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

Factors responsible for the loss of respiratory burst capacity (stimulated extracellular O2-. release) of alveolar macrophages (AM) exposed to prolonged hyperoxia were assessed. Specific pathogen-free rats were exposed to 1 ATA O2 for 24-72 h, and lungs of survivors lavaged. Release of O2-. by cells after addition of concanavalin A, which stimulated AM but not polymorphonuclear leukocytes (PMN), or digitonin, which stimulated both cell types, was measured using cytochrome c reduction +/- superoxide dismutase. O2-. release by AM declined 47.2% (P less than 0.05) after 24 h of hyperoxia and 100% after 60 h. Percent PMN in the lavage was less than 3% at 0-36 h but increased to 16% at 48 h and to 44% at 72 h. Although addition of PMN to AM in vitro caused inhibition of AM O2-. release, the percent PMN required for inhibition was not reached in vivo until after a significant decline in AM O2-.-releasing capacity had already occurred. Cell-free lavage fluid from either control or hyperoxic rats did not affect AM O2-. release. AM in culture for 24 h in hyperoxia lost 76.7% (P less than 0.005) of O2-.-releasing capacity vs. cells incubated in 20% O2, although dye exclusion was unaffected. The results indicate that the major cause of loss of AM O2-. release by hyperoxia is a direct effect of O2 on the cells.
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PMID:Hyperoxia inhibits stimulated superoxide release by rat alveolar macrophages. 629 Apr 36

Rats pretreated with 500 micrograms X kg-1 endotoxin are resistant to the pulmonary toxic effects of normobaric hyperoxia (greater than 95% O2). After endotoxin-pretreatment and exposure to 1.0 ATA O2 for 72 h, such rats are found to have elevated total superoxide dismutase, glutathione peroxidase, and catalase activities in homogenates of whole lungs. Despite increases in these protective antioxidant enzymes which persist in 2.0 ATA O2 (4 h) and 4.0 ATA O2 (1.0 h), such rats do not have improved survival in hyperbaric hyperoxia. Likewise, endotoxin-pretreatment immediately prior to 2.0 or 4.0 ATA O2 exposure does not prolong survival compared to controls. It is likely that lung injury during the normobaric oxygen preexposure and the central nervous system toxicity of hyperbaric oxygen interact to limit survival.
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PMID:The endotoxin-pretreated, oxygen-adapted rat model in hyperbaric hyperoxia. 648 6

Hyperbaric air and hyperbaric hyperoxia, which have been shown to decrease both liver plasma flow and plasma volume in dogs, may potentially affect the disposition of drugs whose distribution and/or elimination are dependent upon those actions. This study examined the effects of those conditions on the disposition of salicylic acid, using the dog as a model. The drug was administered to six mixed-breed dogs as a 10 mg sodium salicylate/kg i.v. bolus at 1 ATA breathing air (control), at 2.8 ATA breathing 100% O2, and at 6 ATA breathing air, followed by serial blood sampling for 8 h. Statistical analysis showed a significant increase (p less than 0.05) in salicylate clearance at 2.8 ATA compared to control with a subsequent, although not statistically significant, increase in elimination half-life. There were no significant differences between the values observed at 6 ATA and either control or 2.8 ATA. As 100% O2 at 2.8 ATA is used during hyperbaric oxygen medical therapy and during decompression, this change in disposition of this commonly used agent may have implications in man. Studies in man must be conducted, however, to determine if the same conclusions apply.
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PMID:Salicylate pharmacokinetics in the dog at 6 ATA in air and at 2.8 ATA in 100% oxygen. 662 74

High hydrostatic pressure has been shown to reverse the anesthetic effects of barbiturates. However, attempts to distinguish between two possible causes of this reversal, changes in drug disposition or changes in drug-receptor interaction, have not been reported. This study examined the possible effects of hyperbaria and hyperbaric hyperoxia on the distribution and clearance of pentobarbital in the dog. The drug was administered to six mixed-breed dogs as a 30 mg/kg i.v. bolus at 1 ATA breathing air, 6 ATA breathing air, and 2.8 ATA breathing 100% oxygen, with serial blood sampling for 12 h. Pharmacokinetic and statistical analyses showed no significant effects of hyperbaria or hyperbaric hyperoxia on the total plasma clearance, volume of distribution or elimination half-life. If pressure reversal of barbiturate anesthesia occurs at these pressures, changes in the disposition of the drug are not the causative factors.
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PMID:Pharmacokinetics of pentobarbital under hyperbaric and hyperbaric hyperoxic conditions in the dog. 665 25

Hyperoxia beyond 1.8 ATA results in a striking reduction of high-pressure neurological syndrome (HPNS) type I convulsion threshold pressures but is without measurable effect on type II convulsions. The synergism is partially or completely reversed by increasing alveolar or tissue CO2 levels. High total pressures (PI) result in striking reductions in the duration of hyperoxic exposure preceding seizure onset (tc). The interaction of hyperoxia and high pressure gives rise to three zones on the PO2-Pt plane. In zone I, Pt less than 30 ATA, the duration of hyperoxia prior to convulsion onset is given by the equation PO2 -- PO2 lim = K/(tc -- tc lim), where PO2 lim and tc lim both decrease with increasing total pressure. Zone II, Pt = 30-50 ATA and PO2 1.8-2.3 ATA, is characterized by a sharp drop in tc, as Pt is increased beyond 30 ATA, to a value near 15 min that is constant within the PO2 limits given. In zone III, Pt greater than 50 ATA and PO2 greater than 0.2 ATA, tc is of the order of 2 min, and the seizures are essentially HPNS seizures only slightly modified by hyperoxia. The data are interpreted as suggesting that zone I represents hyperoxic seizures facilitated by high pressures, whereas zone II represents HPNS type I seizures facilitated by hyperoxia.
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PMID:Synergism of hyperoxia and high helium pressures in the causation of convulsions. 681 23

Patients being treated for a variety of conditions with hyperbaria or hyperbaric hyperoxia, and ill or injured deep sea divers being decompressed, may require concomitant drug therapy. This study examined the possible effects of those conditions on the distribution and elimination of meperidine, using the dog as a model. The drug was administered to six mixed-breed dogs as a 1.4 mg/kg i.v. bolus at 1 ATA breathing air, at 2.8 ATA breathing 100% O2, and at 6 ATA breathing air, and followed by serial blood sampling for 3 h. Statistical analysis showed no effects of hyperbaria or hyperbaric hyperoxia on the elimination half-life, total plasma clearance, or volume of distribution. These studies demonstrated marked differences between man and the dog in the elimination of meperidine. This probably means these results cannot be extrapolated to man.
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PMID:Drug disposition under hyperbaric and hyperbaric hyperoxic conditions: meperidine in the dog. 687 Jul 34

1 The uptake of 5-hydroxytryptamine (5-HT) and beta-phenylethylamine (PEA) and their deamination by monoamine oxidase (MAO) were studied in perfused lung from male and female rats exposed to 100% O(2) at 1 ATA for up to 60 h.2 The uptake and metabolism of 5-HT in lungs from both male and female rats was not changed by exposure to O(2).3 The uptake and metabolism of PEA by lungs from male rats was unchanged. Uptake of PEA by lungs from female rats was inhibited 20% and 62% after 37 h and 50 h exposure respectively.4 MAO activity, both in vitro and in perfused lung, was increased towards PEA after 35 h of hyperoxia.5 Metabolism of PEA in perfused lung, measured over 30 min, was inhibited 52% after 50 h of O(2) hyperoxia.6 These results show that exposure to high concentrations of O(2) damages lung, resulting in inhibition of uptake of PEA and consequently in inhibition of metabolism of PEA.7 These results also indicate that, in lung from female rats, MAO-type B is more susceptible to changes in O(2) tension than MAO type A.
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PMID:Effect of hyperoxia on uptake and metabolism of 5-hydroxytryptamine and beta-phenylethylamine in rat lung: a sex difference. 723 95

The effect of pre-exposure to graded hyperoxia on subsequent survival under hyperbaric conditions was investigated in 250-300 g male Sprague-Dawley rats. The average survival of normal rats was approximately 4 d in 1 ATA O2, 1 d in 1.5 ATA O2, and 16 h in 2 ATA O2. Rats pre-exposed to O2 at 0.8 ATA for 1 week became O2 tolerant and survived a subsequent 1 week in O2 at 1 ATA with zero mortality. These O2-tolerant rats had a three-fold increase of survival duration in O2 at 1.5 ATA, but showed no significant prolongation of survival in 2 ATA O2. Pre-exposure to 0.8 ATA O2 for 2 weeks had no further effect on tolerance. However, rats pre-exposed to O2 at 0.8 ATA for 1 week followed by exposure to O2 at 1 ATA for a second week demonstrated approximately a three-fold increase in subsequent survival at 2 ATA O2. The results indicate that oxygen-tolerant rats remain susceptible to mortality in 1.5-2 ATA O2 and that graded tolerance to O2 develops as a function of the oxygen exposure regimen.
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PMID:The oxygen-adapted rat model: Tolerance to oxygen at 1.5 and 2 ATA. 741 43

Exposure of dark- or light-adapted mice to 1--3 ATA oxygen for times ranging from 15 min to 4 h caused a progressive increase in P-450, which peaked and then decayed. The rate of decay appears to be independent of PO2. A linear, inverse relationship was noted between the PO2 in the range of 1--4 ATA and the duration of exposure needed to obtain maximum P-450 levels. Cytochrome P-450 was induced by hyperoxia in vitro in a suspension of hepatocytes, and this induction was prevented by inhibitors of transcription and translation and by disulfiram. Cytochrome P-450 induction is not a general phenomenon of stress, albeit physical restraint may decrease the level of P-450 induced. Induction was a specific effect of increased oxygen tensions and was not due to pressure per se. Neither equivalent pressures of compressed air in the in vivo experiments nor equivalent pressures of nitrogen in the in vitro experiments induced P-450. Induction in vivo was inhibited by disulfiram and metyrapone. Hyperoxia is the most rapid inducer of P-450 yet found, and this response may represent a protective mechanism against hyperoxia.
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PMID:In vivo and in vitro induction of cytochrome P-450 synthesis in hyperoxia. 742 54

Glutathione (GSH) administered intraperitoneally significantly prolongs the time to initial seizure and survival time of rats exposed to hyperbaric hyperoxia (HBO). Acivicin is an antitumor antibiotic that is an inhibitor of gamma-glutamyl transpeptidase (GGT), an enzyme necessary for the breakdown and transport across cell membranes of GSH. To determine whether acivicin treatment alters GSH-induced protection from HBO, rats were dosed with 25 mg/kg of acivicin or vehicle 1 h before O2 exposure at an inspired O2 fraction of 1.0 at 4 ATA. Immediately before exposure, rats received GSH (1 mmol/kg) or vehicle. Time to seizure and time to death were recorded during exposure by direct observation. In separate groups of rats on the same dosing schedule, plasma GSH, renal GGT, and brain GGT were measured 15 min after the GSH injection without HBO exposure and 100 min after the beginning of HBO exposure. Renal GGT was decreased to 2.5% of control and brain GGT to 37% of control in the acivicin-dosed rats. Plasma GSH increased 3-fold in rats given acivicin alone, 52-fold in rats given GSH alone, and 84-fold in rats receiving both acivicin and GSH. Rats dosed with GSH alone had significantly prolonged times to seizure and death compared with all other groups. Rats dosed with GSH after receiving acivicin were not protected from HBO despite the large increase in plasma GSH that occurred in these animals. GSH treatment did not increase tissue GSH in lung, liver, or brain at 160 or 200 min of exposure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Elimination of glutathione-induced protection from hyperbaric hyperoxia by acivicin. 791 99


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