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

To determine the HbO(2) 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 (HbO(2)), 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 HbO(2) due to the amount of the dissolved O(2) to provide the O(2) consumed by the brain, and therefore no O(2) will be dissociated from the HbO(2). Awake rats were exposed progressively to 15 min normobaric hyperoxia, 100% O(2) (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 HbO(2) in relation to pO(2) 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 HbO(2): linear or logarithmic. These findings show that the increase in brain microcirculatory HbO(2) is due to an increase in O(2) supply by dissolved O(2), reaching a maximum at 2.5 ATA. NADH is oxidized (decreased signal) in parallel to the HbO(2) increase, showing maximal tissue oxygenation and cellular mitochondrial NADH oxidation at 2.5 ATA. In conclusion, in the normoxic brain, the level of microcirculatory HbO(2) is about 50% as compared to the maximal level recorded at 2.5 ATA and the minimal level measured during anoxia.