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

Pulmonary and systemic hemodynamics and arterial blood gases were measured in anesthetized and mechanically ventilated dogs before and after oral or intravenous administration of ethanol. Increases in mean pulmonary artery pressure and pulmonary vascular resistance occurred. Platelet antiserum-induced thrombocytopenia inhibition of prostaglandin synthesis with meclofenamate, or alpha-adrenergic blockade did not alter the pulmonary pressor response to ethanol. However, the increase in resistance following ethanol was abolished by hyperoxia and potentiated by hypoxia. Thus, it appears that the effect of ethanol is to augment hypoxic pulmonary vasoconstriction, whereas ethanol per se has no independent pulmonary pressor activity.
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PMID:Potentiation of hypoxic pulmonary vasoconstriction by ethyl alcohol in dogs. 62 4

Although supplemental fatty acids have been shown to alter the susceptibility of experimental animals to oxidant gases, the relationship between the degree of tissue fatty acyl unsaturation and resistance to oxidant exposure remains undefined. Because vascular endothelial cells have been demonstrated to be sensitive cellular targets in oxidant-induced lung injury, we evaluated the effects of a supplemental fatty acid on the lipid composition and oxidant susceptibility of pulmonary artery endothelial cells (PAEC) in monolayer culture. PAEC were incubated in culture medium supplemented with an ethanolic solution of 0.1 mM cis-vaccenic acid (CVA), an 18-carbon monounsaturated fatty acid, or with the ethanol vehicle alone for 3 h. Cells were then exposed to either control or oxidant (hyperoxia: 95% O2; or hydrogen peroxide: 100 microM) conditions. Oxidant-induced cell injury was assessed by phase-contrast microscopy and by measuring the release of intracellular lactate dehydrogenase. Incubation with CVA increased the CVA content of PAEC lipids and protected cells from oxidant-induced injury for up to 72 h after supplementation. CVA had no effect on nonoxidant-induced cell injury. Although the mechanism by which CVA protects cells against oxidant injury remains undefined, evidence is presented that indicates the mechanism does not involve induction of antioxidant enzyme activity, alterations in the physical state of PAEC membranes, or enhancement of PAEC nucleic acid repair mechanisms. These results define a useful model for exploring the relationship between lipid composition and oxidant susceptibility and suggest that fatty acid modifications may constitute an important strategy for protecting cells against oxidant injury.
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PMID:Fatty acid supplementation protects pulmonary artery endothelial cells from oxidant injury. 222 2

The level of adenosine was measured in monthly biopsied livers from rats fed ethanol and a high fat/low protein diet in order to test a hypothesis that hepatic adenosine is increased due to enhanced breakdown of adenine nucleotides in which ATP and total adenylate pool were decreased by chronic ethanol feeding. The ethanol-fed rats showed a significantly higher average level of adenosine compared to the pair-fed controls. When investigated monthly, however, adenosine in ethanol-fed rats increased only after the decrease in ATP had stabilized and AMP remained unchanged, indicating that these changes were not temporarily related. The average percentage of change in adenosine after acute hyperoxia or hypoxia were variable both in ethanol-fed and pair-fed rats. There was a tendency for a positive correlation between the percentage of change of adenosine and AMP after hyperoxia regardless of ethanol feeding. A negative correlation between the percentage of change of adenosine and energy charge, and a positive correlation between the percentage of change of adenosine and AMP were seen after hypoxia regardless of ethanol feeding. Adenosine levels changed rapidly in response to changes in systemic of pO2 in both the ethanol-fed and control rats, indicating that the liver maintained its normal response to the changes in energy state. The results indicate that chronic ethanol feeding does increase the level of adenosine in the liver and that this level remains responsive to acute changes in pO2.(ABSTRACT TRUNCATED AT 250 WORDS)
Alcohol Clin Exp Res 1988 Aug
PMID:Hepatic adenosine in rats fed ethanol: effect of acute hyperoxia or hypoxia. 305 72

Hyperoxia and hyperbaric hyperoxia increased the rate of cerebral hydrogen peroxide (H2O2) production in unanesthetized rats in vivo, as measured by the H2O2-mediated inactivation of endogenous catalase activity following injection of 3-amino-1,2,4-triazole. Brain catalase activity in rats breathing air (0.2 ATA O2) decreased to 75, 61, and 40% of controls due to endogenous H2O2 production at 30, 60, and 120 min, respectively, after intraperitoneal injection of 3-amino-1,2,4-triazole. The rate of catalase inactivation increased linearly in rats exposed to 0.6 ATA O2 (3 ATA air), 1.0 ATA O2 (normobaric 100% O2) and 3.0 ATA O2 (3 ATA 100% O2) compared with 0.2 ATA O2 (room air). Catalase inactivation was prevented by pretreatment of rats with ethanol (4 g/kg), a competitive substrate for the reactive catalase-H2O2 intermediate, compound I. This confirmed that catalase inactivation by 3-amino-1,2,4-triazole was due to formation of the catalase-H2O2 intermediate, compound I. The linear rate of catalase inactivation allows estimates of the average steady-state H2O2 concentration within brain peroxisomes to be calculated from the formula: [H2O2] = 6.6 pM + 5.6 ATA-1 X pM X [O2], where [O2] is the concentration of oxygen in ATA that the rats are breathing. Thus the H2O2 concentration in brains of rats exposed to room air is calculated to be about 7.7 pM, rises 60% when O2 tension is increased to 100% O2, and increases 300% at 3 ATA 100% O2, where symptoms of central nervous system toxicity first become apparent. These studies support the concept that H2O2 is an important mediator of O2-induced injury to the central nervous system.
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PMID:Hyperoxia increases H2O2 production by brain in vivo. 362 37

The effects of environmental and toxicological factors were tested in a new and "simple" biological system; the collective motility exhibited by ram spermatozoa. Motility of highly concentrated semen (greater than 1 X 10(9) cells/ml) was evaluated objectively with a multichannel reflectospermiograph (RSG) connected to a minicomputer for an on-line analysis. The effect was tested on one of the energy-producing systems in the sperm cells, while the other was inhibited by 2-deoxy-D-glucose or antimycin-A so that the energy source for motility was known. The effects of the addition of ethanol to the semen in various concentrations, as well as various levels of oxygen in the environment were tested. When motility of the sperm cells was driven by mitochondrial respiration, the intensity and duration of motility was inhibited significantly above a threshold level. At the same level of ethanol, the motility was not significantly affected when the energy source was the fructolysis pathway. The effects of oxygen level were tested below and above the normal oxygen level (21% O2). When fructolysis was inhibited, the motility was fully dependent on oxygen supply, namely, that lower levels of oxygen inhibited motility. It was also found that under higher levels of O2 (hyperbaric hyperoxia conditions) the motility was inhibited due to the known oxygen toxicity effects.
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PMID:Sperm cell motility as a new experimental model for toxicological studies. 657 35

Nitrofurantoin, a commonly used urinary antiseptic, is associated with significant pulmonary toxicity. This study used a 51Cr rat lung explant cytotoxicity assay to demonstrate that nitrofurantoin (10(-3) M), when incubated with lung parenchymal cells for 12 h at 37 degrees C, resulted in significant lung cell injury (cytotoxic index of 43 +/- 2). This injury could be reduced (p less than 0.05) by several antioxidants, including superoxide dismutase, 300 U/ml (37 +/- 2); catalase, 1,100 U/ml (27 +/- 2); alpha tocopherol, 10 micrograms/ml (30 +/- 2); ascorbic acid 50 micrograms/ml (37 +/- 2); ethanol, 0.1% (35 +/- 2); dimethyl sulfoxide, 1.0% (37 +/- 2). Additionally, the nitrofurantoin-induced injury could be accelerated in the presence of hyperoxia (95% O2) from 45 +/- 2 to 62 +/- 1, p less than 0.01. These data suggest that nitrofurantoin can directly injure lung parenchymal cells, probably through oxidant mechanisms, and this might suggest alternative approaches in the evaluation and therapy of patients with this disorder.
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PMID:Nitrofurantoin: evidence for the oxidant injury of lung parenchymal cells. 683 54

"Oxidative stress" takes place in animal tissues when the balance between the cellular defense mechanisms (glutathione cycle, superoxide dismutase, catalase, vitamin E, etc.) and conditions capable of triggering oxidative reactions is altered. The oxidative reactions which occur under a variety of conditions were assessed by two non-invasive methods, low-level chemiluminescence and volatile hydrocarbon production. Oxidative stress induced by hyperoxia or organic hydroperoxides in isolated hepatocytes or the perfused liver, respectively, is accompanied by low-level chemiluminescence, the intensity of which is enhanced upon perturbation of the glutathione cycle system, i.e., glutathione depletion and/or selenium deficiency. Oxidative stress during redox cycling of paraquat, when infused into the perfused liver, is not accompanied by light emission, whereas menadione, a substance also capable of redox cycling, was found to elicit photoemission under similar conditions. The basal rates of ethane release by the perfused liver are enhanced during oxidative conditions such as metabolism of hydroperoxides, paraquat redox cycling, and ethanol oxidation. Alkane release during the latter involves the participation of alcohol dehydrogenase and further products of ethanol oxidation, i.e., acetaldehyde, as well as free radicals in some stage of the process. In vivo ethane release by animals with adjuvant arthritis was found higher than in controls, presumably due to a systemic response of liver to inflammation.
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PMID:Active oxygen metabolites and their action in the hepatocyte. Studies on chemiluminescence responses and alkane production. 696 Jun 50

The hypothesis that severe lung damage generated by acid aspiration or a 50-hour exposure to 100% oxygen aggravates ethanol-induced hemorrhagic mucosal lesions in the stomach was examined in the rat. Animals were either given intratracheally with pyrogen-free saline or HCl (pH 1.75) or exposed for 50 h to 100% oxygen before the intragastric application of 1 ml of 50 or 75% ethanol. All rats receiving 50% ethanol were also given 3% monastral blue, 3 min before ethanol administration as a vascular tracer. Lung acid damage and inflammation as assessed by bronchopulmonary lavage were severe. We observed a significant increase in extracellular lactate dehydrogenase beta-glucosaminidase, albumin and the number of polymorphonuclear leukocytes in the lavage fluid. The number of resident macrophages decreased significantly. Blood gas analysis was not influenced. Hemorrhagic gastric mucosal lesions after 50 or 75% ethanol increased from 4.4 or 8.2% to 9.8 or 13.1% after HCl and from 6.7 or 18.2% to 10.6 or 21.6% of the glandular stomach following oxygen exposure. The area of mucosal vascular damage caused by 50% ethanol as revealed by monastral blue labelling was 3.3 and 2.6 times larger in rats with lung damage induced by HCl or hyperoxia, respectively. Thus, severe lung damage predisposes to microvascular damage and aggravates chemically induced hemorrhagic mucosal lesions.
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PMID:Lung damage aggravates gastric mucosal lesions induced by ethanol in the rat. 765 45

We have analyzed the magnitude and uniformity of the expression of manganese superoxide dismutase (Mn SOD) protein in alveolar type II cells of rats exposed to hyperoxia using quantitative colloidal gold immunocytochemistry and morphometric techniques. Sprague-Dawley rats were exposed continuously to normal air or to 85% oxygen for 7 and 14 days. The lungs were fixed by intratracheal instillation of a paraformaldehyde-glutaraldehyde fixative. Lung samples were dehydrated in ethanol and embedded in LR-White. Thin sections for electron microscopy were labeled with anti-rat Mn SOD rabbit antiserum followed by protein-A gold. The labeling density (gold particles/micron 2) over subcellular compartments was determined, and relative organelle volumes were measured using a random point overlay. The results confirm that alveolar type II cells are a locus of Mn SOD response in the lungs of hyperoxic rats and contribute to this response through a combination of changes: an increase of Mn SOD concentration in the mitochondrial matrix, an increase of mitochondrial volume per cell, and type II cell hyperplasia.
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PMID:Quantitative immunocytochemical analysis of Mn SOD in alveolar type II cells of the hyperoxic rat. 794 50

The mutual potentiation of the hepatotoxic effects of ethanol and hypoxia raised the question of whether such an interaction also occurs in the cardiovascular system. Therefore, anaesthetized rats were infused intravenously with ethanol (25 mg/kg x min.) over 90 min. to reach blood ethanol concentrations between 2.2 and 2.6 g/l and were ventilated artificially either with room air, 10% O2/90% N2 or 100% O2. Under normoxic conditions, ethanol produced a slow decrease of mean arterial blood pressure from 130 to 100 mmHg due to the decline in cardiac output and stroke volume (-20%) while heart rate and peripheral resistance remained unchanged. Hypoxia (arterial oxygen tension 35-38 mmHg) without ethanol produced immediate hypotension (-60 mmHg) without decreasing the cardiac output, i.e. by reducing peripheral resistance. In combination with ethanol, hypoxia produced an even stronger hypotension (-90 mmHg) due to reduction in both cardiac output and peripheral resistance. On the other hand, respiration with 100% O2 (arterial oxygen tension about 500 mmHg) elevated peripheral resistance, attenuated ethanol-induced cardiodepression and prevented ethanol-induced hypotension. The lethal doses of ethanol evaluated by infusing 75 mg/kg x min. ethanol until death amounted to 4.1 g/kg with 10% O2, to 5.5 g/kg with 20% O2 (room air) and to 6.9 g/kg with 100% O2. Thus decrease in vascular contractility induced by hypoxia combined with ethanol-induced cardiodepression may result in lethal cardiovascular failure. Hyperoxia, on the other hand, counteracts ethanol-induced cardiodepression and its acute toxicity by raising the vascular contractility.
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PMID:Influence of hypoxia and hyperoxia on the cardiovascular and lethal effects of ethanol. 1019 68


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