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

To evaluate the regulation of endothelial cell Cu,Zn-SOD, we have exposed bovine pulmonary artery endothelial cells in culture to hyperoxia and hypoxia, second messengers or related agonists, hormones, free radical generating systems, endotoxin, and cytokines and have measured Cu,Zn-SOD protein of these cells by an ELISA developed in our laboratory. Control preconfluent and confluent cells in room air contained 196 +/- 18 ng Cu,Zn-SOD/10(6) cells. A23187 (0.33 microM), forskolin (10 microM), isobutylmethylxanthine (0.1 mM), dexamethasone (1 microM), triiodothyronine (1 microM) and retinoic acid (1 microM) failed to alter this level of Cu,Zn-SOD. Exposure to anoxia and hyperoxia both elevated the level approximately 1.5-2.0-fold over 20% oxygen-exposed controls at 48-72 hr. Similarly, exposures to glucose oxidase (0.0075 units/ml), menadione (12.5 microM), xanthine-xanthine oxidase (10 microM, 0.03 units/ml) and H2O2 (0.0005%) increased the level up to two-threefold over controls at 24-48 hr. Lipopolysaccharide, TGF beta 1, TNF alpha, and Il-1 also increased levels of cellular Cu,Zn-SOD, but only in proliferating cells. Il-2, Il-4, interferon-gamma, and GM-CSF had no effect on Cu,Zn-SOD. All treatments that elevated SOD resulted in inhibition of cellular growth, but decreased growth of cells at confluence alone was not associated with increased Cu,Zn-SOD. We propose from these studies that Cu,Zn-SOD of endothelial cells is not under conventional second messenger or hormonal regulation, but that up-regulation of the enzyme is associated with (and perhaps stimulated by) free-radical or oxidant production that also may be influenced by availability of certain cytokines under replicating conditions.
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PMID:Regulation of Cu,Zn-superoxide dismutase in bovine pulmonary artery endothelial cells. 133 80

The influence of 12-, 24- and 48-h normobaric hyperoxia on phospholipid composition of lung surfactant in rats was investigated. Both in surfactant isolated from bronchoalveolar lavage and in surfactant isolated from lung tissue after 12 h breathing of pure oxygen, a decrease in both phosphatidylcholine (particularly in disaturated ones) and phosphatidylglycerol content was observed. This decrease was compensated with concomitant increase in lysophosphoglyceride content. A drop in total phospholipid level in surfactant of oxygen-exposed rats was observed. These data suggest that normobaric hyperoxia causes a substantial changes in lung surfactant composition and type II pneumocyte metabolism.
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PMID:The influence of normobaric hyperoxia on lung surfactant phospholipids in rats. 133 68

Persistent pulmonary hypertension of the newborn (PPHN) characterised by right to left shunting with intense cyanosis is difficult to manage, and in the best of centres carries a 40-60 percent mortality. We report our one year's experience of managing six neonates with PPHN. There were 5 males and 1 female with mean birth weight of 2.59 +/- 0.487 kg and gestation period 39 +/- 2.0 wks and 1 minute Apgar score 2.8 +/- 2.1. Four to six babies were born by cesarean section and 3-6 babies had aspiration pneumonia. All babies presented within 12 hours of age (mean 5.08 +/- 5 hrs) with intense cyanosis and respiratory distress. Diagnosis were confirmed in all by (a) hyperoxia test, (b) simultaneous determination of preductal and postductal paO2 (c) contrast echocardiography and (d) hyperoxia-hyperventilation test. Babies were managed with hyperventilation using mean ventilatory rates of 100 +/- 45 per minute, an inspired oxygen concentration of 100%, peak inspiratory pressures 27 +/- 9 cm of H2O, and expiratory pressures 5 +/- 1.6 cms of H2O, and mean air way pressures of 10.4 +/- 2.7 cms H2O. Alkali therapy was used in 3 of the six babies whereas low dose dopamine was infused in all six babies. Inspite of aggressive ventilatory therapy, only 3 out of 6 babies could be salvaged.
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PMID:Persistent pulmonary arterial hypertension of the newborn. 134 Aug 63

Exercise capacity in patients with stable heart failure may be influenced by prolonged drug treatment or exercise training, but acute interventions are generally thought to have little effect. Cardiorespiratory responses to exercise were studied in 12 consecutive patients with chronic congestive heart failure who underwent serial submaximal and maximal exercise tests at inspired oxygen concentrations of 21% (room air), 30%, and 50%. Mean (SD) exercise duration during progressive testing to maximum exercise capacity was prolonged from 548 (276) s on room air to 632 (285) s on 50% oxygen (p = 0.012). During steady-state exercise at 45 W, oxygen enrichment to 50% was associated with significantly increased arterial oxygen saturation (94.6 [1.9]% to 97.5 [1.3]%), and significantly reduced minute ventilation (36.1 [8.6] l/min to 28.1 [5.9] l/min), cardiac output (7.5 [2.3] l/min to 6.5 [1.9] l/min), and subjective scores for fatigue and breathlessness (13.9 [3.1] to 11.5 [3.5]) compared with room air intermediate changes were observed with 30% inspired oxygen. Increased inspired oxygen concentrations can improve exercise performance acutely and modify the ventilatory response to exercise in patients with heart failure. Hyperoxia reduces ventilatory response and circulatory demand while maintaining oxygen delivery at a given workload. The potential benefits of increased inspired oxygen concentrations in the treatment of chronic heart failure merit further assessment.
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PMID:Effects of increased inspired oxygen concentrations on exercise performance in chronic heart failure. 135 2

The present study was undertaken to investigate the comparative effects of rapid vs graded correction of chronic hypoxia in vitro. Cerebral cortical cell cultures obtained from fetal mice were exposed to 5% O2 for 24 h and returned immediately to room air for the following 24 h (Group I); comparable cultures were exposed to 5% O2 for 24 h followed by 10% O2 for an additional 24 h before return to room air (Group II). At the conclusion of the experimental protocol (time 0), partial pressure of oxygen in the bathing medium of Group I cultures was significantly higher than that of Group II and non-hypoxic controls (151 mmHg vs 124 and 132 mmHg, respectively; P less than 0.05). Throughout the recovery period, Group II cultures evidenced improved neuronal survival (e.g. 35,800 vs 17,700 neurons/culture well at time 0, P less than 0.01), decreased lactate dehydrogenase efflux into the bathing medium, relative preservation of neuronal morphology, as well as higher specific and clonazepam-displaceable benzodiazepine binding and GABA uptake. Glutamate binding was not differentially affected and glutamine synthetase activity, a predominantly glial marker, was only modestly increased after graded reoxygenation. These results demonstrate that gradual reoxygenation after prolonged hypoxia in vitro (i) improves neuronal survival compared to rapid reoxygenation and (ii) delays the manifestations of metabolic dysfunction even though the length of hypoxic exposure is increased. The findings are also consistent with the concept that a period of relative hyperoxia may contribute to hypoxia-induced neuronal injury.
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PMID:Neuroprotective effects of graded reoxygenation following chronic hypoxia in neuronal cell cultures. 134 36

The responses of canine tracheal ciliary beat frequency (CBFt) to total lung, tracheal lumen, and peripheral lung hyperoxia, to tracheal lumen anoxia with or without peripheral lung hypoxia, and to isolated tracheal lumen hyperoxia combined with a beta-antagonist were delineated in anesthetized beagle dogs. CBFt was measured using a heterodyne laser light-scattering technique. When oxygen mixtures were delivered to the whole lung, a dose-dependent increase in maximal CBFt was observed from 6.3 +/- 1.0 Hz on air to 13.8 +/- 1.2 Hz on 100% oxygen. When oxygen mixtures were delivered to the isolated tracheal lumen, a dose-dependent increase in maximal CBFt from 6.9 +/- 1.3 Hz on air to 25.7 +/- 6.3 Hz on 100% oxygen was observed. CBFt was unchanged under conditions of peripheral lung hyperoxia. There were no significant changes from room air baseline CBFt of 7.6 +/- 1.5 Hz due to either isolated tracheal anoxia alone or in combination with alveolar hypoxia. CBFt stimulated with 100% oxygen insuffiated to the isolated tracheal lumen decreased from 14.1 +/- 3.2 to 9.5 +/- 1.9 Hz and from 16.5 +/- 1.2 to 9.7 +/- 1.2 Hz in response to 6 and 18 micrograms/kg of intravenous esmolol, respectively. This study demonstrates that short-term, local hyperoxia stimulates CBFt and that a pulmonary or systemically derived factor can be activated to inhibit this stimulation. It indicates that acute airway anoxia and alveolar and blood hypoxia do not suppress ciliary beat frequency. It also suggests that the adrenergic system is involved in the oxygen-induced stimulation of ciliary beat.
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PMID:Short-term interaction of airway and tissue oxygen tensions on ciliary beat frequency in dogs. 135 65

To study the effects of hyperoxia and beta-adrenergic stimulation on pulmonary surfactant in the neonatal lung, we measured disaturated phosphatidylcholine (DSPC) and [14C]choline incorporation into DSPC, obtained from alveolar lavage and lung tissue. We used an isolated salt-perfused rabbit lung preparation from neonatal rabbits exposed to room air or greater than 95% oxygen for 3 days. There were four experimental groups: room air, basal condition; room air, beta-adrenergic stimulation; hyperoxia, basal conditions; and hyperoxia, beta-adrenergic stimulation. Hyperoxia caused a significant decrease in lavage and intracellular [14C]DSPC specific activity, and a decrease in intracellular DSPC suggesting depressed surfactant synthesis. Beta-stimulation in room air caused a decrease in lavage DSPC, an increase in DSPC, and [14C]DSPC fraction released, consistent with increased uptake for reutilization. With hyperoxia and beta-stimulation, there is an increase in total DSPC in the lavage; lavage [14C]DSPC specific activity is similar to that of the basal hyperoxia group (i.e., depressed compared with the room air state); intracellular [14C]DSPC specific activity does not differ from basal, hyperoxia, or beta-stimulated, room air groups, all being depressed compared with basal, room air conditions. Intracellular DSPC in the beta-stimulated group is less affected by hyperoxia than the basal groups. It appears that prolonged exposure to hyperoxia is manifested primarily by a decrease in [14C]DSPC specific activity suggesting alterations in surfactant synthesis, though DSPC in the lavage is not altered. Beta-adrenergic stimulation may enhance release of newly synthesized surfactant into the alveoli, and possibly enhances uptake for reutilization. The enhancement of surfactant release seems to be preserved after prolonged hyperoxia.
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PMID:Effects of hyperoxia and beta-adrenergic stimulation on pulmonary surfactant in neonatal rabbits. 135 52

Oxygen free radicals and hydroperoxides have been postulated to play a causal role in the aging process, implying that antioxidant enzymes may act as longevity determinants. Catalase (H2O2:H2O2 oxidoreductase; EC1.11.1.6) is the sole enzyme involved in the elimination of H2O2 in Drosophila melanogaster; glutathione peroxidase being absent. A genomic fragment containing the Drosophila catalase gene was used to construct transgenic Drosophila lines by means of P element-mediated transformation. Enhanced levels of catalase (up to 80%) did not prolong the life span of flies, nor did they provide improved protection against oxidative stress induced by hyperoxia or paraquat treatment. However, enhanced resistance to hydrogen peroxide was observed in the overexpressors.
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PMID:The effects of catalase gene overexpression on life span and resistance to oxidative stress in transgenic Drosophila melanogaster. 137 30

According to the free radical theory of aging, loss of cellular function during aging is a consequence of accumulating subcellular damage inflicted by activated oxygen species. In cells, the deleterious effects of activated oxygen species may become manifest when the balance between radical formation and destruction (removal) is disturbed creating a situation denoted as 'oxidative stress'. Cell culture systems are especially useful to study the effects of oxidative stress, in terms of both toxicity and cellular adaptive responses. A better understanding of such processes may be pertinent to fully comprehend the cellular aging process. This article reviews three model systems for oxidative stress: extracellular sources of O2-. and H2O2, and normobaric hyperoxia (elevated ambient oxygen). Methodological and practical aspects of these exposure models are discussed, as well as their prominent effects as observed in cultures of Chinese hamster cell lines. Since chronic exposure models are to be preferred, it is argued that normobaric hyperoxia is a particularly relevant oxidative stress model for in vitro cellular aging studies.
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PMID:Cell culture models for oxidative stress: superoxide and hydrogen peroxide versus normobaric hyperoxia. 138 81

IL-1 and TNF are important mediators in the inflammatory response, and have been associated with endothelial cell damage in the lung. TNF and IL-1 cell-mediated injury has been proposed to occur through an increase in intracellular oxygen free radical production. However, these cytokines have also been shown to protect the lung from hyperoxia-mediated oxidant injury. In this paper we evaluated the response of the antioxidant enzymes, MnSOD and Cu/ZnSOD to IL-1, TNF, and LPS in both rat pulmonary artery and microvascular endothelial cells. These mediators produced an increase in MnSOD but not Cu/ZnSOD expression in both rat pulmonary endothelial cells. An additive effect was observed with co-treatment by the cytokines with LPS. The MnSOD mRNA induction is dependent upon a transcriptional event, but did not require de novo protein synthesis.
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PMID:Regulation of manganese superoxide dismutase: IL-1 and TNF induction in pulmonary artery and microvascular endothelial cells. 138 89


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