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

The CNS tolerance to prolonged normobaric hyperoxia (NH) was investigated using alterations in regional cerebral metabolic rate for glucose (rCMRgl) as a sensitive measure of brain oxygen poisoning. Conscious rats were continuously exposed either to air or to oxygen for 24 h at atmospheric pressure inside a closed and ventilated environmental chamber. The rCMRgl was measured during ongoing air or oxygen exposures by [14C]2-deoxyglucose (2-DG) autoradiographic technique. No significant difference in the rCMRgl of 29 neuroanatomical structures investigated was found between two groups of air- and oxygen-exposed rats. At the same time however, a significant reduction in the respiratory frequency (f) was observed only in the oxygen-exposed rats. It is suggested that brain energy metabolism is not affected at least up to 24 h NH in conscious rats. The NH-induced reduction in f on the other hand, may be due to alterations in afferent inputs from peripheral and central chemoreceptors or lung stretch receptors. Furthermore, since slight changes in rCMRgl of small neuroanatomical structures are not detectable by limited resolution power of [14C]2-DG autoradiographic technique, a subtle NH-induced damage to central respiratory control mechanisms cannot yet be ruled out.
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PMID:Effect of prolonged normobaric hyperoxia on regional cerebral metabolic rate for glucose in conscious rats. 316 79

Oxygen toxicity in the non-ischemic and non-hypoxic heart has not been reported. In an experiment on isolated rat heart lung preparation, the effects of superoxide dismutase (SOD) on oxygen toxicity during hyperoxic perfusion were evaluated with intramyocardial high energy phosphates and the release of creatine phosphokinase (CPK) in the perfusate blood. Although there were no significant differences in high energy phosphates between SOD-treated and untreated hearts, the CPK release from the SOD-treated hearts was significantly less than from the untreated hearts. SOD increased the oxygen pressure of perfusate blood, too. These results indicate that hyperoxia induced cardiac and lung cell damage which was protected by SOD.
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PMID:Protective effects of superoxide dismutase against oxygen toxicity in rat's heart lung preparation. 369 65

Oxygen toxicity is a major complication of normobaric hyperoxia in therapeutic settings. Because alterations in membrane function occurring as a consequence of peroxidation of membrane phospholipid fatty acids may be an early event in the pathogenesis of oxygen-induced injury, we studied the effects of hyperoxia on the ability of the membrane to repair itself by incorporating fatty acid via the pathway for deacylation and reacylation in situ. Although the lung is the major site of clinically significant injury, the erythrocyte is also directly exposed to elevated PO2 in vivo. In this study, incorporation of [9,10(-3)H]-oleic acid into phospholipid has been measured in sheep erythrocytes in vitro after exposure of four animals to normobaric hyperoxia in vivo. [9,10(-3)H]-Oleic acid incorporation into erythrocyte phospholipid decreased within 24 hours and reached 50% of pre-exposure levels after 70 hours of exposure to 100% O2. No significant change in the fatty acid composition of membrane phospholipid was detected under these conditions. In contrast to the results with intact cells, incorporation of [9,10(-3)H]-oleic acid into phospholipid by isolated erythrocyte membranes prepared from the cells of two animals increased after 70 hours of exposure to 100% O2, indicating that the inhibition of fatty acid incorporation in intact erythrocytes does not result from irreversible inactivation of the enzymes involved in acylation of endogenous lysophospholipid. Because the ability of cells to replace membrane phospholipid fatty acids via deacylation and reacylation in situ could be important in the maintenance of membrane integrity during oxidative stress, the decrease in fatty acid incorporation by erythrocytes in vitro may reflect an early event in the pathogenesis of oxygen-induced cellular injury.
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PMID:Normobaric hyperoxia in vivo inhibits fatty acid incorporation into sheep erythrocyte phospholipid in vitro. 396 68

Weanling male rats were fed semi-purified diets supplemented with 0, 60, or 600 IU X g-1 vitamin E or 0, 100 or 1000 ppb selenium. One group was injected daily with vitamin E at a rate equivalent to consumption of 60 IU X kg-1. Animals from all groups were sacrificed after exposure to normobaric oxygen or air for 48 h. Lung tissue was analyzed for the combined activity of prostaglandin dehydrogenase and reductase. Using the decline in enzyme activity as an indicator of susceptibility to oxygen poisoning, protection against hyperoxia was directly related to the level of vitamin E supplementation. Selenium supplemented at 100 ppb provided significant protection when compared to 0 ppb or 1000 ppb. The latter dose may have been marginally toxic. We conclude that dietary supplementation of vitamin E and selenium may influence the relative susceptibility of an animal to pulmonary oxygen poisoning.
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PMID:Effect of dietary vitamin E or selenium on prostaglandin dehydrogenase in hyperoxic rat lung. 608 85

Rats treated with low doses of bacterial endotoxin have been shown to be protected from oxygen poisoning under normobaric conditions. Induction of lung activity of the antioxidant enzymes glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and catalase (CAT) has been reported to occur with endotoxin administration. GSH-Px is a selenoenzyme and selenium-deficient rats have decreased lung GSH-Px activity and enhanced lung toxicity during a hyperoxic exposure. To determine whether bacterial endotoxin administration can provide protection for animals with decreased antioxidant defenses, selenium-deficient and control rats received daily intraperitoneal injections of 250 micrograms/kg bacterial endotoxin or phosphate-buffered saline (PBS) during normobaric exposure to greater than 95% O2. Both groups of animals were protected from hyperoxia by bacterial endotoxin administration despite the extremely low lung GSH-Px activity in the selenium-deficient rats. GSH-Px, SOD, or CAT activities were not induced in the selenium-deficient rats by 48 hr (the time when the selenium-deficient rats treated with PBS began to die). In the selenium-deficient rat, mechanisms other than enzyme induction appear to be providing early protection from hyperoxia.
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PMID:Endotoxin protects selenium-deficient rats from hyperoxia. 669 Jun 38

Survival time in conditions of hyperbaric oxygenation were measured in trout and eels in water, and in frog in water or in gas phase at various temperatures. In eel and trout, the gill surface is altered within 90 min at 15 ata pressure of oxygen. Survival times of the frog during hyperoxia in aquatic or gaseous conditions are only slightly different, in spite of the marked difference in the oxygen concentration of the two media. Oxygen toxicity is well correlated with the aerobic metabolic rate, (1) in a given species adapted to various temperatures; (2) in trout eel and frog observed at the same temperature. The differing O2 toxicities in homeothermic and poikilothermic animals are also related to the differences in metabolic activity.
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PMID:A comparative study of oxygen toxicity in vertebrates. 697 78

Weanling male rats were fed a semi-purified diet containing 10, 20, 40 or 60% of calories as fat having a constant polyunsaturated/saturated fatty acid ratio of 0.7. After 21-28 d of feeding, animals from each treatment group were exposed to pure oxygen at one atmosphere absolute for up to 72 h. Some animals were sacrificed after 0 or 48 h of oxygen exposure and lung tissue analyzed for the activities of the hexose monophosphate shunt and prostaglandin dehydrogenase/reductase. Other animals were exposed to hyperoxia until death. With increasing dietary fat content, the pre-exposure activities of the two enzymes decreased and oxygen-induced mortality increased. There was no dietary effect on enzyme activities after 48 h of hyperoxia. We concluded that both dietary fat content and the pre-exposure activity of prostaglandin dehydrogenase/reductase influenced the relative susceptibility to pulmonary oxygen poisoning.
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PMID:Effect of dietary fat on pulmonary enzymes and toxicity during normobaric hyperoxia. 711 50

The content of N-acetyl-l-asparaginic acid, CoA, CoASAc and the N-acetylaspartate amunohydrolase activity was determined in cerebral areas of rats at the normal level and at different stages of oxygen poisoning. At the preconvulsive stage of the oxygen poisoning the content of N-acetyl-l-asparaginic acid decreases in cerebral hemispheres by 54, in the midbrain and diencephalon by 23, in the medulla oblongata--by 27, and in the cerebellum by 21%. The N-acetylaspartate aminohydrolase activity, vice versa, increases by 58, 62, 57 and 60%, respectively. The content of CoA and CoASAc is unchanged. At the convulsive stage of hyperoxia the content of N-acetyl-l-asparaginic acid in the cerebral hemispheres and cerebellum is unchanged in the midbrain and diencephalon increases by 21% and in the medulla oblongata-by 15%. The n-acetylaspartate aminohydrolase activity in he cerebral hemispheres, midbrain, diencephalon and medulla oblongata is unchanged, in the cerebellum it increases by 100%. The CoA content in the brain decreases by 20%, CoASAc-by 16%.
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PMID:[Effect of hyperbaric oxygenation on N-acetyl-L-asparaginic acid metabolism in different cerebral areas]. 725 21

Oxygen toxicity is attributed to the reaction of oxygen metabolites with cellular components leading to cell destruction. Activation of latent human neutrophil interstitial collagenase by reactive oxygen species has been demonstrated. The potential role of collagenases in hyperoxic lung injury has not been investigated. We studied the effect of hyperoxia on newborn rat lung water content, morphology and ultrastructure, interstitial (type I) and type IV collagenase gene expression and type I and IV collagenolytic activity. We observed that hyperoxia causes pulmonary edema, alters newborn rat lung morphology in a sequential manner and produces ultrastructural alterations, induces type I and increases type IV collagenase mRNA expression, and increases type I and IV collagenolytic activity. A role for type I and IV collagenase in hyperoxic newborn lung injury or in the recovery following the injury is proposed.
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PMID:Hyperoxia induces interstitial (type I) and increases type IV collagenase mRNA expression and increases type I and IV collagenolytic activity in newborn rat lung. 799 51

Time to onset of hyperbaric oxygen-induced convulsions was measured in mice and rats exposed to hyperbaric oxygen (515-585 kPa) under conditions of low humidity (dry gas, < 10% relative humidity) or in a humidified environment (60% relative humidity). At all pressures tested, the duration of convulsive activity was markedly increased (P < 0.001), because of the earlier onset of severe generalized convulsions, in the groups of rodents exposed to the higher humidity. Pulmonary oxygen poisoning was determined by increases in lung wet and dry weights. Such pulmonary damage was also significantly (P < 0.001) increased in the humidified groups. Hyperoxic toxicity was also measured in rats and mice exposed to approximately 100% oxygen (normobaric hyperoxia) under conditions of 30 or 62% relative humidity. In contrast to the results obtained with hyperbaric oxygen exposure, there was slightly less toxicity in the rodents maintained at 62% compared with 30% humidity in normobaric hyperoxia.
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PMID:Effect of humidity on hyperoxic toxicity. 830 49


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