Brain lactate during partial global ischemia and reperfusion: effect of pretreatment with dichloroacetate in a rat model |
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| Authors: | M H Biros R V Dimlich |
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| Affiliation: | 1. Department of Emergency Medicine, University of Cincinnati Medical Center, Cincinnati, Ohio USA.;2. Department of Anatomy and Cell Biology, University of Cincinnati Medical Center, Cincinnati, Ohio USA.;1. Department of Dermatology, University of Alabama at Birmingham, Birmingham, AL, USA;2. Department of Anesthesiology and Perioperative Medicine, University of Alabama at Birmingham, Birmingham, AL, USA;3. Stillman College, 3601 Stillman Blvd, Tuscaloosa, AL, USA;4. Department of Visual Science, University of Alabama at Birmingham, Birmingham, AL, USA;5. Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, IN, USA;1. Neuroscience and Mental Health Research Institute, School of Medicine, Cardiff University, Cardiff CF24 4HQ, UK;2. Division of Neuroscience, School of Bioscience, Cardiff University, Cardiff CF10 3AX, UK;3. Institut National de la Santé et de la Recherche Médicale (INSERM) UMR861, I-Stem, AFM, 91100 Corbeil-Essonnes, France;1. Department of Paediatric Neurology, 2nd Faculty of Medicine, Charles University in Prague and Motol University Hospital, Czech Republic;2. Department of Pathology and Molecular Medicine, 2nd Faculty of Medicine, Charles University in Prague and Motol University Hospital, Czech Republic;1. Department of Microbiology, Tumor and Cell Biology, Nobels väg 16, Karolinska Institutet, 17177 Stockholm, Sweden;2. Department of Biosciences and Nutrition, Novum, Karolinska Institutet, 14183 Huddinge, Sweden;3. Science for Life Laboratory, Division of Translational Medicine and Chemical Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, 17121 Stockholm, Sweden;4. Department of Pharmacology and Pharmacotherapy, Faculty of Medicine, University of Pécs, Szigeti út 12, 7624 Pécs, Hungary;1. Molecular Physiology Group, Leibniz Institute for Neurobiology, D-39118 Magdeburg, Germany;2. Department Neurochemistry, Leibniz Institute for Neurobiology, D-39118 Magdeburg, Germany;3. Presynaptic Plasticity Group, Leibniz Institute for Neurobiology, D-39118 Magdeburg, Germany;4. University of Bordeaux, F-33000 Bordeaux, France;5. CNRS, Interdisciplinary Institute for Neuroscience, UMR 5297, F-33000 Bordeaux, France;6. Bordeaux Imaging Center, UMS 3420 CNRS, US4 INSERM, University of Bordeaux, F-33000 Bordeaux, France;7. Harvard University, Department Molecular and Cellular Biology, Cambridge, MA 02138, USA;8. Otto-von-Guericke-University Magdeburg, Systemverfahrenstechnik, Universitätsplatz 2, D-39106 Magdeburg, Germany;1. Shenzhen Key Laboratory for Neuronal Structural Biology, Biomedical Research Institute, Shenzhen Peking University–The Hong Kong University of Science and Technology Medical Center, Shenzhen, Guangdong Province, China;2. Shenzhen Key Laboratory for Translational Medicine of Dermatology, Biomedical Research Institute, Shenzhen Peking University–The Hong Kong University of Science and Technology Medical Center, Shenzhen, Guangdong Province, China;3. Department of Dermatology, Peking University Shenzhen Hospital, Shenzhen, Guangdong Province, China;4. Division of Life Science, The Hong Kong University of Science and Technology, Clear Water Bay Road, Kowloon, Hong Kong, China |
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| Abstract: | Elevated cerebral lactate levels following cerebral ischemia have been associated with brain cell damage and death. We previously found that pre- or postischemia treatment with dichloroacetate (DCA), presumably by its activation of brain pyruvate dehydrogenase, effectively lowers cerebral lactate levels in rats subjected to 30 minutes of partial global ischemia (PGI) followed by 30 minutes of recirculation. The goal of the present study was to determine the effects of preischemia DCA treatment on cortical lactate levels during the ischemia period or during early recirculation. Rats (four in each group) received preischemia treatment with DCA and were then subjected to 0, 10, or 30 minutes of PGI or 30 minutes of PGI followed by 15 minutes of recirculation. Cortical lactate levels in pretreated animals were not significantly different from lactate levels of untreated rats at any time during PGI, but were significantly lower than levels in untreated rats at 15 minutes of recirculation (P less than .05, ANOVA). These results suggest that preischemia treatment with DCA does not limit the accumulation of cortical lactate during PGI but may promote its clearance during recirculation following PGI. If reperfusion events influence the degree of brain cell injury, DCA may enhance cell recovery by lower cortical lactate levels in the reperfusion period. |
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