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Hyperoxia Results in Increased Aerobic Metabolism Following Acute Brain

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Hyperoxia Results in Increased Aerobic Metabolism Following Acute Brain View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by UCL Discovery Original Article Journal of Cerebral Blood Flow & Metabolism 0(00) 1–11 Hyperoxia results in increased aerobic ! Author(s) 2016 Reprints and permissions: metabolism following acute brain injury sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/0271678X16679171 jcbfm.sagepub.com Arnab Ghosh1,*, David Highton1,*, Christina Kolyva2, Ilias Tachtsidis2, Clare E Elwell2 and Martin Smith1,2,3 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 [ÁpbrO2 30.9 mmHg p < 0.001], reduced LPR [ÁLPR À3.07 p ¼ 0.015], and increased cytochrome c oxidase (CCO) oxidation (Á[oxCCO] þ 0.32 mM p < 0.001) which persisted on return-to-baseline (Á[oxCCO] þ 0.22 mM, p < 0.01), accompa- nied by a 7.5% increase in estimated cerebral metabolic rate for oxygen (p ¼ 0.038). Our results are consistent with an improvement in cellular redox state, suggesting oxygen-limited metabolism above recognised ischaemic pbrO2 thresh- olds. 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. Keywords Brain ischaemia, energy metabolism, mitochondria, near infrared spectroscopy, neurocritical care Received 2 June 2016; Revised 2 September 2016; Accepted 17 October 2016 Introduction reflects oxygen deprivation or a non-ischaemic meta- bolic crisis.8,9 The brain relies on aerobic metabolism to meet its sub- Mitochondria exist and function normally in a near stantial energy needs and, in health, various mechan- anoxic environment, facilitating a diffusion gradient for isms ensure that oxygen (and metabolic substrate) oxygen transport from the microvasculature, and supply is balanced to meet metabolic demand. This bal- ance is often disturbed after acute brain injury in which cerebral hypoxia–ischaemia is a key injury mechanism 1Neurocritical Care, University College London Hospitals, National Hospital for Neurology & Neurosurgery, London, UK associated with poor outcome, irrespective of brain 2 1–3 Department of Medical Physics and Biomedical Engineering, University injury type. Specific neuroprotective therapies have College London, London, UK 4,5 failed to translate into clinical benefit and treatment 3University College London Hospitals National Institute for Health of severe acute brain injury therefore focuses on Research Biomedical Research Centre, London, UK avoiding or minimising secondary cerebral hypoxia– *These authors contributed equally to this work. ischaemia and consequent mitochondrial energy failure by maintaining cerebral oxygen delivery at a level that Corresponding author: 6,7 David Highton, Neurocritical Care, University College London Hospitals, is sufficient to meet metabolic demand. Debate con- National Hospital for Neurology & Neurosurgery, Queen Square, tinues whether depressed aerobic metabolism, which is London WC1N 3BG, UK. common following acute brain injury, predominantly Email: [email protected] 2 Journal of Cerebral Blood Flow & Metabolism offering protection from oxidant damage. Cytochrome limitation or an altered mitochondrial ischaemic c oxidase (CCO), the terminal electron acceptor in the threshold could equally explain these findings. While mitochondrial respiratory chain, is responsible for CCO oxidation status reflects the activity of the respira- reducing oxygen to water. Its low Michaelis–Menton tory chain, it is also dependent on metabolic substrate constant (Km) for oxygen means that oxidative phos- supply, ATP, oxygen, and mediators which modify the 24 phorylation may continue unimpeded in isolated mito- Km for oxygen such as nitric oxide. Understanding 10 chondria with a pO2 less than 1 mmHg. Below a the changes in CCO oxidation status may therefore critical ischaemic threshold, CCO is reduced and, be a useful adjunct for the in-vivo investigation of dif- importantly, oxygen then becomes a rate limiting sub- fusion limitation and mitochondrial dysfunction after strate decreasing oxidative phosphorylation.11,12 acute brain injury. In health, changes of brain tissue pO2 within the We have developed an in-house optical technique, physiological range are not believed to influence cere- incorporating hybrid spatially resolved broadband bral oxygen consumption13 but, following acute brain and frequency domain near infrared spectroscopy injury, a range of disturbances to oxygen transport and (NIRS), optimised for the measurement of the oxida- its utilisation may complicate the relationship between tion state of CCO [oxCCO] in adult brain-injured 25 pO2 and metabolism. Classical ischaemia describes a patients. Spatially resolved cerebral tissue oxygen sat- situation of insufficient oxygen delivery, and therefore uration, also called the tissue oxygenation index (TOI), of maximal extraction of oxygen from haemoglobin, in association with concentrations of oxyhaemoglobin and is characterized by a combination of large oxygen ([HbO2]), deoxyhaemoglobin ([HHb]) and [oxCCO] extraction fraction (OEF) measured by positron emis- may be used to investigate oxygenation of both the sion tomography (PET), cerebral oligaemia, and falling microvasculature and mitochondria.12 A comprehen- 14 cerebral metabolic rate for oxygen (CMRO2). sive multimodal neuromonitoring array, including While prevalent early after acute brain injury, this pic- pbrO2, microdialysis, transcranial Doppler-measured ture is less common beyond the immediate period of cerebral blood flow velocity and NIRS therefore injury after stroke and traumatic brain injury (TBI).15 covers the entire oxygen cascade from the microvascu- Metabolic dysfunction has been identified in the pres- lature (TOI, HbO2, HHb) through the tissue intersti- ence of apparently acceptable tissue oxygenation, where tium (pbrO2) to the mitochrondria ([oxCCO]), and has both diffusion limited oxygen transport and mitochon- potential to predict cellular redox status (microdialysis drial dysfunction have been implicated as alternative LPR, [oxCCO]) and CMRO2 changes estimated using forms of restriction to oxidative metabolism in the pres- NIRS and transcranial Doppler,26 and might therefore 16 ence of a normal interstitial tissue pO2 or OEF. differentiate between diffusion limited oxygen transport Multimodal neuromonitoring with brain tissue pO2 and mitochondrial dysfunction. (pbrO2) and cerebral microdialysis-derived lactate:pyru- The aim of this study was to investigate the oxygen vate ratio (LPR) have enabled investigation of the dependence of mitochondrial metabolism in vivo relationship between oxygen delivery, cerebral tis- following acute brain injury. We hypothesised that nor- sue oxygenation, and cellular redox status in vivo fol- mobaric hyperoxia-induced increases in cerebral lowing TBI,16 aneurysmal subarachnoid haemorrhage oxygen availability would lead to an increase in CCO (SAH),17 and intracerebral haemorrhage (ICH).18,19 oxidation and reduction in microdialysate LPR, sug- Clinical therapy protocols guided by changes in pbrO2 gesting oxygen-limited mitochondrial oxidative metab- seek to maintain oxygen delivery and availability above olism at baseline. 20 a ‘critical’ pO2 threshold for anaerobic metabolism. Although overt ischaemia and anaerobic metabolism has typically been described when pbrO2 falls below Materials and methods 10 mmHg, normobaric hyperoxia and hyperbaric Study participants and protocol hyperoxia may improve LPR and CMRO2 after TBI in the presence of pbrO2 values that are within or After approval by the Research Ethics Committee of above the normal physiological range.21–23 Vespa the National Hospital for Neurology and Neurosurgery et al.16 demonstrated metabolic dysfunction without and Institute of Neurology (04/Q0512/67) and repre- classical ischaemia after TBI based on observation of sentative consent, recordings were carried out in elevated LPR and PET-derived OEF > 0.75. Others 16 sedated, mechanically ventilated acute brain injury have described a similar picture of metabolic dysfunc- patients requiring invasive neuromonitoring to guide tion ‘without hypoxia’ in SAH and ICH.17 However, it clinical management on the neurocritical care unit. is difficult to entirely rule out hypoxia as a cause of such This was performed in accordance with the observations because of the absence of a subcellular Declaration of Helsinki. Inclusion criteria also included marker of oxygenation in these studies. Diffusion baseline inspired fraction of oxygen (FiO2) Ghosh et al. 3 Baseline inspired oxygen Inspired oxygen fraction Inspired oxygen fraction Baseline fraction (typically 30%) 60% 100% Continuous
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