Effect of hyperbaric oxygenation on brain hemodynamics, hemoglobin oxygenation and mitochondrial NADH

To determine the HbO2 oxygenation level at the microcirculation, we used the hyperbaric chamber. The effects of hyperbaric oxygenation (HBO) were tested on vitality parameters in the brain at various pressures. Microcirculatory hemoglobin oxygen saturation (HbO2), cerebral blood flow (CBF) and mitochondrial NADH redox state were assessed in the brain of awake restrained rats using a fiber optic probe. The hypothesis was that HBO may lead to maximal level in microcirculatory HbO2 due to the amount of the dissolved O2 to provide the O2 consumed by the brain, and therefore no O2 will be dissociated from the HbO2. Awake rats were exposed progressively to 15 min normobaric hyperoxia, 100% O2 (NH) and to 90 min hyperbaric hyperoxia (HH) from 1.75 to 6.0 absolute atmospheres (ATA). NH and HH gradually decreased the blood volume measured by tissue reflectance and NADH but increased HbO2 in relation to pO2 in the chamber up to a nearly maximum effect at 2.5 ATA. Two possible approximations were found to describe the relationship between NADH and HbO2: linear or logarithmic. These findings show that the increase in brain microcirculatory HbO2 is due to an increase in O2 supply by dissolved O2, reaching a maximum at 2.5 ATA. NADH is oxidized (decreased signal) in parallel to the HbO2 increase, showing maximal tissue oxygenation and cellular mitochondrial NADH oxidation at 2.5 ATA. In conclusion, in the normoxic brain, the level of microcirculatory HbO2 is about 50% as compared to the maximal level recorded at 2.5 ATA and the minimal level measured during anoxia.