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

The effect of tumor necrosis factor-alpha (TNF) on hyperoxia-induced endothelial injury in vitro was investigated. TNF caused a time- and dose-dependent reduction in the number of viable pulmonary artery endothelial cells. The TNF-mediated endothelial cytotoxicity was more pronounced under hyperoxia (95% O2 and 5% CO2) than under normoxia (95% air and 5% CO2). Pretreatment of endothelial cells with TNF (0.01 micrograms/ml or 240 U/ml) for 18 h at normoxia reduced the intracellular concentration of total glutathione (GSH), whereas the concentration of oxidized GSH was increased. These TNF-treated endothelial cells were more susceptible to hyperoxia- or hydrogen peroxide-mediated cytotoxicity. TNF also induced changes in endothelial morphology and in the distribution and density of actin filaments. Exogenous GSH or L-2-oxothiazolidine-4-carboxylate, which enhanced endothelial GSH concentrations, partially protected endothelial cells against TNF-mediated cytotoxicity, morphologic changes, and actin filament redistribution, especially under the hyperoxic condition. These results suggest an important role of GSH in modulating endothelial response to TNF.
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PMID:Tumor necrosis factor enhances endothelial cell susceptibility to oxygen toxicity: role of glutathione. 195 83

The primary aim of this study was to determine the influence of systemic hyperoxia on sympathetic nervous system behavior at rest and during submaximal exercise in humans. In seven healthy subjects (aged 19-31 yr) we measured postganglionic sympathetic nerve activity to skeletal muscle (MSNA) in the leg, antecubital venous norepinephrine concentrations, heart rate, and arterial blood pressure during normoxic rest (control) followed by 3- to 4-min periods of either hyperoxic (100% O2 breathing) rest, normoxic exercise (rhythmic handgrips at 50% of maximum force), or hyperoxic exercise. During exercise, isocapnia was maintained by adding CO2 to the inspirate as necessary. At rest, hyperoxia lowered MSNA burst frequency (12-42%) and total activity (6-42%) in all subjects; the average reductions were 25 and 23%, respectively (P less than 0.05 vs. control). Heart rate also decreased during hyperoxia (6 +/- 1 beats/min, P less than 0.05), but arterial blood pressure was not affected. During hyperoxic compared with normoxic exercise, there were no differences in the magnitudes of the increases in MSNA burst frequency or total activity, plasma norepinephrine concentrations, or mean arterial blood pressure. In contrast, the increase in heart rate during hyperoxic exercise (13 +/- 2 beats/min) was less than the increase during normoxic exercise (20 +/- 2 beats/min; P less than 0.05). We conclude that, in healthy humans, systemic hyperoxia 1) lowers efferent sympathetic nerve activity to skeletal muscle under resting conditions without altering venous norepinephrine concentrations and 2) has no obvious modulatory effect on the nonactive muscle sympathetic nerve adjustments to rhythmic exercise.
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PMID:Hyperoxia lowers sympathetic activity at rest but not during exercise in humans. 203 99

Almitrine has potential as a tool for testing the physiological role of the peripheral chemoreceptor. The effects of almitrine on CO2 chemosensitivity were studied at rest and during light exercise using a constant inflow technique that avoids the hyperoxia of rebreathing methods. The steady-state ventilatory response to CO2 was measured in two groups of six normal men before and 150 min after 100 mg oral almitrine bismesylate or placebo. One group was studied at rest, the other while pedalling at 50 W. The resting group showed a significant increase in CO2 response slope after almitrine when compared with placebo but there was no significant change in the response intercept. During exercise the individual results were very variable and after almitrine no significant change was seen in either the response slope or intercept. Control ventilation was not affected by almitrine in either group. Even in the absence of marked hyperoxia the effect of almitrine on CO2 sensitivity at rest in small. The lack of effect at 50 W is against any important role for the peripheral chemoreceptor during light exercise but other interpretations are possible.
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PMID:The effect of almitrine on the steady-state ventilatory response to carbon dioxide at rest and during exercise in man. 211 16

1. The ventilatory sensitivity to carbon dioxide obtained from a step-ramp CO2 challenge was compared to the CO2 sensitivity from the steady-state method. 2. Experiments were performed in nine healthy male subjects against a background of hyperoxia and in two subjects against a background of normoxia. 3. In each subject experiments were performed in which the stepwise increase in end-tidal PCO2 above its resting value (A) was varied (range 0-2 kPa) and the subsequent rate of rise of end-tidal PCO2 in time (R) kept constant at 0.6 or 0.8 kPa min-1. 4. The results of the hyperoxic experiments show that the slope of the non-steady-state ventilatory response to CO2 (Sn) is greatly influenced by the magnitude of A. An increase of A of 1 kPa results in a 54% increase of the ratio non-steady-state ventilatory CO2 sensitivity to steady-state ventilatory CO2 sensitivity (Ss). The magnitude of R plays a minor role in determining Sn. The normoxic experiments gave similar results. 5. In experiments performed during hyperoxia Sn approximates Ss when the magnitude of A is 0.5 kPa. 6. The results are discussed and related to a physiological model. Simulations with representative values for the model parameters are in fair agreement with experimental values.
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PMID:On a pseudo-rebreathing technique to assess the ventilatory sensitivity to carbon dioxide in man. 211 56

1. The ventilatory response to isoxic square-wave challenges in end-tidal PCO2 was investigated at three levels of end-tidal PO2 (PET, O2) in nine healthy male subjects. 2. Twenty-seven responses against a background of mild hypoxia (PET, O2 approximately 10 kPa), sixty-seven against a background of normoxia (PET, O2 approximately 14.5 kPa) and seventy-six against a background of hyperoxia (PET, O2 approximately 70 kPa) were collected. 3. The breath-to-breath data were partitioned into a fast and a slow ventilatory component using a two-compartment model. 4. In the normoxic and hypoxic experiments the CO2 sensitivity of the fast component averaged to about 30 and 40% of the total CO2 sensitivity, respectively. In the hyperoxic experiments three subjects had no fast component in their response while in three others the CO2 sensitivity of the fast component averaged to about 24% of the total CO2 sensitivity. In the remaining three subjects the presence of a fast component was doubtful. 5. We argue that the fast component is due to the peripheral chemoreflex loop and the slow component to the central chemoreflex loop. 6. The central CO2 sensitivity and the apnoeic threshold (extrapolated end-tidal CO2 at zero ventilation in the steady state) were 15% smaller in hyperoxia than those in normoxia and hypoxia. In normoxia and mild hypoxia the central CO2 sensitivities were not significantly different. 7. We argue, that apart from peripheral oxygen-carbon dioxide interaction, there is evidence for central oxygen-carbon dioxide interaction in human subjects. 8. We conclude that in general there is a contribution to ventilation of the peripheral chemoreceptors during hyperoxia in man.
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PMID:The influence of oxygen on the ventilatory response to carbon dioxide in man. 212 61

After voluntary hyperventilation, normal humans do not develop a significant ventilatory depression despite low arterial CO2 tension, a phenomenon attributed to activation of a brain stem mechanism referred to as the "afterdischarge." Afterdischarge is one of the factors that promote ventilatory stability. It is not known whether physiological stimuli, such as hypoxia, are able to activate the afterdischarge in humans. To test this, breath-by-breath ventilation (VI) was measured in nine young adults during and immediately after a brief period (35-51 s) of acute hypoxia (end-tidal O2 tension 55 Torr). Hypoxia was terminated by switching to 100% O2 (end-tidal O2 tension of first posthypoxic breath greater than 100 Torr). Brief hypoxia increased VI and decreased end-tidal CO2 tension. In all subjects, termination of hypoxia was followed by a gradual ventilatory decay; hyperoxic VI remained higher than the normoxic baseline for several breaths and, despite the negative chemical stimulus of hyperoxia and hypocapnia, reached a new steady state without an apparent undershoot. We conclude that brief hypoxia is able to activate the afterdischarge mechanism in conscious humans. This contrasts sharply with the ventilatory undershoot that follows relief of sustained hypoxia, thereby suggesting that sustained hypoxia inactivates the afterdischarge mechanism. The present findings are of relevance to the pathogenesis of periodic breathing in a hypoxic environment. Furthermore, brief exposure to hypoxia might be useful for evaluation of the role of afterdischarge in other disorders associated with unstable breathing.
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PMID:Hypoxic exposure and activation of the afterdischarge mechanism in conscious humans. 212 78

The specific ventilatory flow rate (Vw), cardiac output (Vb) and blood respiratory parameters were determined in the carp (Cyprinus carpio) during hyperoxia. Vb changed little during moderate hyperoxia (240-330 Torr) but slightly increased during extreme hyperoxia (430-490 Torr) while Vw decreased. This means that the ventilation-perfusion ratio considerably decreased during hyperoxia. The CO2 tension (PCO2) of blood rose, causing a corresponding decrease in blood pH. The O2 tensions (PO2) of arterial and mixed venous blood increased but remained low (about 40 Torr and 15 Torr, respectively). Consequently, the hemoglobin in the arterial and mixed venous blood was not saturated with O2 (about 80 and 55%, respectively) even during extreme hyperoxia. This indicates that most of the O2 which is consumed by the fish remains transported in a combined form during hyperoxia. During hyperoxia, when the decreased Vw was artificially elevated to the normoxic level, the PO2 of arterial blood (PaO2) rose further and the PCO2 and pH of arterial blood became restored to the normoxic levels. This suggests that the CO2 retention and the depressed increase in PaO2 during hyperoxia are mainly due to the decrease in Vw in the carp.
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PMID:Ventilation, cardiac output and blood respiratory parameters in the carp, Cyprinus carpio, during hyperoxia. 212 16

CO2 single breaths have been performed in 7 men and 7 women in conditions of normoxia (FICO2 congruent to 0.13; FIO2 congruent to 0.21; FIN2 congruent to 0.66) and of hyperoxia (FICO2 congruent to 0.13; FIO2 congruent to 0.87). Ventilatory responses of the subjects and modifications of breathing pattern in the course of the CO2 tests were also explored in the two conditions. The results (mean +/- SEM) show that, whatever the oxygenation, men and women exhibit the same ventilatory response during a CO2 test from a qualitative point of view but with a smaller intensity in women (men: 0.37 +/- 0.088 LBTPS.min-1.Torr-1; women: 0.15 +/- 0.025 LBTPS.min-1.Torr-1; p less than 0.05). Considering men and women together, CO2 tests induced an increase of minute volume VE (p less than 0.001), VT (p less than 0.01) and rate of breathing (NS) but this response is decreased in hyperoxic conditions (p less than 0.05) mainly in men (men: 0.19 +/- 0.043 LBTPS.min-1.Torr-1; women: 0.11 +/- 0.023 LBTPS.min-1.Torr-1). These results show that sensitivity to transient hypercapnia and its interaction with hyperoxia are weaker in women than in men.
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PMID:CO2 chemoreflex drive of ventilation in man: effects of hyperoxia and sex differences. 212 2

Metabolites of arachidonic acid (AA) released into bronchoalveolar lavage fluid of animals exposed to hyperoxia have previously been implicated as mediators of pulmonary oxygen toxicity. The alveolar macrophage (AM) represents an important potential source of these eicosanoids. We have therefore investigated the effects of in vitro hyperoxia (95% O2/5% CO2) versus normoxia (95% air/5% CO2) on the metabolism of AA in the AM of the rat. Exposure to 95% O2 for up to 72 h did not impair the viability or affect the protein content of cultured AMs. Hyperoxia for 24 to 72 h increased the accumulation of free AA liberated from endogenous stores in cultures of resting AMs. Despite this increase in free AA, no changes in synthesis of thromboxane B2, prostaglandin (PG) E2, PGF2 alpha, leukotriene (LT) B4, or LTC4 were observed in resting AMs exposed to hyperoxia for up to 72 h. This was not due to degradation of eicosanoids in hyperoxia. However, formation of cyclooxygenase metabolites from exogenously supplied AA was reduced in hyperoxia-incubated AMs, suggesting that hyperoxia inhibited the cyclooxygenase enzyme. In AMs stimulated with calcium ionophore A23187, both AA release and synthesis of cyclooxygenase and lipoxygenase eicosanoids were augmented after incubation in hyperoxia for 24 to 72 h. The increase in A23187-stimulated LTB4 synthesis caused by hyperoxia was inhibited by the antioxidants catalase, superoxide dismutase, and the intracellular cysteine loading agent L-2-oxothiazolidine-4-carboxylic acid, suggesting that the augmentation by hyperoxia of A23187-induced AA metabolism was mediated by reactive oxygen metabolites. Thus, hyperoxia has complex effects on AA metabolism in the AM, which include the ability to augment the release of AA and formation of bioactive eicosanoids. These findings support a possible role for eicosanoid synthesis by the AM in the pathogenesis of oxygen toxicity of the lung.
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PMID:Complex effects of in vitro hyperoxia on alveolar macrophage arachidonic acid metabolism. 215 14

The relative contributions of O2- and CO2-sensitive chemoreceptor information to centrally generated respiratory patterns have changed dramatically during vertebrate evolution. Chemoafferent input from branchial O2 chemoreceptors modulates centrally generated respiratory patterns but is not critical for respiratory rhythmogenesis in fishes. In air-breathing fishes, branchial O2 chemoreceptors monitoring internal and external stimuli control the relative contributions of the gills and air-breathing organ to net ventilation, and chemoafferent input is necessary for initiating air breathing. In the transition from water to air breathing by amphibious vertebrates, rhythmic patterns of branchial ventilation are completely replaced by arrhythmic and intermittent patterns of air breathing, and there is progressive dependence on CO2 as a source of respiratory drive. Periodic initiation of air breathing in resting animals appears to depend on attaining a threshold level of afferent activity from O2- and CO2/pH-sensitive chemoreceptors, since hyperoxia and/or hypocapnia can abolish air breathing in all air-breathing vertebrates. Conversely, chemoreceptor stimulation in amphibians and reptiles converts intermittent to more continuous air breathing patterns, suggesting that adequate biasing input from chemoreceptors activates a central rhythm generator. Chemoafferent input in homeotherms serves as one of several sources of drive for rhythmic breathing and supplies feedback for blood gas homeostasis in the face of metabolic or environmental change.
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PMID:Chemoreceptor modulation of endogenous respiratory rhythms in vertebrates. 224 Feb 73


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