Post-hypoxic hypothermia reduces cerebrocortical release of NO and excitotoxins.
Thoresen, Marianne 1,4,9,10; Satas, Saulius 1,8; Puka-Sundvall, Malgorzata 2; Whitelaw, Andrew 4,7; Hallstrom, Ase 3; Loberg, Else-Marit 5; Ungerstedt, Urban 3; Steen, Petter Andreas 6,7; Hagberg, Henrik 2
8(15):3359-3362, October 20, 1997.
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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[degrees]C; n = 7) or hypothermia (35[degrees]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.
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