Developmental NeurosciencePost-hypoxic hypothermia reduces cerebrocortical release of NO and excitotoxinsThoresen, Marianne1,4,9,10; Satas, Saulius1,8; Puka-Sundvall, Malgorzata2; Whitelaw, Andrew4,7; Hallström, Åse3; Løberg, Else-Marit5; Ungerstedt, Urban3; Steen, Petter Andreas6,7; Hagberg, Henrik2Author Information 1Institutes of Surgical and Pediatric Research, The National Hospital, Oslo, Norway 2Perinatal Center, Departments of Anatomy and Cell Biology and of Obstetrics and Gynecology, Sahlgrenska University Hospital, Göteborg, Sweden 3Department of Pharmacology and Physiology, Karolinska Institute, Stockholm 4Departments of Paediatrics, Ullevaal University Hospital, Oslo, Norway 5Departments of Pathology, Ullevaal University Hospital, Oslo, Norway 6Departments of Anesthesiology, Ullevaal University Hospital, Oslo, Norway 7Departments of Experimental Medical Research, Ullevaal University Hospital, Oslo, Norway 8Vilnius University Children's Hospital, Lithuania 9Present address: Department of Child Health, St Michael's Hospital, Southwell Street, Bristol BS2 8EG, UK 10Corresponding Author and Address: Marianne Thoresen, Department of Child Health, St Michael's Hospital, Southwell Street, Bristol BS2 8EG, UK ACKNOWLEDGEMENTS: Supported by the Norwegian Research Council (M.T.), Laerdal Foundation for Acute Medicine (M.T., H.H., A.W.), The Norwegian SIDS Society, and FUS, Ullevaal Hospital (M.T.), Swedish Medical Research Council (09455), Sven Jerring Foundation (H.H.), Åke Wiberg Foundation (H.H.), Free Masonry Foundation and the Medical Faculties of Göteborg and the Karolinska Institute. Website publication 3 October 1997 Received 24 July 1997 accepted 9 August 1997 NeuroReport: October 20th, 1997 - Volume 8 - Issue 15 - p 3359-3362 Buy Abstract HYPOTHERMIA applied after hypoxia offers neuroprotection in neonatal animals, but the mechanisms involved remain unknown. Hypoxia was induced in newborn piglets and changes in excitatory amino acids (EAAs) and the citrulline:arginine ratio (CAR) were followed by microdialysis for 5 h. After the 45 min hypoxic insult, the animals were randomized to receive normothermia (39°C; n = 7) or hypothermia (35°C; n = 7). After reoxygenation, extracellular glutamate, aspartate and the excitotoxic index were significantly lower in the cerebral cortex of hypothermic animals than in normothermic animals. A progressive rise of the CAR occurred during reoxygenation in the normothermic group whereas the ratio tended to decrease in the hypothermic group. In conclusion, post-hypoxic hypothermia attenuated NO production and overflow of EAAs. © Lippincott-Raven Publishers.