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Metabolites. 2020 Jul 13;10(7). doi: 10.3390/metabo10070287.

Ethyl Pyruvate Increases Post-Ischemic Levels of Mitochondrial Energy Metabolites: A .

Metabolites

Kevin H Nygaard, Jesper F Havelund, Troels H Nielsen, Carl-Henrik Nordström, Nils J Færgeman, Frantz R Poulsen, Jan Bert Gramsbergen, Axel Forsse

Affiliations

  1. Department of Neurosurgery, Odense University Hospital, University of Southern Denmark, Sdr. Boulevard 29, 5000 Odense C, Denmark.
  2. BRIDGE-Brain Researche-Inter-Disciplinary Guided Excellence, Institute of Clinical Research, University of Southern Denmark, Winsløwparken 19, 5000 Odense C, Denmark.
  3. VILLUM Center for Bioanalytical Sciences, Department of Biochemistry and Molecular Biology, University of Southern Denmark, Campusvej 55, 5230 Odense M, Denmark.
  4. Institute of Molecular Medicine, University of Southern Denmark, 5000 Odense C, Denmark.

PMID: 32668656 PMCID: PMC7407637 DOI: 10.3390/metabo10070287

Abstract

Mitochondrial dysfunction after transient cerebral ischemia can be monitored by cerebral microdialysis (CMD) using changes in the lactate and pyruvate concentrations and ratio. Other metabolites associated with mitochondrial (dys)function are, e.g., tricyclic acid (TCA) and purine metabolites. Ethyl pyruvate (EP) is a putative neuroprotectant, supposedly targeting mitochondrial energy metabolism, but its effect on cerebral energy metabolism has never been described using microdialysis. In this study we monitored the metabolic effects of EP in the endothelin-1 (ET-1) rat model using perfusion with

Keywords: cerebral metabolism; labeled succinate; liquid chromatography—mass spectrometry; mitochondrial dysfunction; transient ischemia

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