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1

Hyperbaric treatment results in decreased ROS production in neonatal hypoxia-ischemia rat model

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Gamdzyk M. , Ziembowicz A. , Salinska E.

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nr Suppl.1

EN

Encephalopathy caused by birth asphyxia results in significant mortality and long-term morbidity. In our previous studies we proved that HBO reduces brain damage in experimental model of birth asphyxia by almost 60%. The aim of present study was to evaluate the effect of hyperbaric oxygen (HBO) on reactive oxygen species (ROS) production and antioxidative enzymes activities – catalase (CAT) and glutathione peroxidase (Gpx) in 7-day old rat brain after hypoxia-ischemia (H-I). In the experimental model of H-I the left (ipsilateral) common carotid artery ligation is followed by 75 min hypoxia. HBO (2,5 ATA) was applied 1, 3 or 6 h after H-I for 60 min. Treatment was repeated for 3 following days. DCF test showed that H-I causes almost 4-fold increase in ROS production in ipsilateral hemisphere, while HBO reduced it by 40%, 24% and 18%, applied 1, 3 and 6 h after H-I, respectively. H-I resulted in 32% increase in catalase activity, probably as a compensation to high ROS concentration. HBO treatment reduced this increase to 4, 5 and 16%, respectively, which is probably a consequence of reduced oxygen radicals production. Similar pattern was observed in activity of Gpx. Our results suggest that HBO reduce synthesis of ROS (which manifests in decreased DCF fluorescence) and also decrease antioxidative enzymes activity. This may be one of the mechanism of HBO neuroprotective and diminishing brain injury effect.

2

Hypobaric hypoxia and hyperbaric treatment prevents neuronal damage and affect antioxidative activity in neonatal hypoxia-ischemia rat model

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Gamdzyk M. , Ziembowicz A. , Salinska E.

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tom 73

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nr 1

PL

Hypoxic–ischemic encephalopathy (HIE) remains a serious condition that causes significant mortality and long-term morbidity. The aim of the study was to evaluate the effect of hyperbaric oxygen (HBO), hyperbaric air (HBA) and hypobaric hypoxia (HH) on neonatal hypoxic–ischemic (HI) brain injury within a therapeutic window of 1–6 h. We used an experimental model of perinatal hypoxia–ischemia on 7-days old rats, where left (ipsilateral) common carotid artery ligation is followed by 75 min hypoxia. HBO, HBA (2.5 ATA) and HH (0.5 atm air) were applied at 1, 3 or 6 h after HI for 60 min. Treatment was repeated for 3 following days. Brain injury was assessed by comparing ipsilateral hemisphere and contralateral hemisphere weight. Based on the evaluation of weight ratio, HH, HBO and HBA treatment, regardless of time of treatment initiation, resulted in significant reduction of brain weight loss. We observed that HBO reduced brain damage by 58.1%, 57.6% and 54.9%, respectively to the time of treatment initiation (1, 3, 6 h after HI), HBA decreased the damage by 29.9%, 38.1% and 22.0% (respectively). HH also significantly lessened brain weight loss, from 38% after untreated hypoxia–ischemia to 12.9%, 23.1% and 23.8% after HH application respectively 1, 3 and 6 h after hypoxia–ischemia. Superoxide dismutase (SOD) activity and glutathione (GSH) concentration were also measured. HI caused decrease in GSH concentration and 6-fold increase in SOD activity in ipsilateral, but not contralateral hemisphere. HBO treatment applied 1 and 3 h after HI significantly increased GSH concentration and decreased SOD activity, the effect of HBA was less pronounced. HH treatment resulted in additional increase in SOD activity in both hemispheres. However, GSH concentration after HH returned to control values. HBO and HBA altered the expression of cytoplasmic SOD1, and these changes corresponded to changes in SOD activity, suggesting significant role of this protein in neuroprotecting properties of HBO. Our results suggest that HBO, HBA and HH may serve in attenuation of the effects of HI. Early treatment gives better results in brain protection. Our results suggest that HBO and HBA probably reduce synthesis of free oxygen radicals, which manifests in decreased SOD activity. HH however, seems to act on different mechanism, because it enhances SOD activity. It may be beneficial, as it helps to neutralize superoxide anion production, provided that this SOD activity increase is accompanied by activation of glutathione peroxidase (GPx) and catalase (CAT). This assumption needs further investigation.

3

Hyperbaric preconditioning combined with post-ischemic hyperbaric therapy prevents ischemia-evoked damage to CA1 hippocampal neurons of Mongolian gerbils

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Malek M. , Gamdzyk M. , Duszczyk M. , Ziembowicz A. , Sobczuk A. , Lazarewicz J. , Salinska E.

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nr S

EN

Lack of the clinically effective pharmacological neuroprotection in different forms of brain ischemia increased the interest in alternative methods of therapy, like hypothermia or induction of brain tolerance by pre- and post-conditioning. The hyperbaric oxygen (HBO) therapy (2.5 atm) applied after ischemia or traumatic brain injury is one of the proposed but still controversial methods. The aim of this study was to find whether HBO and hyperbaric air (HBA) preconditioning followed by hyperbaric treatment applied for 60 min at different times after 3 min forebrain ischemia in gerbils will give a significant protection. The effects of both treatments on brain temperature and animal behaviour were also examined. A telemetric system to measure brain temperature was used and for behavioural observations a nest building test. The density of viable CA1 pyramidal neurons was also quantified. Our results show that HBO preconditioning combined with HBO postischemic therapy significantly reduced ischemia-evoked increase of brain temperature. HBA was also effective. Both treatments significantly increased gerbils’ ability to build a nest in comparison to untreated animals. The best effect was observed when postischemic therapy was applied 1 h after ischemia, but it was also effective 3 h after ischemia. Morphological analysis showed that HBO preconditioning combined with HBO postischemic treatment applied 1 h after ischemia significantly reduced neuronal damage in CA1 region of hippocampus resulting in 85% of surviving neurons compared to 18% of surviving CA1 neurons in the brains of animals subjected to ischemia but not treated with HBO. Our results show that HBO preconditioning combined with HBO therapy after forebrain ischemia in gerbils gives morphological protection which is accompanied by good behavioral results. Apart from inducing tolerance mediated by mild oxidative stress, HBO may affect blood oxygenation and other factors instrumental in brain protection.

4

Antidepressant-like and anxiolytic-like effects of mild hypobaric hypoxia in mice: possible involvement of neuropeptide Y

75%

Duszczyk M. , Gamdzyk M. , Ziembowicz A. , Boguszewski P. M. , Lazarewicz J. W. , Salinska E.

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nr 4

EN

Previous studies have demonstrated that repeated submission of rats to mild hypobaric hypoxia reduces the persistent behavioral and hormonal depressive symptoms induced by exposure to footshock in the learned helplessness paradigm. The aim of this study was to determine whether hypoxic preconditioning of mice can also induce antidepressant- and anxiolyticlike effects that are detectable with the other commonly used behavioral tests, and to determine whether these effects are accompanied by an increase in neuropeptide Y (NPY) in the hippocampus, which may suggest the involvement of NPY in these mechanisms. The intermittent mild hypobaric hypoxia was generated by 2-h exposure of mice to 0.47 atm for 3 consecutive days. In the tail suspension test a significant decrease in the duration of immobility was observed 24 h, but not 48 h after the last hypobaric session. The elevated plus maze trials performed 48 h after preconditioning showed a significant increase in the frequency of open arm entries, a reduction in the duration of closed arm occupancy and substantially more time spent in the open arms in comparison to the control groups. The open field test demonstrated the absence of increases in general activity or unspecific exploratory behavior in hypoxia-preconditioned mice. The EIA test detected a statistically significant but relatively weak increase in the NPY content in the hippocampus 24 h after preconditioning. Together, our data demonstrate that preconditioning of mice with intermittent mild hypobaric hypoxia induces anxiolytic- and antidepressantlike effects. They are accompanied by up-regulation of NPY which may suggest its mechanistic role.