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

Cardiorespiratory responses of four men to submaximal and maximal cycling exercise were observed during 17 days at 18.6 ATA. Inspired gas at pressure consisted of hyperoxic (PO2 = 232 mmHg) and normoxic (PO2 = 159 mmHg) helium mixtures with relative gas densities of 3.8 and 2.8, respectively. The average of pre- and postdive VO2max (1 ATA air), which were not significantly different, was 3.10 liters - min-1. During 5 min of submaximal exercise at 50% of VO2max, no significant difference in work rate, VO2, VCO2, VE, respiratory rate, heart rate (HR), stroke volume, blood pressures, or rectal temperature was noted at 18.6 ATA compared to 1 ATA with either gas mixture. Submaximal HR tended to decrease by 5 to 10 beats - min-1 at pressure, and in hyperoxia the VO2/HR ratio was significantly higher. Maximal exercise was performed to exhaustion at work rates requiring about 120% of VO2max. Significant increased in VO2max of 0.10 liter - min-1 (3%) and in endurance time of 2 min (48%) were found during hyperoxic gas breathing, whereas normoxic values at 18.6 ATA were similar to those at 1 ATA. Significant reductions in maximal HR of 8 beats - min-1 (4%) were observed with both gas mixtures at pressure, and VE was significantly decreased by 36 liters - min-1 (26%) in hyperoxia and 29 liters - min-1 (21%) in normoxia. No change was found in the calculated cardiac output. Maximal voluntary ventilation, which was measured only for the hyperoxic gas, fell significantly by 80 liters - min-1 (40%). Results indicate that aerobic power and endurance performance were affected by oxygen pressure. Normoxic work capacity, however, was not decreased at 18.6 ATA, despite marked reductions in HR and VE.
Undersea Biomed Res 1977 Sep
PMID:Hana kai ii: a 17-day dry saturation dive at 18.6 ATA. V. Maximal oxygen uptake. 91 Mar 18

Neonatal rabbit neuro-epithelial bodies (NEB) were investigated under various experimental conditions with light microscopy, microspectrography, morphometry and electron microscopy. (1) Hypoxia causes a decreased amine fluorescence intensity and an increased secretory exocytosis of dense core vesicles (DCV). Otherwise the NEB appear structurally normal. (2) Hypercapnia also produces a decreased fluorescence and an increased exocytosis; ultrastructurally, however, the dense core of DCV fragmentizes. (3) Hyperoxia does not appear to affect significantly either fluorescence or exocytosis. (4) The uptake of biogenic amines such as 5-HTP and L-DOPA was demonstrated by fluorometry and electron microscopy. (5) Reserpine, on the other hand, provokes an amine depletion with a decrease of the NEB fluorescence and an ultrastructural palor of the DCV. (6) Intratracheally administered nicotine is accompanied by a decreased fluorescence and a distinct exocytosis of fragmented DCV. The reaction of NEB to hypoxia and hypercapnia suggests that these corpuscles could be intrapulmonary chemoreceptors (in addition to the classically known central and peripheral chemoreceptors), inducing a reflex reaction through the liberation of DCV at the corpuscular sensible nerve endings and via the CNS. In addition, they may subserve a local intrapulmonary effect by modulating directly the hypoxic and hypercapnic pulmonary vasoconstriction and thus the V/Q ratio.
Cell Tissue Res 1977 Sep 05
PMID:Intrapulmonary neuro-epithelial bodies in newborn rabbits. Influence of hypoxia, hyperoxia, hypercapnia, nicotine, reserpine, L-DOPA and 5-HTP. 92 15

Hyperoxia has been reported to stimulate both resorption and synthesis of bone in vitro. The effects of increased oxygen tension were re-investigated using calvaria from infant mice maintained in a stationary grid culture system for 48 48 hours with an unsupplemented chemically defined medium. Resting resorption due to osteoclastic activity was demonstrated in the explants in air by Von Kossa staining, histology, and 45 Ca release. Resorption was inhibited by exposure to 95 per cent oxygen or hyperbaric oxygenation at 2 atmospheres pressure. Hyperoxia also depressed new bone formatin by osteoblasts although the production of a new collagen, as measured by the incorporation of 3H-proline, was greater in calvaria cultured in hyperbaric oxygen than in paired explants in 95 per cent oxygen. Thus hyperoxia was toxic for both synthetic and resorptive activity of bone cells; these effects may stem from the loss of vital factors present in natural MEDIA supplements.
Clin Orthop Relat Res 1976 Sep
PMID:The effects of hyperoxia upon bone in organ culture. 95 15

Continuous and interval exposures to 1 atmosphere of oxygen (hyperoxia) were examined using insects. Hyperoxia did not affect hatchability of Heliothis zea or Trichoplusia ni. Continuous hyperoxia was 100% lethal for H. zeal and T. ni. Most insects died as larvae and pupae of H. zea which resulted were deformed, reduced in weight, and failed to emerge. Hyperoxic exposures of T. ni for 48 h at sequential 48-h intervals during development, revealed that first instar and prepupae were most sensitive to hyperoxia and 80% were killed when exposed to only 24 h of hyperoxia as prepupae. T. ni which survived hyperoxia exposures at all development stages tested, were capable of producing progeny. The differential hyperoxic sensitivity and its correlation with specific morphogenetic stages suggest the usefulness of these insect species for studying biochemical sites of oxygen toxicity.
Aviat Space Environ Med 1976 Sep
PMID:Selective toxicity of 1 atmosphere of oxygen during morphogenesis of two Lepidopterans. 97 Nov 74

The growth factors that operate while the lung remodels in hyperoxia are not known. At the lung periphery, high oxygen levels cause cell hypertrophy and hyperplasia, and this results in a thickening of the alveolar-capillary membrane and the walls of its associated microvessels. The present study examines gene expression of platelet-derived growth factor (PDGF) receptor and its ligand in this region of the lung of rats breathing 87% oxygen and compares this with the levels of expression in normal lung. In similar peripheral lung tissue, the proliferative response of specific cell populations has been assessed by [3H]thymidine incorporation and autoradiography. Normal lung expresses PDGF alpha-receptor subunit transcripts of 6.5 and 4.7 kb and PDGF beta-receptor transcripts of 5.5 and 4.5 kb. PDGF A-chain transcripts of 2.9, 2.3, and 1.7 kb are also expressed, each being at 10-fold higher levels than the single 3.5-kb transcript detected for PDGF B-chain. Within hours of breathing high concentrations of oxygen, mRNA levels change rapidly for the PDGF receptor subunits. These levels return to normal after 1 day and then decline over the next 28 days of exposure. PDGF A-chain mRNA increases 12 to 18 h after exposure, but then returns to normal levels. It is the PDGF B-chain mRNA that responds most to hyperoxia by increasing 10-fold on day 3. This increase immediately precedes the proliferative response on day 4 of microvascular adventitial fibroblasts, precursor smooth muscle cells, and epithelial cells but not smooth muscle cells, which do not proliferate until day 28.
Am J Respir Cell Mol Biol 1992 Sep
PMID:Differential regulation of the genes encoding platelet-derived growth factor receptor and its ligand in rat lung during microvascular and alveolar wall remodeling in hyperoxia. 132 10

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.
Mutat Res 1992 Sep
PMID:Cell culture models for oxidative stress: superoxide and hydrogen peroxide versus normobaric hyperoxia. 138 81

The influence of oleic, linoleic (LIN), and eicosapentaenoic (EPA) acids incorporated into cellular lipids on susceptibility to O2-induced toxicity was evaluated in Chinese hamster fibroblasts (HA1) using a clonogenic cell survival assay. Fatty acid incorporation was achieved by incubating HA1 cells in 21% O2 for 72 h in the presence or absence of media supplemented with 25 microM oleic acid, 25 microM LIN, or 2, 4, and 25 microM EPA. This fatty acid incorporation period increased the percentage of composition in phospholipids 2-fold for oleic acid, 6-fold for LIN, and 6- to 20-fold for EPA. Vitamin E, total glutathione, superoxide dismutase activity, glutathione transferase activity, and catalase activity were unchanged, relative to control, in the 25-microM EPA-treated group, and only total glutathione was elevated in the LIN-treated group. After the incorporation period, the cells were placed in non-fatty acid supplemented media and exposed to 95% O2, and clonogenic survival responses were evaluated at time intervals up to 100 h. Sensitization to O2 toxicity in EPA-treated cells was apparent after 24 h of O2 exposure, whereas LIN-treated cells were significantly (p less than 0.05) sensitized to hyperoxia after 54 h of exposure, indicating that EPA was a more potent sensitizer for O2 injury. Furthermore, cells supplemented with 4 and 25 microM EPA were more sensitive to O2 toxicity than cells supplemented with 2 microM EPA. In contrast, cells treated with 25 microM oleic acid were significantly more resistant to O2 toxicity at 51, 72, and 98 h of O2 exposure.(ABSTRACT TRUNCATED AT 250 WORDS)
Pediatr Res 1992 Sep
PMID:The effect of monosaturated and polyunsaturated fatty acids on oxygen toxicity in cultured cells. 140 77

Undernutrition may exacerbate hyperoxia-induced lung injury, a finding that may be of significance in the early clinical management of the premature human infant. Addressing this specific problem, we found that 72 h of food restriction in guinea pig pups delivered 3 days preterm increased mortality rates among pups exposed to 95% oxygen (8/18) and yet had no effect on 21% oxygen (air)-exposed pups (0/10). Reduced tolerance of hyperoxic conditions was not, however, associated with increased lung injury, assessed as pulmonary microvascular leakage. Pulmonary antioxidant enzyme activities [Cu,Zn superoxide dismutase (SOD), Mn SOD, glutathione peroxidase, and catalase] were unaltered by starvation or hyperoxia. Lung glutathione concentration was slightly decreased after food restriction, whereas hyperoxic exposure did not change either lung or bronchoalveolar lavage fluid glutathione concentrations or lung antioxidant enzyme activities. Increased susceptibility to the lethal effects of oxygen in the starved preterm guinea pig pup could not be attributed to a deficiency of pulmonary antioxidant defenses.
Am J Physiol 1992 Sep
PMID:Effect of food restriction on hyperoxia-induced lung injury in preterm guinea pig. 141 61

Oxygen tension in the arterial blood with transcutaneous method (tcPO2) and TBA-active products of venous blood plasma were measured during simulation of extravehicular activity. There was a parallel increase of tcPO2 and the level of TBA-active products upon introduction of hypobaric hyperoxia factor. Detrimental action of lipid peroxidation products on erythrocyte membranes can be one of the factors of anemia during space flight.
Biull Eksp Biol Med 1992 Sep
PMID:[Oxygen tension and water-soluble products of lipid peroxidation in blood of volunteers in hypobaric hyperoxia]. 147 47

Hyperoxia has been suggested as a risk factor for kernicterus. The toxicity of hyperoxia may be mediated by free radicals. We investigated the effects of free radicals, formed by the hypoxanthine/xanthine oxidase system, with and without additional hyperoxia, on the accumulation of bilirubin and albumin in rat brain. Hypoxanthine was infused for 60 min into retrograde carotid catheters in awake, young, male SPRD rats. After 30 min the infusion was briefly interrupted to inject xanthine oxidase 1 U/kg through the same catheter. Group I (controls) received 0.9% NaCl in lieu of hypoxanthine/xanthine oxidase. Groups I and II breathed room air at all times, while group III breathed 90% O2. After 60 min all groups received a bolus dose of 125I-albumin through a peripheral venous catheter, followed by bilirubin 25 mg/kg for 5 min, then bilirubin 35 mg/kg for 55 min. There were no significant differences between the groups as regards serum bilirubin, serum albumin, brain bilirubin, or brain albumin. Neither during normoxic nor hyperoxic conditions did the hypoxanthine/xanthine oxidase system increase the accumulation of bilirubin or albumin in rat brain.
Early Hum Dev 1992 Sep
PMID:The effects of hypoxanthine, xanthine oxidase and hyperoxia on the accumulation of bilirubin and albumin in young rat brain. 149 69


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