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Khellaf A, Garcia NM, Tajsic T, et al. Focally administered succinate improves cerebral metabolism in traumatic brain injury patients with mitochondrial dysfunction. J Cereb Blood Flow Metab. 2021;271678X211042112doi: 10.1177/0271678X211042112.
Khellaf, A., Garcia, N. M., Tajsic, T., Alam, A., Stovell, M. G., Killen, M. J., Howe, D. J., Guilfoyle, M. R., Jalloh, I., Timofeev, I., Murphy, M. P., Carpenter, T. A., Menon, D. K., Ercole, A., Hutchinson, P. J., Carpenter, K. L., Thelin, E. P., & Helmy, A. (2021). Focally administered succinate improves cerebral metabolism in traumatic brain injury patients with mitochondrial dysfunction. Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 271678X211042112. https://doi.org/10.1177/0271678X211042112
Khellaf, Abdelhakim, et al. "Focally administered succinate improves cerebral metabolism in traumatic brain injury patients with mitochondrial dysfunction." Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism vol. (2021): 271678X211042112. doi: https://doi.org/10.1177/0271678X211042112
Khellaf A, Garcia NM, Tajsic T, Alam A, Stovell MG, Killen MJ, Howe DJ, Guilfoyle MR, Jalloh I, Timofeev I, Murphy MP, Carpenter TA, Menon DK, Ercole A, Hutchinson PJ, Carpenter KL, Thelin EP, Helmy A. Focally administered succinate improves cerebral metabolism in traumatic brain injury patients with mitochondrial dysfunction. J Cereb Blood Flow Metab. 2021 Sep 08;271678X211042112. doi: 10.1177/0271678X211042112. Epub 2021 Sep 08. PMID: 34494481.
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J Cereb Blood Flow Metab. 2021 Sep 08;271678X211042112. doi: 10.1177/0271678X211042112. Epub 2021 Sep 08.

Focally administered succinate improves cerebral metabolism in traumatic brain injury patients with mitochondrial dysfunction.

Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism

Abdelhakim Khellaf, Nuria Marco Garcia, Tamara Tajsic, Aftab Alam, Matthew G Stovell, Monica J Killen, Duncan J Howe, Mathew R Guilfoyle, Ibrahim Jalloh, Ivan Timofeev, Michael P Murphy, T Adrian Carpenter, David K Menon, Ari Ercole, Peter J Hutchinson, Keri Lh Carpenter, Eric P Thelin, Adel Helmy

Affiliations

  1. Division of Neurosurgery, Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK.
  2. Division of Neurosurgery, St. Michael's Hospital, University of Toronto, Toronto, Canada.
  3. Department of Neurosurgery, The Walton Centre, Liverpool, UK.
  4. Department of Chemistry, University of Cambridge, Cambridge, UK.
  5. Medical Research Council Mitochondrial Biology Unit, University of Cambridge, Cambridge, UK.
  6. Wolfson Brain Imaging Centre, Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK.
  7. Division of Anaesthesia, Department of Medicine, University of Cambridge, Cambridge, UK.
  8. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
  9. Department of Neurology, Karolinska University Hospital, Stockholm, Sweden.

PMID: 34494481 DOI: 10.1177/0271678X211042112

Abstract

Following traumatic brain injury (TBI), raised cerebral lactate/pyruvate ratio (LPR) reflects impaired energy metabolism. Raised LPR correlates with poor outcome and mortality following TBI. We prospectively recruited patients with TBI requiring neurocritical care and multimodal monitoring, and utilised a tiered management protocol targeting LPR. We identified patients with persistent raised LPR despite adequate cerebral glucose and oxygen provision, which we clinically classified as cerebral 'mitochondrial dysfunction' (MD). In patients with TBI and MD, we administered disodium 2,3-

Keywords: Cerebral metabolism; microdialysis; mitochondrial dysfunction; succinate; traumatic brain injury (Human)

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