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

Rana catesbeiana Shaw tadpoles and adults were maintained at 20-23 degrees C under aerial and aquatic normoxia (PO2 150 mmHg), hyperoxia (PO2 275 mmHg) and hypoxia (PO2 75 mmHg) for 4 weeks, after which the following blood measurements were made: haematocrit, red blood cell count, haemoglobin concentration, mean corpuscular haemoglobin concentration, O2 capacity, O2 equilibrium curve, Bohr shift, Hill's coefficient and intraerythrocytic concentration of nucleotide triphosphates (ATP + GTP) and 2,3-DPG. Normoxic tadpoles had much higher blood O2 affinity (P50 9-10 mmHg) than adults (P50 35 mmHg) but a lower haemoglobin concentration, haematocrit and O2 capacity. The concentration of intraerythrocytic phosphates was higher in normoxic tadpoles than in adults, indicating that the higher O2 affinity of normoxic tadpole blood was due to the haemoglobins themselves, rather than affinity modulators. Chronic hypoxia in tadpoles produced little change in whole blood P50, and no significant change in any other blood variable. In adult bullfrogs, on the other hand, O2 capacity doubled through polycythaemia, and the P50 decreased by 11 mmHg (35%), though apparently not from any significant change in concentration of intraerythrocytic phosphates. Hyperoxia produced no haematological changes in either larvae or adults. In adult bullfrogs exposed to chronic hypoxia, the morphology of the gas exchange organs does not change (Burggren & Mwalukomo, 1983), but instead profound adjustments occur in the blood, favouring O2 transport under these conditions. The blood of the tadpole shows little or no response to chronic hypoxia, with morphological adjustments in skin, gills and lungs constituting the major response.
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PMID:Respiration during chronic hypoxia and hyperoxia in larval and adult bullfrogs (Rana catesbeiana). II. Changes in respiratory properties of whole blood. 660 82

We analyzed brain tissue in 139 rats for adenosine and its metabolites, inosine and hypoxanthine, during the initial 120 seconds of seizures induced by bicuculline. We also measured ATP, ADP, AMP, phosphocreatine (PCr), and lactate. We divided the rats into four groups by adjustment of their preictal arterial oxygen tension: group I, PaO2 > 200 mm Hg; group II PaO2 = 50 mm Hg; and group III: PaO2 = 100 mm Hg. We treated a fourth group whose PaO2 = 100 mm Hg with phentolamine to block the 44% rise in blood pressure which occurred with the onset of seizures. PaCO2 was maintained between 30 anf 40 mm Hg in all groups. Brain tissue was sampled rapidly after 0, 10, 20, 30, 60, and 120 seconds of seizures by the freeze-blow technique. With normoxia (PaO2 = 100 mm Hg) or hyperoxia (PaO2 > 200 mm Hg), adenosine increased within ten seconds of the onset of seizures and remained elevated even after 120 seconds. Elevations in inosine and hypoxanthine were delayed compared to the increases in adenosine. A reduction in PaO2 (50 mm Hg) or systemic blood pressure during seizures caused a further augmentation in the increase in brain adenosine levels. During the seizure period, transient changes in adenine nucleotides and energy charge were observed, but PCr remained depressed and lactate continued to rise. The rapid and sustained increase in cerebral adenosine levels, temporally paralleling the changes in cerebral blood flow, supports the role for adenosine in the regulation of cerebral blood flow.
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PMID:Changes in brain adenosine during bicuculline-induced seizures in rats. Effects of hypoxia and altered systemic blood pressure. 677 98

To determine what biochemical indexes might be useful in measuring the endothelial response to hyperoxia in vitro we exposed endothelial cell monolayers (ECM) from pig aortas to either hyperoxic (95% O2:5% CO2, 1 atm) or control conditions (95% air:5% CO2) and made the following measurements: (a) DNA and protein contents remaining in the ECM; (b) lactate dehydrogenase (LDH) activity in the medium; (c) the net uptake of rubidium (Rb+), adenine, and adenosine; and (d) cellular ATP and medium lactate. Twelve hours of hyperoxic exposure did not cause significant changes. After 24 or 48 h of hyperoxia, DNA and protein contents were decreased; LDH activity and the protein-to-DNA ratio were increased; adenosine uptake was decreased per ECM but was unchanged when corrected for culture DNA and protein contents. Adenine uptake was unaltered as were cellular ATP content and medium lactate concentration. The net Rb+ uptake-to-DNA ratio was increased after 24 h but not after 48 h of hyperoxia. The extent of the DNA and LDH changes indicated that the cellular disturbance caused by hyperoxia was progressive from 12 to 48 h. Presence of superoxide dismutase (250 U/ml) prevented both the increase of LDH activity and the decrease of protein after 48 h but did not affect the decrease of DNA. These results suggest that the cells remaining in the ECM after hyperoxia have normal biochemical function and may represent a subpopulation of cells more resistant to oxygen toxicity than the damaged cells.
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PMID:Effects of hyperoxia on biochemical indexes of pig aortic endothelial function. 688 2

Breathing of 100% oxygen at ambient pressure causes disorders in mouse brain organic phosphate phosphocreatine (PC), ATP, ADP, and AMP. The fast increase in PC level attains a maximum augmentation of about 50% after 16-18 h of exposure with subsequent slight alterations between 18 and 50 h. The initial losses (a) in ATP amount to approximately 20% after 4 h; (b) in ADP, 32% after 6-8 h; and (c) in AMP, about 40% after 30 min and 50% after 50 h. contrary to the continual decrease in AMP, the ATP and ADP values exhibit a later increase to a constant level during the full time of exposure up to 50 h. The initial loss in adenosine nucleotides points to an intense effect of hyperoxia in nerve cell metabolism with subsequent attainment of a new adenylate equilibrium at lower concentrations. The increased but constant level of PC may be due to an inhibition of the oxygen sensitive SH-groups, which are an essential center in the creatine kinase. Although the absolute concentration of AMP is by far the lowest of the three nucleotides, the continual decrease in AMP is of considerable importance because of its direct response to ATP via adenylate kinase reaction.
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PMID:Brain energy metabolism in mice exposed to oxygen at 1 atmosphere absolute. 733 82

Exposure to hyperoxia causes alveolar macrophage (AM) injury. The present study investigates the roles of intracellular antioxidant enzymes and of glutathione in the protection of AMs against hyperoxia in a biphasic cell culture system in aerobiosis. The effect of normoxia or hyperoxia on the integrity of AMs was related to indices of cell injury (ATP cell content and lactate dehydrogenase release into culture medium) and cell mass (protein content of AMs). Antioxidant activities were measured in guinea-pig AMs exposed to 95% O2 or to normoxia (control cells) for 3 days. A 3-day AM culture in normoxia showed a significant decrease in protein and catalase, whereas ATP cell content, superoxide dismutase (SOD) (both Cu,Zn-SOD and Mn-SOD) and glutathione peroxidase (GPx) activities significantly increased. The content of reduced glutathione (GSH) did not change. Using the ATP content in AMs expressed as a cell injury index (CII), AM injury increased with increasing O2 exposure time (1 day: 13 +/- 4.4%; 2 days: 34 +/- 3.8%; 3 days: 40 +/- 4.1%; 4 days: 55 +/- 7.3%; 6 days: 87.5 +/- 5.4%). Exposure to 95% O2 for 3 days was associated with a significant decrease in ATP cell content, protein, catalase and GSH to the total glutathione ratio, whereas SOD, GSH and total glutathione did not change significantly. The GPx activities increased significantly. There was no significant correlation between the AM CII and SOD or GPx content. In contrast, a significant correlation was observed between hyperoxia-induced AM CII and catalase content (r = 0.71) and glutathione content (r = 0.71).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relationship between oxygen-induced alveolar macrophage injury and cell antioxidant defence. 774 27

Hypoxia is the alleged stimulus for initiation of increase of carbonic anhydrase II (CAII) and 2,3-diphosphoglycerate (2,3-DPG) synthesis of red blood cells from late chick embryos. The PO2-dependent regulation of red cell metabolism is mediated by unknown humoral factors [Million et al., Am. J. Physiol. 261 (Regulatory Integrative Comp. Physiol. 30): R1188-R1196, 1991]. In the present investigation we have analyzed whether interindividual differences in egg size (which result in different surface area-to-mass ratios) affect the timing of initiation of 2,3-DPG and CAII synthesis in late chick embryos. We also investigated the effect of extracellular adenine nucleotides on red cell organic phosphate pattern and O2 affinity to test whether the inhibitory effect of normal or elevated PO2 on 2,3-DPG synthesis and the concomitant increase of ATP (and O2 half-saturation pressure) can be mimicked by these agents. The results show that differences in egg size affect the timing of CAII and 2,3-DPG synthesis, indicating that PO2-dependent regulation of red cell function allows adjustment to the properties of the individual egg. We also found that extracellular ATP, which is rapidly degraded to AMP by red cell ectoenzymes, can alter the red cell phosphate pattern and O2 affinity, i.e., significantly increase red cell ATP, decrease red cell 2,3-DPG and O2 affinity, and thus mimic the effect of normoxia and hyperoxia. These findings suggest that extracellular adenine nucleotides may be involved in the PO2-dependent regulation of embryonic red cell metabolism.
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PMID:Control of red cell function of late chick embryos: role of extracellular ATP/AMP and egg size. 806 66

In the ventilated ischemic lung, oxygen tension will increase at a time when glucose depletion may impair antioxidant defenses, thereby predisposing the lung to injury mediated by oxygen radicals. In the unventilated ischemic lung, however, glucose depletion in the setting of low oxygen tension may decrease production of ATP, leading to injury by a different mechanism. In this study, we evaluated the role of both oxygen tension and glucose concentration on ischemic injury in isolated ferret lungs. Injury, defined as an increase in vascular permeability, was assessed by measurement of filtration coefficient (Kf) and osmotic reflection coefficient for albumin (sigma alb) after 3 h of normothermic (37 degrees C) ischemia without reperfusion. Lungs were ventilated with either 95% O2-5% CO2 or 0% O2-5% CO2. The vasculature was flushed with physiological salt solution containing either 15 mM glucose (hyperoxia-glucose, anoxia-glucose), 15 mM sucrose (hyperoxia-sucrose, anoxia-sucrose), or no substrate (hyperoxia-no substrate, anoxia-no substrate) (n = 6 for each condition). Kf and sigma alb in hyperoxia-no substrate group did not differ from values in minimally ischemic normoxic normoglycemic ferret lungs. Without glucose, ischemic injury was worse in anoxic than in hyperoxic lungs. With glucose, ischemic injury was worse in hyperoxic than in anoxic lungs. Glucose exacerbated injury in hyperoxic, but not anoxic, lungs. These results indicate that ischemic injury in these lungs depended on both oxygen tension and glucose concentration and suggest that both oxygen radical generation and ATP depletion during ischemia may contribute to the development of this injury.
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PMID:Effects of oxygen tension and glucose concentration on ischemic injury in ventilated ferret lungs. 822 35

To examine the potential impact of fluid dynamic boundary layers on cutaneous ion exchange, we investigated how bulk flow of dilute Na+ solutions (< or = 1.0 mmol l-1) over the skin of intact frogs (Rana catesbeiana and Rana pipiens) affects cutaneous Na+ uptake (JNa(in)) and transepithelial potential (TEP). Cessation of stirring resulted in a 14-35% decrease in TEP and a 14-65% decrease in JNa(in). Two weeks' acclimation to an unstirred bath increased JNa(in) to levels 70% greater than in frogs acclimated to a continuously stirred bath and to levels comparable to those of frogs acclimated to deionized water. These effects are consistent with depletion of Na+ in the boundary layer, but are also consistent with depletion of O2 in the boundary layer, which might limit generation of ATP consumed by ATPases responsible for cutaneous Na+ uptake. To investigate this latter possibility, we measured TEP and JNa(in) while manipulating the PO2 of well-stirred external media at constant [Na+]. Hyperoxia (PO2 > or = 97 kPa) increased JNa(in) by 28% and had little or no effect on TEP. Hypoxia (PO2 < or = 1.5 kPa) reduced JNa(in) by 48% and decreased TEP by 22%. These results suggest that ionic and gaseous boundary layers may interact to affect cutaneous ion transport.
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PMID:Bulk flow of the medium and cutaneous sodium uptake in frogs: potential significance of sodium and oxygen boundary layers. 844 Sep 67

A new micromethod for the determination of sphingomyelin in samples suspended in aqueous solutions, and modified micromethods for determining phosphatidylcholine and phosphatidylglycerol were used to determine phosphatidylcholine and sphingomyelin (detection limits of 1.8 mumol/l), and phosphatidylglycerol (detection limit of 2.3 mumol/l) in lipid dispersions, membranes from sheep erythrocytes and platelets, and pulmonary surfactants from rats of different ages and rats maintained under normobaric hyperoxia for 2 days prior to their sacrifice. The procedures are easy to perform, accurate, require less sample than conventional methods and can also be applied directly to aqueous samples. Phospholipase C and sphingomyelinase were used to release phosphorylcholine from phosphatidylglycerol and sphingomyelin, respectively. The choline released from phosphorylcholine by alkaline phosphatase is reconverted to phosphorylcholine by ATP and choline kinase. In the phophatidylglycerol determination, phospholipase D was used to release glycerol and phosphatidate. The glycerol formed was converted to glycerolphosphate using ATP and glycerol kinase. In all cases, the ADP thus formed was determined by following the enzymatic conversion of NADH to NAD at 340 nm in an coupled pyruvate kinase/lactate dehydrogenase system. Significant variations in the phospholipid composition of rat pulmonary surfactant were found during development; in particular there was an increase in the phosphatidylglycerol content of adult rats as compared with younger rats. Hyperoxia produced changes in the phosphatidylglycerol content of surfactant from adult rats, but not from 2-day old rats.
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PMID:Enzymatic determination of phosphatidylcholine, sphingomyelin and phosphatidylglycerol in lipid dispersions, blood cell membranes and rat pulmonary surfactant. 870 43

The recent immunopurification and cloning of various lung Na+ channel proteins has provided the necessary tools to study Na+ transport at a fundamental level across a number of epithelial tissues. Various macroscopic measurements of Na+ transport have shown that Na+ ions enter the cytoplasm of alveolar cells mainly through amiloride-inhibitable Na+ channels. Molecular biology studies have shown the existence of three Na+ channel subunit mRNAs (alpha-, beta-, and gamma-rENaC) in mature fetal (FDLE) and adult alveolar type II (ATII) cells. Patch-clamp studies have demonstrated the existence of various types of amiloride-inhibitable Na+ channels, located in the apical membranes of FDLE and ATII cells. beta-Agonists and agents that enhance intracellular adenosine 3',5'-cyclic monophosphate levels increase the open probability of these channels, leading to increased Na+ transport across the alveolar epithelium in vivo. Immunopurification of a putative channel protein from adult ATII cells showed that it contains an amiloride-binding subunit with a molecular mass of 150 kDa. When this protein was reconstituted in planar lipid bilayers, it exhibited single channels with a conductance of 25 pS, which were moderately selective for Na+ over K+. The open probability of these channels was increased by the addition of protein kinase A (PKA) and ATP, and was decreased to the same extent by addition of [N-ethyl-N-isopropyl]-2'-4'-amiloride (EIPA) and amiloride (1 microM each) in the apical side of the bilayer, in agreement with the results of patch-clamp studies in ATII cells. Exposure of rats to sublethal hyperoxia increased alpha-rENaC mRNA and the functional expression of Na+ channels in alveolar epithelial cells and limited alveolar edema. These findings indicate that alveolar epithelial channels contain at least one family of amiloride-sensitive Na+ channel proteins, which displays a number of unique properties, including sensitivity to EIPA.
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PMID:Biophysical and molecular properties of amiloride-inhibitable Na+ channels in alveolar epithelial cells. 876 Jan 27


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