Hyperoxia results in increased aerobic metabolism following acute brain injury

Article


Ghosh, A., Highton, D., Kolyva, C., Tachtsidis, I., Elwell, C. and Smith, M. 2017. Hyperoxia results in increased aerobic metabolism following acute brain injury. Journal of Cerebral Blood Flow and Metabolism. 37 (8), pp. 2910-2920. https://doi.org/10.1177/0271678x16679171
TypeArticle
TitleHyperoxia results in increased aerobic metabolism following acute brain injury
AuthorsGhosh, A., Highton, D., Kolyva, C., Tachtsidis, I., Elwell, C. and Smith, M.
Abstract

Acute brain injury is associated with depressed aerobic metabolism. Below a critical mitochondrial pO2 cytochrome c oxidase, the terminal electron acceptor in the mitochondrial respiratory chain, fails to sustain oxidative phosphorylation. After acute brain injury, this ischaemic threshold might be shifted into apparently normal levels of tissue oxygenation. We investigated the oxygen dependency of aerobic metabolism in 16 acutely brain-injured patients using a 120-min normobaric hyperoxia challenge in the acute phase (24–72 h) post-injury and multimodal neuromonitoring, including transcranial Doppler ultrasound-measured cerebral blood flow velocity, cerebral microdialysis-derived lactate-pyruvate ratio (LPR), brain tissue pO2 (pbrO2), and tissue oxygenation index and cytochrome c oxidase oxidation state (oxCCO) measured using broadband spectroscopy. Increased inspired oxygen resulted in increased pbrO2 [ΔpbrO2 30.9 mmHg p < 0.001], reduced LPR [ΔLPR −3.07 p = 0.015], and increased cytochrome c oxidase (CCO) oxidation (Δ[oxCCO] + 0.32 µM p < 0.001) which persisted on return-to-baseline (Δ[oxCCO] + 0.22 µM, p < 0.01), accompanied by a 7.5% increase in estimated cerebral metabolic rate for oxygen (p = 0.038). Our results are consistent with an improvement in cellular redox state, suggesting oxygen-limited metabolism above recognised ischaemic pbrO2 thresholds. Diffusion limitation or mitochondrial inhibition might explain these findings. Further investigation is warranted to establish optimal oxygenation to sustain aerobic metabolism after acute brain injury.

Research GroupBiophysics and Bioengineering group
LanguageEnglish
PublisherSage
JournalJournal of Cerebral Blood Flow and Metabolism
ISSN0271-678X
Publication dates
Online01 Jan 2017
Print01 Aug 2017
Publication process dates
Deposited05 Apr 2018
Accepted17 Oct 2016
Output statusPublished
Publisher's version
License
Digital Object Identifier (DOI)https://doi.org/10.1177/0271678x16679171
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