, 89.6 mL/100 g/min) during hypoxia, and the temporal delay and rate constant for the response to hypoxia were 185 s (95% CI: 132 s, 230 s) and 0.0035 s(-1) (95% CI: 0.0019 s(-1), 0.0046 s(-1)), respectively. Recovery from hypoxia was faster with a delay of 20 s (95% CI: -38 s, 38 s) and a rate constant of 0.0069 s(-1) (95% CI: 0.0020 s(-1), 0.0103 s(-1)). R-2*, an index of blood oxygenation obtained simultaneously with the CBF measurement, increased from 30.33 s(-1) (CI: 30.31 s(-1), 30.34 s(-1)) to 31.48 s(-1) (CI: 31.47 s(-1), 31.49 s(-1)) with hypoxia. The delay and rate constant for changes in R-2* were 24 s (95% CI: 21 s, 26 s) and 0.0392 s(-1) (95% CI: 0.0333 s(-1), 0.045 s(-1) ), respectively, for the hypoxic response, and 12 s (95% CI: 10 s, 13 s) and 0.0921 s(-1) (95% CI: 0.0744 s(-1), 0.1098 s(-1)/) during the return to normoxia, confirming rapid changes in blood oxygenation with the end-tidal forcing system. CBF and R-2* reactivity to hypoxia differed between subjects, but only R-2* reactivity to hypoxia differed significantly between brain regions. (c) 2013 The Authors. NMR in Biomedicine published by John Wiley & Sons, Ltd.
dc.description.grantingagencyNatural Sciences and Engineering Research Council - Collaborative Research & Development Grant
dc.description.grantingagencyOther
dc.identifier.citationHarris, A. D., Murphy, K., Diaz, C. M., Saxena, N., Hall, J. E., Liu, T. T., & Wise, R. G. (2013). Cerebral blood flow response to acute hypoxic hypoxia. NMR in Biomedicine, 26(12), 1844–1852. https://doi.org/10.1002/nbm.3026
dc.identifier.doi10.1002/nbm.3026
dc.identifier.doihttp://dx.doi.org/10.11575/PRISM/38519
dc.identifier.issn0952-3480
dc.identifier.urihttp://hdl.handle.net/1880/112927
dc.language.isoeng
dc.publisherWiley
dc.publisher.hasversionPublisher's version
dc.publisher.policyhttps://authorservices.wiley.com/author-resources/Journal-Authors/licensing/self-archiving.html
dc.rights© 2013 The Authors
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/
dc.subjectarterial spin labelling (ASL)
dc.subjectblood oxygenation
dc.subjectcerebral blood flow (CBF)
dc.subjectcerebral perfusion
dc.subjecthypoxia
dc.subjectR2*
dc.subjecttemporal dynamics
dc.titleCerebral blood flow response to acute hypoxic hypoxia
dc.typejournal article
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