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

The total Mg2+-ATPase and Na+, K+-ATPase activity was studied in the fractions of "400 g X for 20 min" and "900 g X for 30 min" conditionally called the fraction of the external cellular membranes and total fraction of mitochondria. The subcellular fractions were isolated from great hemispheres and stem part of the rat brain. The brain of control animals and those during a severe spasmodic attact induced by the oxygen action at a pressure of 6 ati was studied. The total ATPase activity is established to be practically the same in the studied brain areas and unchanged with hyperoxia. Hyperoxia accompanying by convulsions results in an increase in the activity of Mg2+-ATPase and in a decrease in that of Na+, K+-ATPase both in the cerebral cortex and the stem part. The authors suppose that the decrease in the enzyme activity may occur due to an inhibitory effect on it of the lipids reoxidation products formed in the brain with hyperoxia.
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PMID:[ATPase activity of subcellular rat brain fractions following hyperoxia]. 13 79

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 effect of hyperbaric oxygenation (6 atmospheres) on the content of polyamines spermine and spermidine in the rat brain and liver was studied. A decrease of the spermidine content in the brain and liver during oxygen convulsions and four hours after decompression was revealed. The spermine content in the brain during oxygen convulsions decreased as well, but four hours after decompression it increased significantly not eaching the control level. The spermine content in the liver failed to alter during oxygen convulsions, but the next four hours rose sharply. The role of polyamines in the regulation of protein biosynthetic processes under hyperoxia is discussed.
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PMID:[Spermine and spermidine polyamines in the brain and liver of rats under hyperoxic action]. 62 75

Activity of glutaminase (both phosphate-dependent and phosphate-independent forms of the enzyme) as well as glutamate decarboxylase activity were studied in hyperoxia (6 ati) and under conditions of protection by means of arginine from the effect of hyperoxia. In hyperoxia activity of phosphate-dependent and phosphate-independent forms of glutaminase was decreased by 45% and 51%, respectively. At the same time, glutamate decarboxylase activity was decreased by 32%. Arginine showed a protective effect, delaying the time of oxygen convulsions onset by 2.5-fold. The low activities of glutaminases were maintained but the glutamate decarboxylase activity was increased and even exceeded the control level by 29%. A mechanism of the protective effect of arginine is discussed.
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PMID:[Protective effect of arginine in hyperoxia. Activity of cerebral glutaminase and glutamate decarboxylase]. 66 82

Water-insoluble proteins of rat brain were studied as affected by hyperbaric oxygenation (oxygen pressure 6 at.ga. convulsion state). Solubilization of proteins under effect of hyperoxia and triton X-100 increases by 32-81%. Changes in the amino acidic composition of proteins extracted by 0.5% triton X-100 are characterized by an increase in the amount of aspartic acid, cystin, leucine and isoleucine and by a decrease in the amount of histidine, arginine and methionine. Electrophoresis in 7.5% polyacrylamide gel of proteins in the 0.5% triton X-100 extract showed changes in the number and mobility of protein bands.
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PMID:[Effect of hyperoxia on water-insoluble proteins of the brain]. 68 68

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 concentration-related viscosity (formula: see text) of DNP-solutions in 4.0 M urea, 0.0005 M tris-buffer (pH 7.5) isolated from cell nuclei of cerebral hemispheres and testicles was determined for mongrel and Wistar rats of 5 groups: I -- normal, II -- after the action of 6 gauge atmospheres of pure oxygen before convulsions beginning, III -- 1 hour, IV -- 4 hours, V -- 12 hours after decompression. It was noted that the concentration-related viscosity of these DNP was equal both for mongrel and inbred rats. No differences in the polymerity degree of brain DNP were detected in all groups of animals under study. The viscosity of testicular DNP was found to decrease by 13.3% 1 hour and 10.3% 4 hours after decompression, whereas 12 hours after it does not differ from the control. Differences in the resistance degree of the brain and testicular DNP to the action of hyperoxia may depend on the cell division rates in these tissues.
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PMID:[Degree of polymerization of rat cerebral hemisphere and testicular DNP-complex during hyperoxia and following it]. 86 17

Double-beam recording visible cytospectrophotometry showed that 30-minute convulsions due to 6 at. ga. hyperoxia result in a decrease in the RNA and protein content per cell in layer V neurons of the cerebral motor cortex and in the motoneurons of spinal cord anterior horn in albino rats. A decrease is also found in the glial cells, except for a spinal cord neuroglia. A decrease in the RNA content in the neurons as well as the protein content in the neurons and glia of the spinal cord is more pronounced than in similar structures of the cerebral motor cortex. The quantity of RNA and protein in the neurons and neuroglia of the cerebral cortex remins decreased for 24 h after hyperoxia cessation. In the spinal cord motoneurons the level of the RNA and protein becomes normal 3 h after hyperoxia, and 24 h later it exceeds the initial one.
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PMID:[Effect of hyperoxia on RNA and protein concentration in cortical and spinal motor neurons and surrounding neuroglia]. 86 37

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

Two hundred suckling mice from 20 litters were used for determining their functional development of the hyperoxic convulsion mechanism. It was found that 1 to 12-day-old mice did not develop convulsion when they were subjected to oxygen under high pressure. The hyperoxic convulsion was observed in 1 of 10 13-day-old (10%), 3 of 10 14-day-old (30%), 16 of 20 15-day-old (80%) and all of 16-day-old mice (100%). This finding indicates that the hyperoxic convulsion mechanism of the young mice takes 13-16 days for functional maturation. Besides, it was shown that hyperoxia could cause pulmonary damage, the incidence of which also increased with age of suckling mice.
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PMID:High oxygen pressure-induced convulsions in suckling mice. 123 37


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