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

Hyperoxia activates superoxide dismutase (SOD) while inactivating catalase and glutathione peroxidase in polymorphonuclear leucocytes (PMN) and alveolar marcophages (AM) obtained from guinea-pigs exposed to 85% oxygen for 90 h. The influence of these altered enzyme activities on the rate of oxygen consumption and release of superoxide anion (O--2) and hydrogen peroxide (H2O2) was investigated. By 18 h O--2 released from resting PMN increased two-fold and remained elevated through the entire periods of the study, whereas H2O2 release and oxygen consumption at the same time points remained normal. At 66 h PMN phagocytizing opsonized zymosan particles released additional quantities of O--2 and H2O2 and consumed significantly more oxygen compared to the usual increase noted at earlier time points. Although oxygen consumption was almost two-fold higher in AM than PMN, phagocytizing AM released three-fold less O--2 and five-fold less H2O2 than did PMN. Furthermore, AM of animals exposed to hyperoxia no longer exhibited enhanced O--2 production upon exposure to opsonized zymosan. Hydrogen peroxide release progressively decreased at rest but progressively increased during phagocytosis of opsonized zymosan during the 90 h exposure to hyperoxia. No changes in oxygen consumption of AM occurred during hyperoxia. The divergent oxidative responses in PMN and AM of guinea-pigs exposed to hyperoxia suggest different biochemical adaptive mechanisms.
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PMID:Effect of hyperoxia on superoxide anion and hydrogen peroxide production of polymorphonuclear leucocytes and alveolar macrophages. 19 22

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

Theoretical and experimental investigations have shown that the oxygen pressure field of an organ reflects the state of the oxygen supply of a tissue. Unfortunately it is practically impossible to measure the total oxygen pressure field. Meaurements of arterial and venous PO2 or of the mean tissue PO2 do not reveal the local tissue situation. Measurements together with K. Kunze and M. Kessler lead us to the conclusion, that the oxygen pressure field can be characterized sufficiently well by a PO2-histogram. Under normal conditions the PO2-histogram is bell shaped with a steeper left side. The form and position is rather consistent. In hypoxia low PO2 values increase causing a leftward shift of the histogram; in hyperoxia the bell shaped form is destroyed and the form becomes broader and irregular. The form of the histogram gives also information about the state of the regulation of the microflow. It can be measured by PO2 microelectrodes as well as by multiwire surface electrodes. Both techniques have been applied successfully with patients.
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PMID:[The significance of the local oxygen pressure and of the PO2 histogram for the evaluation of the state of oxygen supply to various organs (author's transl)]. 19 96

In order to investigate the effects of high concentrations of oxygen on the lung, experiments were performed on 18 baboons exposed to a humidified environment of 95% oxygen for five days. Open lung biopsies for biochemical assay, histologic and electron microscopic analysis and measurement of tissue respiration were performed before and after oxygen exposure. Pulmonary function was evaluated by measurement of arterial blood gases, compliance, closing capacity (CC), functional residual capacity (FRC), total lung capacity (TLC), residual volume (RV) and vital capacity (VC) before and after exposure and then at seven and 14 days in the animals which recovered. Six baboons removed from the oxygen environment after 96--110 hours and exposed to room air died within three to 20 hours of profound hypoxemia (PaO2 40 +/- 6). The remaining 12 baboons were successfully weaned to room air over a three day period with a return of ABGs to control values (PaO2 89+/- 2). Electron microscopic analysis of alveolar membranes exposed to 120 hours of hyperoxia demonstrated endothelial cell swelling, interstitial alveolar membrane edema, and an increased predominance of Type II pneumocytes. Lung volume measurements showed significant decreases in TLC (25%), VC (34%), CC/TLC (28%) and dynamic compliance (47%). Biochemical studies indicated a shift toward anaerobic metabolism with a decrese in tissue oxygen consumption, reduced cytochrome oxidase activity, and increased lung lactic acid production. These changes were all found to be reversible in the 12 baboons slowly weaned back to room air.
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PMID:Reversible pulmonary oxygen toxicity in the primate. 21 38

To study the ultrastructural effects of hyperoxia on the kidney, young adult Sprague Dawley rats were exposed to 3 atmospheres absolute (ATAs) of pure oxygen for 5 hours and were killed in a time sequence varying from immediately to 30 days after exposure. Their renal cortices were processed for electron microscopy. Selective mitochondrial changes were observed within sublethally and transiently altered proximal tubular epithelial cells. The most consistent finding was the accumulation of 0.08 mu to 0.5 mu round to ovoid homogeneous matrical inclusions which frequently formed larger confluent amorphous masses. The inclusions stained intensely with lead and uranium but appeared homogeneously electron-lucent in unstained sections. Energy-dispersive x-ray analysis revealed that they did not contain calcium or phosphorus. The inclusions were different from the innately electron-opaque flocculent densities commonly found in pathologically altered mitochondria. Since the mitochondria containing them were removed by autophagocytosis, it is suggested that the inclusions were associated with selective mitochondrial degeneration induced by hyperoxia. No glomerular lesions were found.
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PMID:Selective mitochondrial degeneration in renal tubules following hyperbaric oxygen exposure. 22 8

Before exposure of man to hyperbaric hyperoxia the blood plasma possessed marked erythropoietic activity. Erythropoietins disappeared completely and erythropoiesis inhibitors appeared in the plasma of persons untrained to hyperbaric hyperoxia after a 24-hour exposure to hyperoxic conditions (25% of oxygen in the inhaled air) in the high pressure chamber corresponding to the depth of 63 metres. A reduction of the peripheral red blood indices was observed by that time.
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PMID:[Plasma erythropoiesis inhibitors in humans during hyperbaric hyperoxia]. 42 Sep 29

Substrate specificity of monoamine oxidase (MAO) of the A type from rat brain and liver tissues was altered after exposure of rats to an increased oxygen pressure [4 ati O2, 1 hr]. Simultaneously with a decrease in monoamine deaminating activity the enzyme acquired an ability to deaminate several substances, which are not MAO substrates in normal state, in particular, aminosugars. Activity of MAO of the B type was not altered in brain under hyperoxia. Alterations in catalytic properties of MAO of the A type were apparently important in development of the oxygen intoxication.
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PMID:[Type A and B monoamine oxidase activity in hyperbaric oxygenation]. 45 1

Equipment has been developed for the servo-control of arterial oxygen tension in sick, newborn babies. Using an indwelling umbilical arterial oxygen electrode as sensor, the equipment successfully regulated the administration of oxygen to 12 newborn babies with respiratory distress syndrome, significantly improving the stability of arterial oxygen tension and lessening the duration of episodes of hypoxia and hyperoxia.
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PMID:New technique for servo-control of arterial oxygen tension in preterm infants. 45 11

Changes of the oxygen tension in the surface layers of cerebral cortex (PtO2) and arterial blood (PaO2) in the conditions of hyperoxia occurred in anesthetized rabbits: raising of O2 partial pressure in altitude chamber to 1.0 and 2.0 kgs/cm2 increased PaO2 from 76.5 +/- 11.4 mm Hg to 472.3 +/- 63.1 and 1138.0 +/- 79.4 mm Hg respectively. Raising of O2 partial pressure in altitude chamber from 0.2 to 6.0 kgs/cm2 increased PtO2 from 34.9 +/- 12.0 to 1087.5 +/- 149.8 mm Hg. Obvious defence reactions of the organism developed at the moment of transition from air breathing to pure oxygen breathing under the pressure of 1.0 kgs/cm2. High effectiveness of these reactions preserved with the raising of pressure to 3.0 kgs/cm2 and weakened with the further raising of pressure to 4.0-6.0 kgs/cm2. With prolongation of exposure to the 2.0-3.0 kgs/cm2 pressure the defence reactions slackened as well.
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PMID:[Effect of hyperoxia on oxygen tension in the blood and brain tissue]. 45 65

Recent data demonstrate that the magnitude of the heat loss that occurs from the respiratory tract during exercise correlates with the degree of post-exertional obstruction that develops in asthmatics. Respiratory heat loss relates directly to the minute ventilation and heat capacity of the inspired gas and inversely to its water content and temperature. Because it has been shown that inhaling 100% oxygen during exercise blunts the obstructive response, we wondered if this effect could be accounted for by differing values of heat exchange with air and oxygen breathing. To examine this question, we studied 10 asthmatics by measuring multiple aspects of pulmonary mechanics before and after four bouts of exhausting leg work during which the subjects inhaled either air or oxygen conditioned to provide widely differing thermal burdens on their airways. Under all inspired gas conditions, oxygen breathing produced significantly less obstruction than air. Minute ventilation was also significantly less with oxygen as was the total heat lost. As the latter fell, so did the magnitude of the postexercise obstruction. When the differences in ventilation and respiratory heat loss between air and oxygen were eliminated by eucapnic hyperventilation, the differences in the obstructive responses also disappeared. Thus, the effects of hyperoxia on exercise-induced asthma can be accounteed for solely by alterations in heat exchange.
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PMID:A critical assessment of the mechanism by which hyperoxia attenuates exercise-induced asthma. 45 67


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