POSTHYPOXIC HYPOTHERMIA REDUCES CEREBROCORTICAL RELEASE OF NO AND EXCITOTOXINS

HYPOTHERMIA applied after hypoxia offers neuroprotection in neonatal a nimals, but the mechanisms involved remain unknown. Hypoxia was induce d 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 ri se of the CAR occurred during reoxygenation in the normothermic group whereas the ratio tended to decrease in the hypothermic group. In conc lusion, post-hypoxic hypothermia attenuated NO production and overflow of EAAs.