Basic physiology of hyperbaric oxygen in brain

Abstract

Oxygen is the proverbial 'double-edged sword' in that it is a necessity for life in moderation and toxic and detrimental to life in excess. This too is the dilemma in hyperbaric oxygen (HBO) treatment in cerebral ischemic-anoxic insults such as stroke, head injury, near drowning, asphyxia, cardiac arrest, etc., i.e. the brain at risk, where regions of ischemia are beside regions of marked hyperemia. The natural heterogeneity of normal brain tissue oxygenation compounds the problem with different microvascular brain regions living at various levels of oxygenation from 0 to arterial PO(2) as an added complication. The application of HBO, whether normobaric or hyperbaric, will result in brain tissue oxygenation ranging from normoxic to highly hyperoxic with the latter possibly exacerbating the injury sustained. On this basis, the application of multiple therapeutic interventions may be considered, for example, HBO in combination with free radical scavengers or inhibitors of free radical generating enzymes. Despite these difficulties in moderating oxygen delivery to treat cerebral ischemic-anoxic insults, overwhelming preclinical evidence indicates that HBO administered during or within 2 hours post-insult effectively attenuates the severity of brain damage sustained. The primary disconnection between pre-clinical and clinical efficacy of HBO then appears to be the time of application. Clinically, HBO therapy is applied at the earliest 6 hours post-insult but usually between 12 hours or longer post-insult. Pre-hospital application of HBO may be required for clear-cut demonstration of clinical efficacy.

Effect of hyperbaric oxygen on lipid peroxidation and visual development in neonatal rats with hypoxia-ischemia brain damage

“…Animal experiments and clinical trials have shown that HBO performed within 6 h after HIBD may achieve favorable outcomes and promote the long-term neurological recovery (3)(4)(5)(6). In addition, numerous studies in China have demonstrated that HBO can reduce the disability and mortality of HIBD (7).…”

The possible protective mechanism of Hyperbaric oxygen (HBO) in memory impairments induced by Aβ25–35 in rats

“…Food pellets and water were freely available throughout the experiment. Forty-eight rats were randomly divided into four groups: control group (rats with no injection), Sham group (physiological saline injected), model group (Aβ 25-35 injected) and HBO group (Aβ [25][26][27][28][29][30][31][32][33][34][35] injected+2ATA HBO treatment). Aβ [25][26][27][28][29][30][31][32][33][34][35] (SIGMA, USA, A4559) was dissolved at a concentration of 1g/L in sterile saline and incubated at 37°C for 7 days before use.…”

“…The present study aimed to determine the effect of Hyperbaric oxygen (HBO) on Aß 25-35 induced cognitive deficits and oxidative stress and apoptosis effects in rats. Rats were given an injection of aggregated Aß [25][26][27][28][29][30][31][32][33][34][35] . After treatment with HBO for 20days, the learning and memory ability, hippocampus neuronal apoptosis, the activity of SOD, GSH content and the MDA level and mRNA and proteins expression of Bcl-2 and Bax were detected.…”

“…The deposition of Aβ in the hippocampus and temporal cortex is recognized as an early and critical event in the pathogenesis of AD [2]. Aβ peptide fragment 25-35 (Aβ [25][26][27][28][29][30][31][32][33][34][35] ), an active fragment of toxic Aβ, has been shown to be toxic to neurons [3] and have the potential to induce oxidative stress and impairment of spatial learning and memory correlate with cell loss in rat hippocampus [4].…”

“…After treatment with HBO for 20days, the learning and memory ability, hippocampus neuronal apoptosis, the activity of SOD, GSH content and the MDA level and mRNA and proteins expression of Bcl-2 and Bax were detected. Our results demonstrated that HBO could significantly improved the apoptosis hippocampus neuronal induced by Aß [25][26][27][28][29][30][31][32][33][34][35] , involving the improvement of the learning and memory impairment, which accompanied of increasing the gene and protein expression of bcl-2 and enhancing the activity of SOD and GSH content. These findings suggest that treatment of HBO might prevent the Aß 25-35 induced learning and memory impairment by increasing the gene and protein expression of bcl-2 and enhancing the activity of SOD and GSH content to alleviate the apoptosis hippocampus neuronal.…”