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

The oxygen consumption rates (VO2) of 9 albacore tuna, Thunnus alalunga (8.5-12 kg) were measured at sea in a swimming respirometer to determine the effects of relative swimming velocity, ambient O2 tension, and water temperature. Significant positive relationships were obtained between tail-beat frequency and relative speed and between relative speed and VO2. The albacore metabolic rate was not appreciably affected by exposure to water temperatures ranging from 13.5 degrees to 16.9 degrees C. Brief exposure to hyperoxia (200-400 mmHg), which was done to reduce the initial stress upon fish in the respirometer, did not affect VO2. Hypoxia (50-99 mmHg), however, did tend to reduce VO2 and affect swimming velocity.
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PMID:O2 tension, swimming-velocity, and thermal effects on the metabolic rate of the Pacific albacore Thunnus alalunga. 292 Aug 15

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

We recently reported that endotoxin infusion before O2 exposure significantly reduced or delayed the onset of pulmonary edema formation and respiratory failure by reducing the oxidant stress of O2 exposure. Despite these beneficial effects of endotoxin treatment, lung microvascular permeability eventually increased, but postmortem lung water content was less than expected. Prolonged O2 breathing blunts or abolishes the pulmonary constrictor response to alveolar hypoxia in some species, and it is possible that the loss of this response could contribute further to edema formation. To determine whether the reduction in lung edema observed in endotoxin-treated, O2-exposed lambs was linked to the preservation of hypoxic pulmonary vasoconstriction (HPV), we measured pulmonary vascular resistance before and after 8 min of isocarbic hypoxia (inspired O2 fraction 0.12) during each day of O2 exposure. In six control lambs, the pressor response to hypoxia was abolished after 72 h in O2, and the lambs developed respiratory failure shortly thereafter. In six endotoxin-treated lambs, HPV was preserved for as long as 144 h of O2 exposure. In two control O2-exposed lambs in whom HPV was abolished, the infusion of either angiotensin or prostaglandin H2 analogue increased pulmonary vascular resistance by greater than 75%. We conclude that in lambs 1) hyperoxia abolishes the pulmonary vascular response to hypoxia, 2) endotoxin pretreatment reduces acute O2-induced lung injury and preserves the pulmonary constrictor response to hypoxia, and 3) the loss of HPV during O2 exposure may be the result of oxidant-mediated injury to the hypoxia response itself and not the result of diffuse damage to the vasoconstrictor effector mechanism.
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PMID:Effect of endotoxin pretreatment on the pulmonary vascular response to hypoxia in O2-exposed lambs. 305 85

Growth of the chick embryo is accelerated by brief (72-hr) exposure to 60% O2 beginning on day 16 of incubation, and acute (2-3 hr) hyperoxia stimulates oxygen consumption (VO2). However, the increment in VO2 that accompanies acute exposure to 60% O2 is only about half that required to account for the degree of growth acceleration observed during 72 hr of hyperoxia. We tested the hypothesis that the magnitude of the oxygen-induced change in embryonic metabolism depends on the length of exposure by making daily measurements of embryonic VO2 during brief (72-hr) exposure to 60% or 15% O2. White leghorn eggs were incubated in 21% O2 for 15 days. On day 16 the experimental eggs were switched to 60% or 15% O2; control eggs were maintained in 21% O2. Oxygen consumption and CO2 production (VCO2) were measured daily. Embryo and organ weights were compared on day 18. Wet and dry weights of briefly hyperoxic embryos were significantly greater than those of normoxic controls. The relative increase in wet weight was significant for the heart and liver but not the brain. Oxygen consumption increased 7% relative to control after 24 hr of hyperoxia and 17% after 72 hr; VO2/gm embryo was 9% greater than control on day 18. Normal growth deceleration was exaggerated by hypoxia; mean wet and dry weights of the briefly hypoxic embryos were significantly less than those of controls. Organ wet weights also showed growth retardation, although the relative decrease in brain weight was not significant. Body water concentration increased in briefly hypoxic embryos. Oxygen consumption was 13% less than control after 24 hr and 17% less after 72 hr.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Modulation of growth and metabolism of the chick embryo by a brief (72-hr) change in oxygen availability. 311 Mar 63

Among vertebrates, adult amphibians are known to be especially tolerant to exposure to high environmental oxygen tensions. To clarify the basis for this high O2 tolerance, adult Rana ridibunda perezi frogs were acclimated for 15 days to water-air phases with either 149 mm Hg O2 (normoxia) or 710 mm Hg O2 (hyperoxia). At the end of the acclimation, various morphometric and biochemical parameters related to oxidative stress were measured in seven organs and tissues. Hyperoxia acclimation did not change either the total weight of the animals or the total and relative wet weights of the organs studied, except for the brain, which showed weight increases in the hyperoxic group. In vivo tissue peroxidation increased in the kidney; decreased in the skeletal muscle and skin; and did not change in the liver, lung, brain, and heart after hyperoxic exposures. Whereas liver, lung, and skin showed glutathione peroxidase (GSH-Px) activities with both cumene hydroperoxide (cumene-OOH) and H2O2 as substrates, skeletal muscle only showed H2O2 GSH-Px activity. Hyperoxia acclimation did not change either catalase (CAT) or GSH-Px activities in any organ, except for the liver in which CAT activity was induced by hyperoxia. Thus hyperoxia tolerance in this species does not need the induction of H2O2-detoxifying enzymes in the majority of the organs. It is suggested that the high O2 tolerance of this amphibian species is related to its comparatively high constitutive GSH-Px activities.
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PMID:Effect of hyperoxia acclimation on catalase and glutathione peroxidase activities and in vivo peroxidation products in various tissues of the frog Rana ridibunda perezi. 318 4

Fluorescence anisotropy measurements are widely used as sensitive indicators of cell membrane fluidity. 1-[4-(trimethylamino)phenyl]-6-phenyl hexa-1,3,5-triene (TMA-DPH) is a cationic fluorescent aromatic hydrocarbon that anchors at the lipid-water interface of membrane lipid bilayers. Its uptake into porcine pulmonary artery and aortic endothelial cells was monitored and the probe remained specifically localized on the cell surface for at least 4 h. It can therefore be recommended for use for specific plasma membrane lipid fluidity measurements in these cells. The effect of hyperoxia on plasma membrane fluidity was measured by using TMA-DPH. In both cell types, hyperoxic damage resulted in decreases in plasma membrane fluidity. Recovery was achieved 48 h after a 42-h hyperoxic exposure. These results indicate that TMA-DPH is a sensitive probe of plasma membrane lipid domains of pulmonary artery and aortic endothelial cells and that hyperoxia causes reversible changes in the physical state of superficial lipid domains of the plasma membrane of these cells.
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PMID:Plasma membrane fluidity measurements in intact endothelial cells: effect of hyperoxia on fluorescence anisotropies of 1-[4-(trimethylamino)phenyl]-6-phenyl hexa-1,3,5-triene. 333 80

The effects of cytochrome P-450 inducers on O2 toxicity were studied in mice. We first examined three cytochrome P-450 inducers, which differ by their specific tissue affinity: phenobarbital sodium (PB), essentially active in the liver, and 3-methylcholanthrene (3-MC) and beta-naphthoflavone (BNF), which are also active in the lung. Both BNF and 3-MC increased the survival rate and significantly decreased pulmonary edema (pulmonary water and wet-to-dry weight ratio) in C57BL/6J mice exposed to hyperoxia (O2 greater than or equal to 95%), whereas PB had no protective effect. In the second part of this study, we compared the action of BNF in two strains of mice. In one (C57BL/6J), cytochrome P-450 can be induced by aromatic hydrocarbons, whereas in the other (DBA/2J) cytochrome P-450 is not inducible by these compounds. Protection against O2 toxicity was assessed in terms of lethality and pulmonary edema and of lung lipid peroxidation (assessed by measuring malondialdehyde). BNF only protected against O2 toxicity in the inducible strain. This protective effect of BNF on O2 toxicity in C57BL/6J mice was associated mainly with a large increase in the components of the cytochrome P-450 system (cytochrome P-450 and cytochrome b5) in the lung. The activity of pulmonary superoxide dismutase was also slightly increased, but the enhancement was not statistically significant. In contrast, in DBA/2J mice neither the components of the cytochrome P-450 system nor the activity of superoxide dismutase showed any increase.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Genetic differences in response to pulmonary cytochrome P-450 inducers and oxygen toxicity. 337 72

The effect of intrapleural pressure on the hypoxic pulmonary vasoconstrictor (HPV) responses to atelectasis and hypoxia were measured in two groups of anesthetized closed chest dogs. The right lung was continuously ventilated with 100% O2. The left lung was initially ventilated with 100% O2 (hyperoxia) but subsequently underwent either reabsorption atelectasis (atelectasis; group I) or ventilation with a hypoxic gas mixture (hypoxia; group II). The mean intrapleural pressure in the left hemithorax was 5.4 cm H2O during hyperoxia, but with left lung atelectasis decreased significantly to -3.8 cm H2O by 15 minutes and to -4.2 cm H2O by 90 minutes. Venous admixture (% VA) increased significantly from 10.3% during hyperoxia to 33.2% at 15 minutes of left lung atelectasis and to 34.6% at 90 minutes. However, after sternotomy with the left lung still atelectatic, the %VA decreased significantly to 25.4% For the hypoxia group, %VA increased significantly from 9.2% during hyperoxia to 29.9% at 15 minutes of left lung hypoxia and 25.1% at 90 minutes. HPV diverted blood flow away from both atelectatic lung and hypoxic lung. However, due to the negative intrapleural pressure generated during left lung resorption atelectasis when the chest was closed, HPV was less effective during atelectasis than during hypoxia.
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PMID:The effect of pleural pressure on the hypoxic pulmonary vasoconstrictor response in closed chest dogs. 339 64

The effect of normobaric hyperoxia on voluntary salt intake was investigated in conscious male SHR (n = 16). The animals were housed individually in metabolic cages and given free access to food, water and 2.5% NaCl-solution. The exposure of the rats to 40% oxygen in nitrogen for four days resulted in a significant enhancement of the salt intake. The present experiment further clarifies the relationship between chemoreceptor activity and salt intake. Hypobaric hypoxia as well as the pharmacological substance almitrine, both stimuli of the carotid bodies, decrease the voluntary salt intake in SHR significantly, whereas hyperoxia, characterized by lowering of the chemoreceptor activity, increases the salt intake. Our studies support the hypothesis that chemoreceptor activity has a modulating influence on salt appetite in SHR.
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PMID:The link between chemoreceptor activity and voluntary salt intake in spontaneously hypertensive rats: a hypothesis. 345 82

Red cell structure and function were examined in rats exposed to 80% oxygen: 20% nitrogen for five days and compared with red cells from air-breathing animals. Evidence of red cell destruction was noted in the animals exposed to hyperoxia. Osmotic fragility was found to be reduced in red cells from oxygen exposed rats (p less than 0.05), also, red cell haemolysis in hydrogen peroxide was noted to be greater (p less than 0.001) in these animals. Inorganic phosphate ion transport was significantly reduced (p less than 0.001) in the red cells from rats receiving oxygen for 5 days. The results demonstrate a decreased ability of the red cell to transport anions and suggest an impairment of the normal movement of water across the membrane following exposure to oxygen.
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PMID:Inorganic phosphate transport across the red blood cell membrane: the effect of exposure to hyperoxia. 362 12


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