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Query: UMLS:C0242706 (hyperoxia)
 5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Toxicity to the central nervous system (CNS) by hyperbaric oxygen (HBO) presumably relates to increased production of reactive oxygen species. The sites of generation of reactive oxygen species during HBO, however, have not been fully characterized in the brain. We investigated the relationship between regional generation of hydrogen peroxide (H2O2) in the brain in the presence of an irreversible inhibitor of catalase, aminotriazole (ATZ), and protection from CNS O2 toxicity by a monoamine oxidase (MAO) inhibitor, pargyline. At 6 ATA of oxygen, pargyline significantly protected rats from CNS O2 toxicity whereas ATZ enhanced O2 toxicity. In animals pretreated with ATZ, HBO inactivated 21-40% more catalase than air exposure in the six brain regions studied. Because ATZ-mediated inactivation of catalase was H2O2 dependent, the decrease in catalase activity during hyperoxia was proportional to the intracellular production of H2O2. Pargyline, administered 30 min before HBO, inhibited MAO by greater than 90%, prevented ATZ inhibition of catalase activity during HBO, and reversed the augmentation of CNS O2 toxicity by ATZ. These findings indicate that H2O2 generated by MAO during hyperoxia is important to the pathogenesis of CNS O2 toxicity in rats.
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PMID:Prevention of H2O2 generation by monoamine oxidase protects against CNS O2 toxicity. 175 1

Decreased oxygen delivery and cellular hypoxia are important factors in the pathophysiology of hemorrhagic shock. We studied the effects of 100% oxygen at 1 and 3 ATA (atmosphere absolute) in a severe model of hemorrhagic shock induced by bleeding 50% of the total blood volume in rats. Post-treatment with 100% oxygen at 1 and 3 ATA maintained mean arterial blood pressure (MABP) in hemorrhaged rats at significantly higher values compared to untreated controls (P less than 0.01 at 1 and 3 ATA). Treatment with oxygen attenuated the increase in plasma activities of the lysosomal hydrolase cathepsin D (P less than 0.05 at 1 ATA; P less than 0.01 at 3 ATA). Oxygen at 3 ATA also attenuated the plasma accumulation of free amino-nitrogen compounds (P less than 0.05). Furthermore, hyperoxia prevented the final increase in hematocrit (P less than 0.05 at 1 ATA; P less than 0.01 at 3 ATA). Hemorrhaged rats treated with oxygen also exhibited a significantly longer survival time (P less than 0.01 at both doses), and higher survival rates (50% at 1 ATA and 100% at 3 ATA; P less than 0.05 and P less than 0.01, respectively) than untreated shock rats. No significant effect on any of the above mentioned variables was found in hemorrhaged rats treated with 7% oxygen at 3 ATA (oxygen pressure 0.2 ATA), indicating that all salutary effects can be attributed to oxygen and not to the increased ambient pressure per se. Our results indicate that 100% oxygen in normobaric and hyperbaric conditions exerts important beneficial effects in hemorrhagic shock and may be a useful drug for the treatment of this condition.
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PMID:Oxygen therapy in hemorrhagic shock. 204 10

The effect of inhibition of rat brain glutathione reductase, under conditions of normoxia and hyperoxia, on tissue ratios of reduced:oxidized glutathione was tested. Under conditions of normoxia, inhibition of brain glutathione reductase by approximately 50%, had no effect on reduced or oxidized glutathione in any of the three brain regions analyzed. After exposure of rats to 4 ATA 100% oxygen for one hour, in the presence of the same degree of enzyme inhibition, significant increases in oxidized glutathione in the cortical and subcortical areas of the brain were detected. Coupled with small, but nonsignificant decreases in reduced glutathione, a highly significant decrease in the ratio of reduced:oxidized glutathione was demonstrated in these two brain regions. These results indicate that under the conditions of an increased oxidizing environment, inhibition of brain glutathione reductase enhances the oxidative stress experienced by this organ.
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PMID:The effect of 1,3 bis-(2-chloroethyl)-1-nitrosourea on rat brain glutathione status under conditions of normoxia and hyperoxia. 234 84

Rats exposed to hyperbaric hyperoxia experience severe central nervous system and lung toxicity. Exogenous glutathione administration has been shown to protect rats from the effects of hyperbaric hyperoxia. To explore the hypothesis that decreases in tissue glutathione (GSH) could increase the susceptibility of rats to hyperbaric hyperoxia, we administered diethyl maleate (DEM) (a compound that conjugates with GSH and rapidly lowers tissue levels) and measured tissue GSH levels. DEM administration decreased plasma GSH by 86%, liver GSH by 82%, and brain GSH by 45% between 2 and 4 h after injection with values returning to normal by 24 h. We then treated rats with DEM or saline and began exposure at 2 h after treatment to 100% oxygen at 4 ATA. Time-to-convulsion and time-to-death were recorded. Rats that received DEM 2 h before exposure seized earlier and died earlier than controls. Intraperitoneal administration of GSH to DEM-treated rats abolished the enhanced toxicity occurring during a hyperbaric hyperoxic exposure. DEM appears to increase the toxicity of rats exposed to hyperbaric hyperoxia by lowering tissue GSH levels, and replenishment of lung and brain GSH by exogenous administration reverses these effects.
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PMID:Depletion of tissue glutathione with diethyl maleate enhances hyperbaric oxygen toxicity. 236 Jun 43

Research on endotoxin protection from oxygen toxicity is presently limited to the rat model since only rats have been protected by endotoxin. This study reports that endotoxin also extends survival of adult male mice in hyperoxia (greater than 99% oxygen at 1 ATA). Initially, 4-month-old male mice were treated with Boivin-extracted E. coli endotoxin and placed in hyperoxia. Zymosan-primed mice receiving 2 or 10 micrograms endotoxin, and unprimed mice receiving 10-40 micrograms endotoxin, showed moderate protection against hyperoxia; 11/15 Boivin-treated mice survived 120 hours exposure to hyperoxia with time-of-death in hyperoxia = 126.7 +/- 4.4 hours (mean +/- SEM, n = 15). This contrasts with untreated male mice; 0/4 survived 120 hours exposure to hyperoxia with mean survival = 103.5 +/- 3.5 hours. Mice receiving 20 or 60 micrograms Westphal-extracted endotoxin were not protected nor were older female mice receiving 20 micrograms Boivin-extracted endotoxin. This study suggests that age, sex, the extraction method used to obtain endotoxin, and possibly the time of year when endotoxin is administered, are important variables in allowing endotoxin to extend survival of mice in hyperoxia.
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PMID:Endotoxin extends survival of adult mice in hyperoxia. 240 1

In order to clarify the early phenomena involved in the lung reaction to hyperoxia, twenty adult male rats were exposed to 100% oxygen at 1 ATA. Morphological pulmonary lesions were detectable after only 24 h hyperoxia, and included vasoconstriction and perivascular oedema, bronchiolar constriction, and pericyte reaction. The lesions were irregularly scattered within the lung parenchyma and occurred preferentially in areas centred on bronchiolo-vascular stems. Even at the latest stages, pulmonary heterogeneity was obvious, from the coexistence of areas damaged at different times. Neuro-epithelial-bodies were found under the bronchiolar epithelium; the morphological aspect of the neuro-endocrine cells observed was consistent with hyperoxia-induced modulation of their secretory activity. Taken together, our findings show the speed of development of hyperoxia-induced pulmonary changes and raise some pathogenic considerations.
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PMID:Early bronchopulmonary lesions in rat lung after normobaric 100% oxygen exposure and their evolution. A light and electron microscopic study. 249 93

Exposure of rats to 100% O2 at high pressure (greater than 2.0 ATA) results in generalized convulsions and death within several hours. The tripeptide, glutathione, has been shown to protect rats exposed to hyperbaric hyperoxia with delayed onset of seizures and prolonged survival. To investigate the hypothesis that glutathione exerts its protective effects via the glutathione redox cycle, we injected selenium-deficient rats and their selenium-supplemented controls with either glutathione (1 mmol/kg) or an equivolume of saline before exposure to 100% O2 at 4 ATA. Selenium-deficient rats exhibit marked reduction in liver glutathione peroxidase activity (GSH-Px). Glutathione administration significantly delayed both the onset of seizures and time to death in the control animals. In selenium-deficient rats, however, glutathione administration was not protective, having no significant effects on time to seizure or time to death. We also measured changes in glutathione concentrations in lung, liver, and brain of these same groups of animals exposed either to hyperbaric hyperoxia or to room air. In control rats, lung and brain glutathione concentrations did not change with the hyperbaric exposure regardless of glutathione pretreatment status, but hepatic glutathione concentration declined significantly during the exposure when glutathione was not supplied. If these animals were pretreated with glutathione, the decline in hepatic glutathione concentrations did not occur. In selenium-deficient rats, the hyperbaric exposure did not result in changes in lung, brain, or liver glutathione concentrations either in the glutathione-pretreated or in the saline-pretreated animals. Exogenous GSH administration does not protect selenium-deficient rats from hyperbaric hyperoxia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of selenium deficiency on glutathione-induced protection from hyperbaric hyperoxia in rat. 261 Feb 68

Hyperoxia affects O2 chemoreception in the highly perfused carotid bodies and causes a reduction of the ventilatory hypoxic drive (HD) as was shown for anesthetized cats and awake rats. We looked for a quantitative description of such an effect on HD as a function of both O2 pressure and exposure duration. Ventilation of rats was measured using the barometric method before and after hyperbaric O2 (HBO) exposure, at either air, 80% O2, or 4% O2. We used three exposure durations: 180, 550 and 900 min. The O2 pressure ranged between 1.2 and 3.0 ATA. At each time duration we used four to five groups of rats at a range of O2 pressures that yielded the full scale of effect on HD but avoided obvious lasting difficulties in breathing. HBO caused a reduction of breathing frequency and elevation of tidal volume in both air and 80% O2 but almost no change in minute ventilation. Hypoxic minute ventilation (4% O2) decreased after HBO, mainly through reduced frequency. HD was described by a power function of O2 pressure for each HBO duration. HD did not decline below 20% of the full control response. Ventilatory HD diminution is pictured as a function of both O2 pressure and HBO duration. The dependency of HD on exposure time and on pressure is similar to other known toxic effects of HBO.
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PMID:Attenuation of hypoxic ventilation by hyperbaric O2: effects of pressure and exposure time. 270 14

Prolonged exposure of C57B16 mice to pure O2 at 1 ATA induced pulmonary edema associated with involution of lymphoid system and depressed immunity. The consequences of these toxic events were evaluated by 1) mortality rate, 2) determination of pulmonary water, 3) thymic and splenic cellularity, and 4) humoral (primary antibodies) and cellular (mitogenic) immune responses. Pretreatment of mice with 125 mg kg-1 of diethyldithiocarbamate (DDC) several days before exposure to O2 resulted in 1) an increase in animal survival (92-100% vs. 59% O2 controls), 2) a reduction in pulmonary edema, 3) partial stabilization of thymus and spleen lymphocyte populations, and 4) restoration of the humoral response (specific antibodies appeared earlier than in O2 control animals) and improvement of the mitogenic proliferative response of the spleen cells after hyperoxia. None of these effects were observed when DDC treatment coincided with the beginning of exposure. Our results indicated that DDC protects mice from both pulmonary and lymphoid hyperoxic injury, but only in a partial manner. It is suggested that the mechanism of this antioxidative property is indirect.
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PMID:Diethyldithiocarbamate provides partial protection against pulmonary and lymphoid oxygen toxicity. 300 45

To evaluate the relative contributions of three possible mechanisms that can be advanced to explain the observation that hyperoxia decreases serotonin uptake by endothelial cells, we examined the effect of high O2 tensions on Na+-K+-ATPase activity, ATP content, and plasma membrane fluidity in cultured endothelial cells. Confluent monolayers of pulmonary artery and aortic endothelial cells were exposed to 95% O2 (hyperoxia) or 20% O2 (controls) in 5% CO2 at 1 ATA for 4-42 h. Exposure to high O2 tensions had no effect on Na+-K+-ATPase activity or ATP content in pulmonary artery or aortic endothelial cells in culture. However, hyperoxia decreased the fluidity of the plasma membrane of pulmonary artery and aortic endothelial cells in culture, and the time course for the decrease in fluidity parallels that of the hyperoxic inhibition of serotonin transport. These results indicate that hyperoxia decreases fluidity in the hydrophobic core of the plasma membranes of cultured endothelial cells. Such decreases in plasma membrane fluidity may be responsible for hyperoxia-induced alterations in membrane function including decreases in transmembrane transport of amines.
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PMID:Hyperoxia reduces plasma membrane fluidity: a mechanism for endothelial cell dysfunction. 300 28


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