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

1. In response to an acute exercise-induced metabolic acidosis, the fall of arterial pH is constrained by the magnitude of the compensatory hyperventilation. To determine the role of the carotid bodies in this regulatory process, subjects performed prolonged (24 min) square-wave cycle ergometry from a background of unloaded cycling at inspired oxygen fractions (FI,O2) of 0.12 O2 (high carotid body gain), 0.21 O2 (normal carotid body gain) and 0.80 O2 (low carotid body gain). The work rates were selected to provide the same exercise intensity, despite the different inspirates; i.e. resulting in a constant increase in arterial blood [lactate] (delta [L-] approximately 4 mequiv l-1. 2. Ventilatory and pulmonary gas exchange variables were computed breath-by-breath and arterial blood was sampled at intervals throughout the tests and analysed subsequently for [lactate], [pyruvate], arterial partial pressures of oxygen and carbon dioxide (PO2, PCO2), pH, [bicarbonate] and [potassium]. 3. Hypoxia markedly reduced, and hyperoxia magnified, the transient decrease in arterial pH following exercise onset. However, there was a slow acid-base compensatory component, even when carotid chemosensitivity was suppressed by hyperoxia. We therefore conclude that, in humans, carotid body chemosensitivity plays a dominant role in constraining variations of arterial pH in response to the acute metabolic acidosis of heavy exercise, but that secondary-presumably central chemosensory-mechanisms subserve a slower compensatory role.
J Physiol 1991 Dec
PMID:Role of the carotid bodies in the respiratory compensation for the metabolic acidosis of exercise in humans. 182 63

Hyperoxic lung injury is an unfortunate consequence of ventilatory oxygen therapy that is necessary to sustain life in certain clinical situations. The biochemical events that accompany hyperoxia of the lung, and the molecular mechanisms underlying these events, are incompletely understood. To better understand hyperoxic lung injury, our laboratory has cloned a set of genes corresponding to mRNAs that increase in abundance in the lungs of hyperoxic rabbits. In this report, we focus on three hyperoxia-induced cDNA clones, which encode surfactant apoprotein A (SP-A), the tissue inhibitor of metalloproteinases (TIMP), and metallothionein. In situ hybridizations and RNA dot blots of isolated lung cell populations indicate that the abundance of mRNA encoding all three proteins is increased by hyperoxia in specific cell types. SP-A mRNA increases in type II alveolar epithelial cells and in bronchiolar epithelial cells. TIMP mRNA increases in interstitial fibroblasts, in chondrocytes of the cartilage surrounding airways, and in endothelial cells of a specific subset of vessels, probably venules. Metallothionein transcripts also increase in chondrocytes and pulmonary fibroblasts. A comparison of the increase in these mRNAs during hyperoxic exposure in adults and newborns indicates that adults respond faster and to a greater extent than newborns and suggests that the rate and extent of these increases is correlated with the time course and severity of the injury.
Am J Respir Cell Mol Biol 1991 Dec
PMID:Cell-specific alterations in expression of hyperoxia-induced mRNAs of lung. 195 78

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.
Am J Respir Cell Mol Biol 1991 Dec
PMID:Tumor necrosis factor enhances endothelial cell susceptibility to oxygen toxicity: role of glutathione. 195 83

Persons with chronic mountain sickness (CMS) hypoventilate and are more hypoxemic than normal individuals, but the cause of the hypoventilation is unclear. Studies of 14 patients with CMS and 11 healthy age-matched control subjects residing in Lhasa, Tibet, China (3,658 m) were conducted to test the hypothesis that hypoventilation, blunted hypoxic ventilatory responsiveness (HVR), and hypoxic ventilatory depression of CMS were due to increased endogenous opioid production. Patients with CMS compared with control subjects exhibited hypoventilation (end-tidal carbon dioxide pressure [PETCO2] = 36.6 +/- 1.0 versus 31.5 +/- 0.5 mm Hg, p less than 0.05), lower tidal volume (VT = 0.54 +/- 0.02 versus 0.61 +/- 0.02 ml BTPS, p less than 0.05), blunted HVR (shape parameter A = 17 +/- 8 versus 114 +/- 22 mm Hg/L BTPS/min, p less than 0.05), and a depressant effect of ambient hypoxia on ventilation (delta PETCO2 with acute hyperoxia = -3.5 +/- 0.5 versus -1.0 +/- 0.6 mm Hg, p less than 0.05). Reduced forced expiratory volume in 1 s to vital capacity ratios (FEV1/VC) and a higher proportion of cigarette smokers in the group of patients with CMS compared with control subjects suggested that at least some patients with CMS had mild airway obstructive lung disease. Naloxone infusion (0.14 mg/kg) to six patients with CMS did not change resting VT, PETCO2, HVR, or SaO2.(ABSTRACT TRUNCATED AT 250 WORDS)
Am Rev Respir Dis 1990 Dec
PMID:Decreased ventilation and hypoxic ventilatory responsiveness are not reversed by naloxone in Lhasa residents with chronic mountain sickness. 225 47

Thirteen pregnant women who subsequently were delivered of infants with birth weights less than the 3rd percentile were studied for examination of fetal heart rate and fetal activity patients during maternal administration of oxygen at a concentration of 50% or room air for 2 hours. None of the fetuses was acidotic at birth. Maternal transcutaneous PO2 levels increased from 79 +/- 3 mm Hg to 158 +/- 10 mm Hg for the 2 hours of observation. The results indicated that maternal hyperoxia produced sustained fetal breathing activity that was almost 100% higher than that in room air (analysis of variance, p = 0.024). Gross fetal body movements, fetal heart rate accelerations, and fetal heart rate variability increased significantly with increasing observation time (analysis of variance, p less than 0.01), but were not significantly altered by maternal hyperoxia or room air. We conclude that despite significant change in fetal breathing activity, ultrasonographic observation of fetal behavioral activity during maternal hyperoxia could not be used to differentiate severely growth-retarded from normally grown human fetuses. We speculate that altered fetal heart rate and fetal body movement patterns usually associated with intrauterine growth retardation might be related to altered development of the fetal central nervous system and are not reversible during prolonged maternal administration of oxygen.
Am J Obstet Gynecol 1990 Dec
PMID:The effect of maternal hyperoxia on behavioral activity in growth-retarded human fetuses. 225 1

The Fischer rat is known for its susceptibility to develop liver necrosis when challenged with paraquat (Smith et al., J. Pharmacol. Exp. Ther. 235: 172-177, 1985). We postulated that other organs, specifically the lung, may also be more susceptible to injury and examined whether lungs from Fischer (F) rats were injured more easily when challenged with active oxygen species than Sprague-Dawley (SD) rat lungs. We aimed to investigate whether increased susceptibility to oxidant injury was related to differences in lung antioxidant defenses. Perfused lungs from both rat strains were challenged by addition of H2O2 to the perfusate or by short-term hyperoxic ventilation. To assess nonoxidant modes of lung injury, we examined lung responses after exposure to protamine sulfate or neutrophil elastase. Intravascular H2O2 or 3 h in vitro hyperoxia caused lung edema in F but not SD rats, and elastase injured F rat lungs more than the lungs from SD rats. Protamine, however, injured the lungs from both strains to a similar degree. Catalase, but not superoxide dismutase or allopurinol, protected F rat lungs against edema, resulting from 3 h in vitro hyperoxia. The lung homogenate levels for reduced glutathione or conjugated dienes and the activities of lung tissue catalase, glutathione peroxidase, and cytochrome P-450 were not different between the two strains. Lung tissue ATP levels, however, were lower in F than in SD rats. Although the F rat strain appears to have an altered oxidant-antioxidant defense balance, the exact cause of the greater susceptibility to oxidant stress of the F rat strain remains elusive.
Am J Physiol 1990 Dec
PMID:Lung injury in Fischer but not Sprague-Dawley rats after short-term hyperoxia. 226 Jun 76

Tracheal insufflation of tumor necrosis factor (TNF) enhances pulmonary antioxidant enzyme activities and protects rats against oxygen toxicity (J. Appl. Physiol. 68: 1211-1219, 1990). We now report that tracheal insufflation of TNF selectively induced pulmonary Mn-superoxide dismutase (SOD) mRNA in normoxia- and hyperoxia-exposed rats, leading to increased amounts of Mn-SOD specific protein and enzyme activity. Tracheal insufflation of TNF had no effect on the levels of pulmonary Cu,Zn-SOD mRNA or specific protein. Hyperoxia alone also selectively induced pulmonary Mn-SOD mRNA. However, the hyperoxia-induced increase in Mn-SOD mRNA was not associated with an increase in Mn-SOD specific protein or enzyme activity. The results suggest that the increased pulmonary Mn-SOD in TNF-insufflated rats may contribute to the TNF-induced protection against oxygen toxicity.
Am J Physiol 1990 Dec
PMID:Molecular basis for tumor necrosis factor-induced increase in pulmonary superoxide dismutase activities. 226 Jun 78

The effect of graded systemic hyperoxia on vitreal PO2 distribution has been determined for the rat eye. Oxygen tension profiles were measured, using oxygen-sensitive microelectrodes, as a function of distance from the internal limiting membrane as the inspired oxygen percentage was increased in 10% steps from 20-100%. Depending on the original touching location of the microelectrode on the retina, there could be substantial PO2 gradients within 500 microns of the retina; at greater distances vitreal PO2 was constant and a function of the inspired oxygen percentage. Whatever the location of the microelectrode in the vitreous, PO2 rose with increasing hyperoxia. The relationship between vitreal PO2 and inspired oxygen was nonlinear with a central relatively flat region between 50-80% inspired oxygen. The ratio between vitreal PO2 during 100% O2 breathing and air breathing was 3.42 +/- 1.08 (standard deviation, n = 7). Possible explanations for the plateau region are the maintenance of a relatively constant PO2 by vascular autoregulation and/or the buffering of capillary PO2 by hemoglobin. The rat eye, therefore, responds to hyperoxia similarly to that of the cat and monkey but differs from that of the miniature pig where there is no rise in preretinal PO2 during hyperoxia.
Invest Ophthalmol Vis Sci 1990 Dec
PMID:The response of rat vitreal oxygen tension to stepwise increases in inspired percentage oxygen. 226 89

The concomitant treatment of rats with bleomycin and hyperoxia results in synergistic development of pulmonary injury. We exposed rats to 70% oxygen for 72 hr following an intratracheal instillation of bleomycin (0.2 U/kg body wt). Animals were killed 15, 30, 60 and 90 days after treatment for hydroxyproline, cell kinetics, and histopathologic analysis. A 16% increase in hydroxyproline over controls was seen 15 days after treatment which was manifested by the proliferation phase of diffuse alveolar damage and an increase in cell labeling by tritiated thymidine. Thirty days after treatment the hydroxyproline remained elevated while lung injury appeared to be healing with a residual focal interstitial pneumonitis and a drop in cell labeling. Between 60 and 90 days, there was an additional significant increase in hydroxyproline to 44% over controls. Diffuse interstitial pneumonitis with fibrosis was observed. Cell labeling remained constant between 60 and 90 days. We conclude that the treatment of rats with bleomycin and hyperoxia results in slowly progressive pulmonary fibrosis. The increase in hydroxyproline in the chronic phase was not accompanied by an increase in cell proliferation, and therefore may have resulted from an increase in cellular production of hydroxyproline rather than increased number of cells producing collagen.
Exp Mol Pathol 1985 Dec
PMID:Progressive pulmonary fibrosis in rats: a biochemical, cell kinetic, and morphologic analysis. 241 89

Four patients with retinitis pigmentosa and either disc or peripheral retinal neovascularization with recurrent vitreous hemorrhage are described. One patient with peripheral retinal neovascularization also had rubeosis and neovascular glaucoma. The effects of relative hyperoxia on the retinal microcirculation in retinitis pigmentosa as well as intraocular inflammation may account for such changes. Laser photocoagulation appears effective in preventing vitreous hemorrhage in these patients, but systemic administration of corticosteroids did not cause the new vessels to regress.
Ophthalmology 1986 Dec
PMID:Retinitis pigmentosa and retinal neovascularization. 243 59


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