MULTIPARAMETRIC MONITORING OF THE AWAKE BRAIN EXPOSED TO CARBON-MONOXIDE

We have applied in vivo real-time techniques to monitor the physiologi cal changes associated with exposure to a pattern of carbon monoxide ( CO) known to cause brain oxidative stress. Using a multiparametric mon itoring device connected to the brain, we exposed unanesthetized rats to two levels of CO, 0.1 and 0.3% in air. Energy metabolism was evalua ted by the optical monitoring of relative cerebral blood flow (CBF) an d intramitochondrial redox state. Ionic homeostasis was assessed by me asurements of K+, Ca2+, and H+ or Na+ levels in the extracellular spac e. The electrical parameters monitored were the electrocorticogram and direct current steady potential. Under 1,000 ppm of CO, the CBF was i ncreased significantly without any measurable change in the NADH redox state, suggesting that the cause for the increased CBF was not hypoxi a. Exposing the awake rat to 1,000 ppm of CO (40 min) followed by 3,00 0 ppm of CO (20 min) led to an increase in CBF followed by episodes of spontaneous brain depolarizations characterized by changes in ionic h omeostasis and blood flow. These changes were similar to those recorde d under cortical spreading depression. In most animals exposed to 3,00 0 ppm of CO, spontaneous oscillations in CBF and NADH redox state that were negatively correlated were recorded. The results indicate that a n inspired CO level of 0.1% had effects largely restricted to blood fl ow, whereas at a higher CO level an additional impairment in energy su pply resulted in a complex pattern of effects similar to that caused b y brain ischemia.