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

The content of homocarnosine, gamma-amino butyric acid and histidine was studied in the brain of newborn, 1, 7, 14, 21 and 30-day rabbits in normalcy and under hyperoxia. For 30 days of the postnatal life the amount of peptide in the animal brain is 2.5, histidine 1.6, gamma-amino butyric acid--2.2 times as high. At the preconvulsive stage of oxygen poisoning the content of homocarnosine lowers sharply in the brain of rabbits of all age groups. The most considerable decrease is observed in the brain of 14, 21 and 30-day rabbits by 53, 60 and 85%, respectively. The content of gamma-amino butyric acid lowers only in the brain of 21 and 30-day animals by 39 and 47%, respectively; the content of histidine in these animals under hyperoxia, vice versa, increases by 10 and 25%.
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PMID:[Content of homocarnosine, gamma-amino butyric acid and histidine in brain tissue of different age normal rabbits and under hyperoxia]. 45 27

A rise of hemoglobin concentration accompanied by an increase of the total iron in the blood serum of white mice was found under oxygen pressure of 4 atm for an hour (preconvulsive state) and 6 atm (convulsive state). Changes in correlations of hemoglobin fractions in the blood serum were detected in both stages of oxygen poisoning by disc-electrophoresis in 7.5% polyacrylamide gel. A rise of transferrin concentration under these conditions (hyperoxia) was observed. The deflections occurred were less pronounced following administration of urea to the animals before hyperbaric oxygenation.
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PMID:[Hemoglobin, transferrin and total iron content in the blood serum in hyperoxia and during the protective action of urea]. 46 81

The homocarnosine content and homocarnosine synthetase activity were studied in the brain of rats in normal state and under hyperoxia. The homocarnosine content is higher in phylogenetically old brain areas as compared with that in the cerebral hemispheres. Its nonuniform distribution in the brain is associated with different activity of homocarnosine-carnosine synthetase in the corresponding brain areas. At the preconvulsive stage of oxygen poisoning the homocarnosine content in all the brain areas does not change, the homocarnosine-carnosine synthetase activity is 32% lower. At the convulsive stage of hyperoxia the homocarnosine amount in the cerebral hemisphere decreases by 33%, in the midbrain and diencephalon -- by 70, in the medulla oblongata -- by 60, in the cerebellum -- by 58%. The decrease in the homocarnosine content correlates with that in the activity of homocarnosine-carnosine synthetase in the corresponding brain areas; in the cerebral hemispheres -- by 33%, in the midbrain and diencephalon -- by 50, in the medulla oblongata -- by 49, in the cerebellum -- by 40%.
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PMID:[Homocarnosine content and homocarnosine-carnosine synthetase activity in brain areas of hyperoxic rats]. 51 82

The content of glutamic, asparaginic and gamma-aminobutyric (GABA) acids in norm and under hyperoxia was determined in different cerebral areas of susliks living in places at different heights above sea level. In susliks at a height of 1700-2000 m above sea level the content of glutamate aspartate and GABA lowers significantly as compared to that in susliks at a height of 500-600 m above sea level. Under the effect of oxygen 6 at. ga at the 22nd minute on the average there occur convulsions in susliks living both in high mountains and middle mountains. Acute oxygen poisoning is not accompanied by noticeable shifts in the content of free dicarboxylic amino acids in the studied cerebral areas of middle-mountain susliks and is characterized only by an increase of the GABA content in the cerebellum. In high-mountain susliks the content of glutamate under these conditions increases in great cerebral hemispheres, while the asparate content lowers in cerebral hemispheres and cerebellum. In the latter the drop in the content of GABA is statistically significant.
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PMID:[Content of dicarboxylic acids and GABA in normal suslik brain and under the effect of oxygen at higher pressure]. 55 58

The content of homocarnosine, GAMA, histidine, glutaminic acid and activity of glutamate decarboxylase were studied in four regions of rats brain: cerebral hemispheres, midbrain, diencephalon and cerebellum, in norm and under hyperoxia. A considerable decrease in the content of homocarnosine, GAMA and histidine is observed in all the studied regions of the rat brain in the convulsion stage of oxygen poisoning. A decrease in the glutamate decarboxylase activity is the reason for a drop in the GAMA content. Homocarnosine in the brain is bound functionally with the GAMA level.
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PMID:[Metabolism of homocarnosine and gamma-amino butyric acid in different regions of rat brain under hyperoxia]. 72 92

The influence of hypoxic acclimatization at altitudes of 0, 5,000, or 15,000 ft on the relative susceptibility to acute oxygen poisoning was determined in 288 adult female mice. After acclimatization periods of 1, 2, 4, or 8 wk, the mice were exposed to oxygen at high pressures (OHP) of 4, 6, or 9 ATA and the times to convulsion and death recorded. A factorial analysis of variance indicated that altitude and OHP level had inverse, log-linear effects on both parameters. The duration of acclimatization progressively decreased the time to death. The onset of convulsions and death was independent of body weight. There were significant interactions on the measured parameters between various combinations of altitude, OHP level, and duration of acclimatization. While alterations in the metabolism of gamma-aminobutyric acid and high-energy compounds are common to both hypoxia and hyperoxia, the most plausible explanation of the results relates to the decrease in buffer base induced by hypoxic acclimatization which might have caused CO2 potentiation of OHP symptoms.
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PMID:Relative susceptibility of altitude-acclimatized mice to acute oxygen toxicity. 112 Jul 52

For studying the mechanism of hyperoxia toxic effect on metabolism in the rat brain localization of lysosomes enzymes - acid phosphatase, DNase II and acid peptid-hydrolases were investigated in the brain subcellular fractions under different phases of oxygen poisoning and in the in vitro experiments. Under hyperoxia redistribution of the lysosome enzymes is found between the fraction enriched with lysosomes and the soluble one. The character of redistribution evidences for disturbance of permeability in the brain lysosome membranes under hyperoxia. Urea possessing a protective effect under these conditions prevents from labilization of lysosome enzymes which is evoked by the effect of oxygen hyperoxia. When studying manifestation of the effect of lysosome hydrolases release on the substrate level there were found constancy of DNA content in the brain under hyperoxia and a decrease in polymeric property of the brain DNA an hour after the beginning of the terminal phase of oxygen poisoning.
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PMID:[Lysosome enzymes of brain in hyperoxia and under the effect of urea]. 120 6

Oxygen toxicity to the lung is characterized by injury of the pulmonary capillary endothelium with progressive loss of functioning alveolar-capillary units. Current concepts suggest that the risk of O2 toxicity in human subjects is greatly increased with O2 concentrations exceeding 50% to 60%, although there are no data to support a cellular basis for this apparent threshold of toxicity. Our study suggests that a cellular threshold may exist in human pulmonary endothelial cells for O2 toxicity. Hyperoxia was directly toxic to cultured human pulmonary artery endothelial (HPAE) cells, with impairment of replicative function, expressed as growth impairment (GI) index, monitored by two independent parameters: cell number determination and tritiated thymidine incorporation. Impaired cell growth occurred as early as 8 hours after beginning exposure to 95% O2 and with concentrations as low as 60% during a 48-hour incubation. For example, 60% O2 resulted in an impairment of HPAE cell growth at 48 hours with a GI index (cell number) of 37.5 +/- 2.1 (p less than 0.001, comparison with control cells in normoxia). Furthermore, 95% O2 impaired cell growth, as monitored by tritiated thymidine incorporation, as early as 8 hours after exposure (GI index of 43.6 +/- 4.9) however, the injury was completely reversible when cells were reincubated in normoxia for 6 hours (GI index of 4.2 +/- 4.7), p less than 0.001. O2 toxicity was associated with an increase in cellular glutathione levels but was not associated with a detectable loss of antioxidant enzyme activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Oxygen-mediated impairment of human pulmonary endothelial cell growth: evidence for a specific threshold of toxicity. 246 57

Although oxygen has been known to be toxic for more than 200 years, the clinical importance of oxygen toxicity was not appreciated until an epidemic of retrolental fibroplasia occurred in the early 1950s. Oxygen at high partial pressures is toxic to the respiratory, cardiovascular, nervous, and gastrointestinal systems. Toxicity results from the formation of oxygen-free radicals. These arise within mitochondria as oxygen is reduced to water, as byproducts of prostaglandin and thromboxane synthesis, and by the xanthine oxidase catalyzed reduction of xanthine or hypoxanthine. They are also produced by activated macrophages as part of the immune response. Superoxide anion is the radical most commonly produced. It dismutes to hydrogen peroxide, which is able to diffuse through lipid membranes. Hydrogen peroxide reacts with transition metals to produce the highly reactive hydroxyl radical which can initiate chain reactions of lipid peroxidation leading to cell rupture. Oxygen radical scavengers such as superoxide dismutase and catalase protect the body against normal levels of oxygen-free radicals. Oxygen toxicity can result from either reperfusion of ischemic tissue or prolonged exposure to high concentrations of oxygen. Limiting hyperoxia to maintain arterial oxygen percent saturation (SaO2) greater than or equal to 90% is recommended.
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PMID:Oxygen toxicity: an introduction. 267 91

1. Small mammals have been used to study the effects of O2 toxicity. The aim of the present study was to investigate whether body size should be considered when applying the results of these studies to man. 2. Oxygen toxicity is enhanced as perfusion and metabolism increase: specific animal tissues of high perfusion are more susceptible to O2 toxicity. Exercise, high metabolic rate, and increased brain blood flow enhance O2 toxicity. 3. Increased specific O2 consumption and perfusion as body mass decreases may enhance O2 toxicity in small mammals. 4. Survival time in normobaric hyperoxia (1 atm O2) and the time to first appearance of convulsions in hyperbaric oxygen (4-5 atm) were collected from the literature and showed no relation to body size. 5. Known difference in antioxidant enzyme activity cannot explain the findings. 6. Independence of tissue PO2 on body size, or equal rates of free radical formation and degradation, are suggested as possible mechanisms. 7. Small mammals can serve as a good model for O2 toxicity in man.
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PMID:Oxygen toxicity is not related to mammalian body size. 290 37


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