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

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

By the method of Astrup-Zigaard-Andersen the acid-base balance in the blood of men and dogs exposed to hypercapnic atmospheres with a normal, increased and decreased oxygen content was investigated in 164 experiments. Variations in the acid-base equilibrium were compared with changes of physiological functions. The relationship between the acid-base balance and the carbon dioxide concentration as well as the oxygen concentration in the breathing air was established. The toxic effects of sharp hypercapnia and hyperoxia were shown to cumulate. The positive effect of moderate hypercapnia on the tolerance to normobaric hypoxia in long-term experiments was noted.
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PMID:[Blood acid-base equilibrium during breathing of hypercapnic gas mixtures]. 112 99

Tissue gas tensions were measured in healing rabbit tibias by means of an implanted Silastic tonometer. During the course of the healing, tissue oxygen tensions increased progressively and carbon dioxide tensions underwent a gradual decline. In all phases of repair, bone tissue gases responded to systemic hyperoxia and hypercarbia. Occlusion of local circulation resulted in tissue anoxia and accumulation of carbon dioxide. Acetazolamide, an inhibitor of carbonic anhydrase, elevated the carbon dioxide tension in the bone but not in the blood which supports earlier data indicating the presence of a functional carbonic anhydrase system in actively metabolizing bone tissue.
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PMID:Tissue oxygen and carbon dioxide tensions in healing rabbit tibias. 114 19

To evaluate the effect of different levels of arterial oxygen content on hemodynamic parameters during exercise nine subjects performed submaximal bicycle or treadmill exercise and maximal treadmill exercise under three different experimental conditions: 1) breathing room air (control); 2) breathing 50% oxygen (hyperoxia); 3) after rebreathing a carbon monoxide gas mixture (hypoxia). Maximal oxygen consumption (Vo2 max) was significantly higher in hyperoxia (4.99 1/min) and significantly lower in hypoxia (3.80 1/min) than in the control experiment (4.43 1/min). Physical performance changes in parallel with Vo2 max. Maximal cardiac output (Qmax) was similar in hyperoxia as in control but was significantly lower in hypoxia mainly due to a decreased stroke volume. A correlation was found between Vo2 max and transported oxygen, i.e., Cao2 times Amax, thus suggesting that central circulation is an important limiting factor for human maximal aerobic power. During submaximal work HR was decreased in hyperoxia and increased in hypoxia. Corresponding Q values were unchanged except for a reduction during high submaximal exercise in hyperoxia.
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PMID:Effect of changes in arterial oxygen content on circulation and physical performance. 115 May 96

Three to five hours after 5-hour exposure of rabbits to high oxygen pressure (2 ata) the erythropoietin proved to disappear from both the arterial and the venous blood plasma of the kidneys. At the same time the blood plasma from the renal vein began to suppress the mitotic activity of erythroblastic cells in the bone marrow culture. These data testify to the fact that under hyperbaric hyperoxia the kidneys secreted the inhibitor of erythropoiesis. No erythropoiesis inhibitor was revealed 24 hours after the hyperoxia.
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PMID:[Erythropoietic function of the kidneys under conditions of abnormally high oxygen pressure]. 119 66

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

Pulmonary gas exchange has been studied in 14 healthy smokers and 16 healthy nonsmokers (mean age: 36 years) breathing hypoxic, normoxic and hyperoxic gas mixtures, in a sitting position, at rest and on exercise. Alveolar-arterial oxygen tension difference is increased in smokers in hypoxia, at rest and on exercise, and the pulmonary diffusing capacity for oxygen is decreased. In normoxia the alveolar-arterial oxygen tension difference is increased on exercise. There is no difference between the two groups in hyperoxia. For the whole group there exists a negative relationship between (A-a)DO2 in normoxia and the diffusion indices measured on exercise. Arterio-alveolar carbon dioxide tension difference and the ratio physiological dead space/tidal volume are almost identical in both groups in any condition. A diffusion defect seems to be the more constant alteration of gas exchange in asymptomatic smokers.
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PMID:Pulmonary gas exchange in asymptomatic smokers and nonsmokers. 120 96

Distribution of N-acetyl-alpha-l-glutaminic peptide (NAAG) and N-acetyl-l-aspartic acid (NAAA) in brain of different age chickens was studied in norm and under hyperoxia. The content of NAAG in the chicken brain during the first four weeks of life is more than 6 times as high and that of NAAA-4.3 times as high as their level in newborns. After the effect of a high pressure of oxygen (3.25 atm. on birds for 60 min) the content of NAAG lowers considerably in the brain of 14-, 21- and 30-day chickens, that of NAAA in them increases.
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PMID:[Content of N-acetyl-alpha-l-aspartyl-l-glutamate in bird brain in ontogenesis and under hyperoxia]. 120 54

The active and passive transport of radioactive calcium was studied in experiments on the brain and liver mitochondria, homogenates of brain and erythrocytes of albino rats subjected to the toxic effect of oxygen under pressure. The processes of the Ca2+ active transport preparations under examination are established to be inhibited after the effect of hyperoxia. The passive transport is considerably less dependent on the previous effect of oxygen. A conclusion is drawn on the prevailing sensitivity of the calcium energy-dependent transport to the damaging effect of hyperoxia.
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PMID:[Effect of hyperoxia on calcium transport in mitochondria of brain and liver]. 121 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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