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

Despite the seriousness of pulmonary O2 toxicity, patients can generally withstand 1 atm. of PO2 for at least 24 hours. Also, there is no evidence that clinically relevant pulmonary O2 toxicity occurs in humans at inspired partial pressures below 0.4 to 0.5 ATA, even with prolonged exposures. Neither is there clinical or experimental evidence to indicate that patients with preexisting pulmonary disease are more sensitive to O2 toxicity than are normal volunteers. Although the florid manifestations of pulmonary O2 toxicity may have dire consequences, a lower dosage of O2, though still potentially toxic, may well be acceptable. The lung itself can generate some level of self-protection with prolonged O2 exposure, ultimately healing itself to a significant degree. Therefore, no patient should be exposed to dangerous levels of hypoxia out of fear of causing pulmonary O2 toxicity. Pulmonary hyperoxia and systemic hypoxia can usually be avoided with skillful, titrated management of respiratory insufficiency.
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PMID:Clinical manifestations of pulmonary oxygen toxicity. 616 47

Bradycardia has been observed in animals and humans upon exposure to various hyperbaric environments. However, the relative contribution of ambient pressure, gas density, inert gas species, and inspired O2 tension has not been defined. By means of cutaneous ECG leads, the heart rates of unanesthetized rats were recorded and compared in 11 separate thermo-neutral environments. Ambient pressures applied were 1, 3, and 10 ATA, O2 partial pressure PO2 ranged from 140 to 1,590 Torr, and gas densities were varied from 0.40 to 11.45 g/l, utilizing either N2-O2 or He-O2 mixtures. The exposure heart rates were averaged over a 30-min period and compared with a preceding control value obtained in 1 ATA normoxic He or N2. Significant bradycardia was associated with hyperoxia in environments containing either He or N2, with a magnitude proportional to log PO2. On the other hand, under normoxic conditions bradycardia was not observed despite the similar density, pressure, and inert gas components. It is concluded that hyperoxia is the most important variable of those considered in the development of hyperbaric bradycardia.
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PMID:Contribution of environmental factors in development of hyperbaric bradycardia. 626 92

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


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