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

An investigation of acid and neutral triacylglycerol lipases in rat lung tissue has been carried out. The effect of high oxygen concentration in the inspired gas mixture on the activities of the two triacylglycerol lipases has been studied. Hyperoxia had a strong inhibitory effect on both enzymes, the degree of inhibition being dependent on the duration of exposure. Dibutyryl-3',5' AMP and NaF restored completely the activities of the inhibited triacylglycerol lipases, while adrenaline and caffeine had no effect. The possible mechanisms of the effects of oxygen on lung triacylglycerol lipases are discussed.
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PMID:[Effect of hyperoxia on triacylglycerol lipase activity of the rat lung (author's transl)]. 19 50

We have studied the effect of various compounds, known as antioxidants, on the level of hyperoxia (80-90% O2)-induced chromosomal aberrations in Chinese hamster ovary cells: ascorbic acid, alpha-tocopherol, carnosine, imidazole-4-acetic acid, glutathione monoethylester, N-acetylcysteine and ethoxyquin. Carnosine (beta-alanyl-histidine) appeared to be the only compound that reduced chromosomal breakage. The effect was also present in cultures post-treated with caffeine (at 2.5 mM, 3 h before harvest), indicating that the apparent protection was not due to selective arrest of chromosomally damaged cells in the G2 phase of the cell cycle. Imidazole-4-acetic acid, a compound structurally very similar to carnosine, had no detectable effect. Ascorbic acid, N-acetylcysteine, glutathione monoethylester and ethoxyquin were found to have a pro-oxidant effect, i.e. they apparently potentiated the clastogenic effect of hyperoxia. Carnosine is the first compound shown to protect against the clastogenicity of normobaric hyperoxia and may thus be a useful tool in elucidating the underlying mechanism.
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PMID:Effect of antioxidants on hyperoxia-induced chromosomal breakage in Chinese hamster ovary cells: protection by carnosine. 194 22

In carotid body-denervated cats, moderate hypoxia, or even normoxia when compared to hyperoxia, provokes a significant depression of the respiratory output. This is observed in conscious or anesthetized or decerebrated animals. On the other hand, more severe hypoxia induces tachypnea (hypoxic tachypnea of Miller and Tenney, Respir. Physiol. 23: 31-39, 1975) in conscious cats, whereas the same hypoxia is followed by marked respiratory depression or apnea in the anesthetized or decerebrated animals. Hypoxic tachypnea can be partly or completely reversed by injection of dopa or xanthines such as caffeine or aminophylline. This suggests that alterations in brain monoamine metabolism by hypoxia may be responsible for the alterations in suprapontine respiratory control systems, resulting the tachypnea. Mild hypercapnia can also reverse hypoxic tachypnea. It is concluded that the ventilatory response to hypoxia of conscious animals results from stimulation of peripheral chemoreceptors, inhibition of brain stem neurons, and finally involvement of suprapontine structures that seems to be mediated by depletion of monoamines.
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PMID:Possible alterations in brain monoamine metabolism during hypoxia-induced tachypnea in cats. 677 76

This study characterized the effects of caffeine (1.0-30.0 mg/kg) and nicotine (0.1-3.0 mg/kg) administered alone and in combination on ventilation in unanesthetized rhesus monkeys. In seated monkeys prepared with a head plethysmograph, ventilation was measured during exposure to air (normocapnia), CO2 (3%, 4% and 5%) mixed in air (hypercapnia), 10% O2 mixed in N2 (hypoxia) and 100% O2 (hyperoxia). Caffeine produced marked, dose-dependent increases in ventilation during conditions of normocapnia and hypercapnia. In contrast, acute administration of nicotine had less pronounced respiratory-stimulant effects during all conditions. The joint effects of caffeine and nicotine on ventilation generally did not differ from those obtained with caffeine alone. Chronic administration of nicotine (1.0 mg/kg/day) for 4 consecutive wk via osmotic pumps significantly decreased the half-life of caffeine but had little effect on ventilation or on sensitivity to the respiratory-stimulant effects of caffeine. Two primary metabolites of caffeine, theophylline and paraxanthine, were active as respiratory stimulants and were equipotent to caffeine, and the joint effects of caffeine and its metabolites were additive. The results indicate that caffeine and nicotine stimulate respiration through different pharmacological mechanisms, in contrast to caffeine and its metabolites which exhibit a similar pharmacological profile. Moreover, significant pharmacokinetic interactions may be obtained when caffeine and nicotine are coadministered.
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PMID:Effects of caffeine on ventilation during acute and chronic nicotine administration in rhesus monkeys. 779 Oct 79

This study characterized in rhesus monkeys the effects of selected adenosine agonists on ventilation during normal atmospheric conditions and during conditions of hypercapnia, hypoxia and hyperoxia. In seated, unanesthetized monkeys prepared with a head plethysmograph, ventilation during exposure to air, CO2 (3, 4 and 5%) mixed in air (hypercapnia), 10% O2 mixed in N2 (hypoxia) and 100% O2 (hyperoxia) was measured during cumulative dosing with each drug. The nonselective (A1/A2) agonist, 5'-N-ethylcarboxamidadenosine (NECA), the peripherally active, A2-selective agonist, CGS 21680 [2-(carboxyethylphenylamino)adenosine-5'-carboxamide], and the A1-selective agonists, N6-cyclohexyladenosine and N6-cyclopentyladenosine, increased respiratory frequency (f), but had no significant effect on minute volume (VE) during exposure to air. The relative potencies for increasing f corresponded closely with their potencies for binding at A2 receptors. NECA and CGS 21680 increased f in a dose-dependent manner during exposure to 3% CO2, but proportional increases in f were less pronounced as the concentration of CO2 increased. NECA and CGS 21680 also increased f during hypoxia, but neither had a significant effect on f during subsequent hyperoxia. The highest dose of CHA and CPA decreased f below control values during exposure to 5% CO2 and decreased f and VE during hyperoxia. In contrast, the adenosine antagonist, caffeine, and the selective phosphodiesterase inhibitor, rolipram, increased f and VE under all conditions. During hypercapnia, the magnitude of the increases in f was similar at each concentration of CO2 studied. Caffeine and rolipram increased f and VE during hypoxia, and f and VE remained elevated during hyperoxia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of adenosine agonists on ventilation during hypercapnia, hypoxia and hyperoxia in rhesus monkeys. 849 37

We tested the effect of caffeine, on hyperoxia-induced seizures. Thirty-seven rats with chronic cortical electrodes were injected i.p. with caffeine (1.25, 2.5, and 10 mg/kg) or vehicle before exposure to 0.5 MPa oxygen and 17 rats to oxygen with 5% CO2 at 0.5 MPa. EEG monitoring and spectral analysis of EEG activity were carried out. Caffeine significantly prolonged the latent period to the onset of seizures (P < 0.05 in ANOVA), in a dose-related manner. Our results suggest that caffeine may be used in low doses for protection against hyperoxia-induced seizures.
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PMID:Caffeine attenuates CNS oxygen toxicity in rats. 857 77

To enhance the cytogenetic expression of the fragile X chromosome, we studied the effects of hyperoxia and caffeine on the induction of fragile Xq27.3. A lymphoblastoid cell line (GM 06912) derived from a fragile X male proband was cultured in RPMI 1640 containing 16% dialyzed fetal calf serum. The cells were synchronously subjected to one of 3 different atmospheric oxygen tensions (21%, 21.3 kPa, normoxic; 40%, 40.5 kPa, hyperoxic; or 60%, 60.8 kPa, hyperoxic) during the last 24 hours of the 72 hour culture, immediately after the addition of 2'-deoxy-5-fluorouridine (FUdR) at 25 ng/ml. To study the enhancing effect of caffeine, with or without hyperoxia, a second set of cultures was additionally subjected to caffeine (2.5 mM) during the last 6 hours of the culture. When the fragility of hyperoxic cells (38.1 kPa dissolved oxygen) was compared to that of normoxic control cells (13.3 kPa dissolved oxygen), the difference was significant (P < 0.05). These data suggest that there is a mean increase in the fragile Xq27.3 expressivity as the dissolved oxygen tension increases. Additionally, we observed that caffeine, with or without hyperoxia, significantly (P < 0.05) suppressed the expression of the fragile X site in this lymphoblastoid cell line.
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PMID:Effects of hyperoxia and caffeine on the expression of fragile site at Xq27.3. 883 39

The effect of hyperbaric hyperoxia on the pharmacokinetics of caffeine was investigated in human volunteers. Some 600 ml of coffee were administered to 2 volunteers and blood samples were serially collected for 24 h. The volunteers entered a hyperbaric chamber 2.5 h following coffee ingestion for a total period of 110 min (0.25 MPa, alternating 100% O2-breathing for 20 min and air breathing for 5 min). The concentrations of caffeine in serum was determined by high pressure liquid chromatography. The caffeine amount ingested was determined by analyzing an aliquot of the coffee beverage. Data were analyzed assuming linear kinetics and an open one-compartment model. Effects of hyperbaric hyperoxia on caffeine disposition were investigated using a runs test. Moreover, a one-population t-test was applied to residuals, separately for data from the initial normobaric period, the hyperbaric period and the terminal normobaric period. Pharmacokinetic parameters were similar to established literature data on caffeine [Volunteer 1: maximal concentration (Cmax: 6.13 mg.L-1 at Tmax: 55 min, half-time of elimination (T1/2: 180 min, total clearance (Cl): 3.41 ml.min-1.kg-1; volume of distribution (Vd: 0.88 I.kg-1; Volunteer 2: Cmax: 6.23 mg.L-1, Tmax: 94 min, T1/2: 283 min, Cl: 1.90 ml.min-1.kg-1, Vd: 0.77 L.kg-1). The runs test as well as the analysis of residuals gave no evidence for alterations of caffeine disposition by hyperoxia (p > 0.05). The pharmacokinetics of caffeine do not seem to be influenced in a clinically relevant way in humans during a stay for 100 min at 0.25 MPa, alternating 100% O2 and air breathing.
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PMID:Caffeine pharmacokinetics during hyperbaric hyperoxia in humans. 912 91

1. Hyperbaric or hyperoxic or both conditions may affect the disposition of drugs by (1) changes in the catalytic activity of drug metabolizing enzymes, (2) hemodynamic changes and (3) changes in membrane permeability, affecting drug distribution. 2. In isolated microsome preparations from rat liver, the metabolism rate of aniline, but not of amidopirin, is reduced by hyperoxia. In vivo, the clearance of salicylic acid is enhanced in the dog at 2.8 ATA and 100% O2, but not at 6 ATA and air, for reasons that are still unknown. The disposition of theophylline, pentobarbital or pethidine is not affected in dogs by hyperbaric or hyperoxic conditions. 3. In human volunteers, hyperbaric or hyperoxic or both conditions do not affect the disposition of gentamycin (2.4 bar, 100% O2), caffeine or lidocaine (2.5 bar, 100% O2). 4. In conclusion, a single exposure to hyperbaric or hyperoxic conditions does not seem to affect single-dose pharmacokinetics of drugs eliminated by the kidney (gentamycin) or by the liver with a capacity-limited clearance (pentobarbital, theophylline, caffeine) or with a perfusion-limited clearance (pethidine, lidocaine). The enhancement of salicylic acid clearance in dogs under hyperoxic conditions remains unclear.
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PMID:Effects of hyperbaric and hyperoxic conditions on the disposition of drugs: theoretical considerations and a review of the literature. 988 65

Reactive oxygen species produced during hyperoxia damage DNA, inhibit proliferation in G1- through p53-dependent activation of p21(Cip1/WAF1/Sdi1), and kill cells. Because checkpoint activation protects cells from genotoxic stress, we investigated cell proliferation and survival of the murine type II epithelial cell line MLE15 during hyperoxia. These cells were chosen for study because they express Simian large and small-T antigens, which transform cells in part by disrupting the p53-dependent G1 checkpoint. Cell counts, 5-bromo-2'-deoxyuridine labeling, and flow cytometry revealed that hyperoxia slowed cell cycle progression after one replication, resulting in a pronounced G2 arrest by 72 h. Addition of caffeine, which inactivates the G2 checkpoint, diminished the percentage of hyperoxic cells in G2 and increased the percentage in sub-G1 and G1. Abrogation of the G2 checkpoint was associated with enhanced oxygen-induced DNA strand breaks and cell death. Caffeine did not affect DNA integrity or viability of cells exposed to room air. Similarly, caffeine abrogated the G2 checkpoint in hyperoxic A549 epithelial cells and enhanced oxygen-induced toxicity. These data indicate that hyperoxia rapidly inhibits proliferation after one cell cycle and that the G2 checkpoint is critical for limiting DNA damage and cell death.
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PMID:Activation of the G2 cell cycle checkpoint enhances survival of epithelial cells exposed to hyperoxia. 1238 47


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