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.

Effect of hyperbaric oxygenation on intracranial pressure elevation rate in rats during the early phase of severe traumatic brain injury.

Intracranial pressure (ICP) was monitored to evaluate the therapeutic effect of hyperbaric oxygen (HBO(2)) treatment following traumatic brain injury (TBI). This subject is controversial. The aim of our study was to determine whether HBO(2) treatment has a therapeutic effect on ICP dynamics and survival following severe fluid percussion brain injury (FPBI) in rats. Changes in ICP level were analyzed every 30 min during an 8-h monitoring period following trauma and at the end of experiment (20 h). The control (A) and experimental (B) groups consisted of 7 and 4 rats, respectively. Group B was subjected to 1.5 atmospheres absolute (ATA) 100% oxygen for 60 min beginning 2 h after FPBI. No significant differences in ICP were noted between groups A and B before and after HBO(2) treatment until 3.5 h after trauma. At 4 h, for the first time, the difference became significant (P = 0.025; n = 11) and remained significant (P < 0.05) for all measurement points until end of monitoring, when mean ICP values reached 37.17 +/- 14.25 and 20.25 +/- 2.63 mm Hg in groups A and B, respectively. Linear approximation models showed different trends (b1 = 3.80 +/- 0.23; r(2) = 0.65, P < 0.001 and b1 = 1.56 +/- 0.25; r(2) = 0.77, P < 0.001) for groups A and B, respectively. Covariance analysis confirmed significant differences between slopes for groups A and B (F = 148.04, P < 0.001; df = 2,177), i.e., a significant difference in mean rate of ICP elevation. By the end of the experiment, 3 out of 7 rats from group A had died, but none from group B. We conclude that the application of HBO(2) during the early phase of severe FPBI significantly diminished ICP elevation rate and decreased mortality level.

Optimal dosing as a necessary condition for the efficacy of hyperbaric oxygen therapy in acute ischemic stroke: a critical review.

The effectiveness of hyperbaric oxygen therapy (HBOT) in clinical and experimental acute ischemic stroke (AIS) has been controversial for many years. However, in the literature, no data was found on the dose/effect of HBOT in patients with AIS. We analyzed retrospectively the published data of clinical studies performed in different hyperbaric centers (a total of 265 patients). The dose of HBOT (DHBOT) was calculated considering the product intrabarochamber pO2 (ATA), the duration of a single HBOT exposure (hours), and the number of HBOT treatments. Efficacy of HBOT (EfHBOT) data regarding the number of patients who showed significant clinical improvement of their neurologic status in the course of the treatment HBOT (the percentage of the total number of patients). The level of EfHBOT in each study was compared with a corresponding value of DHBOT. A comparison of the data shows a pronounced tendency for higher values of EfHBOT as the level of the average values of the total DHBOT increases. The coefficient of correlation between these parameters appears to be fairly high (r = 0.92). The maximum possible value of EfHBOT is 100%, which corresponded to the average values of DHBOT at a level of no less than 30 agreed units. The examined data suggest that applying optimal total DHBOT may provide a maximum possible EfHBOT in treating patients with AIS.