Inhibition of GABA-Transaminase and GABA-Transporters in the Brain by Vigabatrin and Tiagabine Prevents Seizure Development in Rats Breathing Hyperbaric Oxygen

Oxygen is a potent cerebral vasoconstrictor, but excessive exposure to hyperbaric oxygen (HBO2) can reverse this vasoconstriction by stimulating brain nitric oxide (NO) production, which increases cerebral blood flow (CBF)—a predictor of O2 convulsions. We tested the hypothesis that phosphodiesterase (PDE)-5 blockers, specifically sildenafil and tadalafil, increase CBF in HBO2 and accelerate seizure development. To estimate changes in cerebrovascular responses to hyperoxia, CBF was measured by hydrogen clearance in anesthetized rats, either control animals or those pretreated with one of these blockers, with the NO inhibitor Nω-nitro-l-arginine methyl ester (l-NAME), with the NO donor S-nitroso- N-acetylpenicillamine (SNAP), or with a blocker combined with l-NAME. Animals were exposed to 30% O2 at 1 atm absolute (ATA) (“air”) or to 100% O2 at 4 or 6 ATA. EEG spikes indicated central nervous system CNS O2 toxicity. The effects of PDE-5 blockade varied as a positive function of ambient Po2. In air, CBF did not increase significantly, except after pretreatment with SNAP. However, at 6 ATA O2, mean values for CBF increased and values for seizure latency decreased, both significantly; pretreatment with l-NAME abolished these effects. Conscious rats treated with sildenafil before HBO2 were also more susceptible to CNS O2 toxicity, as demonstrated by significantly shortened convulsive latency. Decreases in regional CBF reflect net vasoconstriction in the brain regions studied, since mean arterial pressures remained constant or increased throughout. Thus PDE-5 blockers oppose the protective vasoconstriction that is the initial response to hyperbaric hyperoxia, decreasing the safety of HBO2 by hastening onset of CNS O2 toxicity.

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Reduced Matrix Metalloproteinase-9 Activity and Cell Death After Global Ischemia in the Brain Preconditioned with Hyperbaric Oxygen

Brain Edema XIV - Acta Neurochirurgica Supplementum ◽

10.1007/978-3-211-98811-4_7 ◽

2009 ◽

pp. 47-49 ◽

Cited By ~ 20

Author(s):

Robert P. Ostrowski ◽

Vikram Jadhav ◽

Wanqiu Chen ◽

John H. Zhang

Keyword(s):

Cell Death ◽

Matrix Metalloproteinase ◽

Hyperbaric Oxygen ◽

Matrix Metalloproteinase 9 ◽

Global Ischemia ◽

The Brain ◽

Metalloproteinase 9

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Acutely administered melatonin reduces oxidative damage in lung and brain induced by hyperbaric oxygen

Journal of Applied Physiology ◽

10.1152/jappl.1997.83.2.354 ◽

1997 ◽

Vol 83 (2) ◽

pp. 354-358 ◽

Cited By ~ 68

Author(s):

Marta I. Pablos ◽

Russel J. Reiter ◽

Jin-Ing Chuang ◽

Genaro G. Ortiz ◽

Juan M. Guerrero ◽

...

Keyword(s):

Lipid Peroxidation ◽

Oxidative Damage ◽

Hyperbaric Oxygen ◽

Antioxidative Enzymes ◽

Melatonin Receptors ◽

Cellular Damage ◽

Oxygen Exposure ◽

Glutathione Status ◽

Hyperbaric Oxygen Exposure ◽

The Brain

Pablos, Marta I., Russel J. Reiter, Jin-Ing Chuang, Genaro G. Ortiz, Juan M. Guerrero, Ewa Sewerynek, Maria T. Agapito, Daniela Melchiorri, Richard Lawrence, and Susan M. Deneke. Acutely administered melatonin reduces oxidative damage in lung and brain induced by hyperbaric oxygen. J. Appl. Physiol. 83(2): 354–358, 1997.—Hyperbaric oxygen exposure rapidly induces lipid peroxidation and cellular damage in a variety of organs. In this study, we demonstrate that the exposure of rats to 4 atmospheres of 100% oxygen for 90 min is associated with increased levels of lipid peroxidation products [malonaldehyde (MDA) and 4-hydroxyalkenals (4-HDA)] and with changes in the activities of two antioxidative enzymes [glutathione peroxidase (GPX) and glutathione reductase (GR)], as well as in the glutathione status in the lungs and in the brain. Products of lipid peroxidation increased after hyperbaric hyperoxia, both GPX and GR activities were decreased, and levels of total glutathione (reduced+oxidized) and glutathione disulfide (oxidized glutathione) increased in both lung and brain areas (cerebral cortex, hippocampus, hypothalamus, striatum, and cerebellum) but not in liver. When animals were injected with melatonin (10 mg/kg) immediately before the 90-min hyperbaric oxygen exposure, all measurements of oxidative damage were prevented and were similar to those in untreated control animals. Melatonin’s actions may be related to a variety of mechanisms, some of which remain to be identified, including its ability to directly scavenge free radicals and its induction of antioxidative enzymes via specific melatonin receptors.

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The effect of hyperbaric oxygen therapy on the nervous system. Systematic review

Polish Hyperbaric Research ◽

10.1515/phr-2015-0020 ◽

2015 ◽

Vol 53 (4) ◽

Cited By ~ 1

Author(s):

Sławomir Kujawski ◽

Agnieszka Kujawska ◽

Mariusz Kozakiewicz ◽

Romuald Olszański ◽

Piotr Siermontowski ◽

...

Keyword(s):

Nervous System ◽

Hyperbaric Oxygen ◽

Hyperbaric Oxygen Therapy ◽

Oxygen Therapy ◽

Arterial Blood ◽

Randomised Control Trials ◽

Methodological Problems ◽

The Brain ◽

Methods Of Treatment

Abstract Hyperbaric oxygen therapy (HBOT) is found among the interests of researchers who seek new methods of treatment of diseases of the nervous system. An increase of the partial pressure of oxygen in arterial blood within the appropriate range leads to numerous changes in the cells of the brain tissue. In this paper we analyse the results of selected articles describing HBOT used on pathologies of the nervous system such as stroke, autism, multiple sclerosis and cerebral palsy as well as in the course of research on animal models. The results are promising, although some studies struggled with numerous methodological problems and differences in the applied protocols, which resulted in conflicting results in individual interventions. In consequence, the need for further studies in randomised control trials and determination of the protocol by an international group of researchers dedicated to the use of HBOT was emphasised.

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