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Delayed hypothermia prevents decreases in N-acetylaspartate and reduced glutathione in the cerebral cortex of the neonatal pig following transient hypoxia-ischaemia |
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| Authors: | Brooks Keith J Hargreaves Iain Bhakoo Kishore Sellwood Mark O'Brien Francis Noone Martina Sakata Yasuko Cady Ernest Wylezinska Marzena Thornton John Ordidge Roger Nguyen Quyen Clemence Matthew Wyatt John Bates Timothy E |
| Affiliation: | (1) Department of Paediatrics, University College London Medical School, London, WC1E 6JJ, United Kingdom;(2) Department of Clinical Biochemistry, National Hospital for Neurology and Neurosurgery, Queen Square, London, WC1N 3BG, United Kingdom;(3) Robert Steiner MR Unit, MRC Clinical Sciences Centre, Faculty of Medicine, Imperial College of Science, Technology and Medicine Hammersmith Campus Du Cane Road, London, W12 ONN, United Kingdom;(4) Department of Medical Physics and Bioengineering, University College Hospital NHS Trusts, 1st Floor, Shropshire House, 11-20 Capper Street, London, WC1E 6JA, United Kingdom;(5) MRC Applied Neuroscience Group, School of Biomedical Sciences, University of Nottingham Medical School, Queens Medical Centre, Nottingham, NG7 2UH, United Kingdom |
| Abstract: | The effects of normothermia and delayed hypothermia on the levels of N-acetylaspartate (NAA), reduced glutathione (GSH) and the activities of mitochondrial complex I, II-III, IV and citrate synthase were measured in brain homogenates obtained from anaesthetized neonatal pigs following transient in vivo hypoxia-ischaemia. In the normothermic animals there was a significant decrease in complex I activity and in the levels of GSH and NAA when compared to the controls. Delayed hypothermia preserved NAA and GSH at control levels and enhanced the rate of complex II-III activity. There was correlation (R = 0.79) between GSH and NAA levels when data from all three experimental groups were analyzed. Citrate synthase activity was not significantly different in the three groups, indicating maintenance of mitochondrial integrity. These data suggest that delayed hypothermia affords protection of integrated mitochondrial function in the neonatal brain following transient hypoxia-ischaemia. |
| Keywords: | Neonatal brain hypoxia-ischemia hypothermia neuroprotection |
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