EFFECTS OF MILD HYPOTHERMIA ON NITRIC-OXIDE SYNTHESIS FOLLOWING CONTUSION TRAUMA IN THE RAT

The exact mechanism of hypothermic cerebroprotection after traumatic b rain injury (TBI) is not fully understood. The present study was condu cted to investigate the effects of mild hypothermia on trauma-induced synthesis of nitric oxide (NO), which has been implicated in the patho genesis of ischemic brain damage associated with glutamate neurotoxici ty. Cerebral contusion was created in the rat parietal cortex by a wei ght-drop method, and extracellular concentrations of the NO end produc ts nitrite and nitrate were measured using in vivo brain microdialysis and capillary electrophoresis under normothermic (37 degrees C) and m ild hypothermic (32 degrees C) conditions. In normothermic animals, th e level of NO end products increased markedly 10 min after contusion, reaching a maximum level at 20 min. In the hypothermic rats, such incr eases were absent. Although it is unknown whether endothelial NO synth ase, neuronal NO synthase, or both caused the elevation of the NO end products seen in the normothermic animals, the present results indicat e that inhibition of NO synthesis may play a part in hypothermic cereb roprotection following TBI.