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

The effect of hyperoxia on lactate production and release and the mitochondrial NAD+-to-NADH ratio was studied in the in situ canine gastrocnemius to determine whether elevated PO2 altered metabolic regulation. Dogs breathed either air (21% O2) [arterial O2 partial pressure (PaO2) 90 mmHg; n = 8] or hyperoxia (100% O2) (PaO2 546 mmHg; n = 8). The left muscle was stimulated for 10 min at 3 Hz and then both right and left muscles were quick frozen in N2. Hyperoxia did not affect O2 uptake, blood flow, and developed tension. Activity increased glucose 6-phosphate (G-6-P), D-fructose 6-phosphate (F-6-P), NH3, lactate, and F-6-P/F-1,6-P in both treatment groups. No significant differences in arterial or venous lactate, muscle lactate, glucose uptake, or glycogen depletion were noted in hyperoxia. Cytoplasmic NAD+/NADH was in a more oxidized state in hyperoxia at rest but not during activity. The increase in NH3 with stimulation was significantly larger in hyperoxia. Activity decreased alpha-ketoglutarate in hyperoxia but not in air. At stimulation, the estimated mitochondrial NAD+/NADH increased in both groups suggesting that hypoxia was not present. Thus hyperoxia did not affect mitochondrial redox state or lactate production and release in active muscle.
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PMID:Hyperoxia, mitochondrial redox state, and lactate metabolism of in situ canine muscle. 361 62

Our earlier studies have shown that local cortical blood flow (CoBF) in the rabbit has been autoregulated in a narrow range of mean arterial blood pressure (MABP) and autoregulation of cortical oxygen tension (bPO2) has been maintained in a wider range (75-110 mmHg) than that of CoBF. In the present studies, bPO2, NAD/NADH redox state, and CoBF were measured under the various conditions of hypoxia and hyperoxia to discuss the critical level of cortical oxidative metabolism and autoregulation of CoBF in relation to oxidative metabolism. New Zealand white rabbits were anesthetized with pentobarbital sodium intraperitoneally and paralyzed with gallamine triethiodide intravenously. They were ventilated artificially maintaining normal blood gas analysis. NAD/NADH redox state was measured with a compensated fluorometer with a reflectance device to correct for hemodynamic artefacts and bPO2 was monitored continuously with the polarographical method. They were measured simultaneously. CoBF was monitored with the thermal diffusion cerebral blood flow monitor of Flowtronics. Hypoxia and hyperoxia were produced by decreasing or increasing the inspired oxygen concentration. Arterial blood samples were obtained for blood gas determination before and during the episode of hypoxia or hyperoxia. A definite reduction of NADH began at a 50% decrease of PaO2. It corresponded to 70 mmHg of PaO2. Below 50% decrease of PaO2, NADH was reduced largely. This was statistically significant (p less than 0.01). Although, the oxidation of NADH occurred in the moderate hyperoxic state, no oxidation of NADH occurred more than 6.1% of full scale even in the condition of higher PaO2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effect of hypoxia and hyperoxia on cortical oxidative metabolism in relation to cerebral blood flow autoregulation]. 396 89

A previous report from this laboratory (Bender, D.A., Magboul, B.I. and Wynick, D. (1982) Brit. J. Nutr. 48, 119-127) suggested that the hydrolysis of the nicotinamide nucleotides NAD and NADP may be an important factor in controlling the tissue content of these coenzymes. Further studies presented here support this suggestion. Both nuclear poly(ADPribose) synthetase and microsomal NAD glycohydrolase showed activity towards both NAD+ and NADP+, and the two nucleotides were mutually competitive. The reduced nucleotides, NADH and NADPH, were not substrates for either enzyme. In rats that were maintained for 24 h under conditions of hypoxia (O2/N2, 1:9) there was an increase in the proportion of nicotinamide nucleotides present in the liver in the reduced form, and an increase in the total concentration of nucleotides in the liver. In rats that were maintained for 24 h under conditions of hyperoxia (O2/N2, 7:3) there was no change in either the proportion of nicotinamide nucleotides in the liver present in the reduced form or in the total tissue control of the nucleotides. There was an increase in the urinary excretion of kynurenine suggesting an increase in the oxidative metabolism of tryptophan.
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PMID:The role of catabolism in controlling tissue concentrations of nicotinamide nucleotide coenzymes. 630 51

Porcine lung and liver nuclei generated superoxide (O-2) at a rate which increased with increasing oxygen concentration. NADH-dependent O-2 generation increased from 0 to 2.21 +/- 0.11 nmol/min per mg protein for lung nuclei and from 0.16 +/- 0.09 to 1.34 +/- 0.14 nmol/min per mg protein for liver nuclei, when oxygen concentration increased from 0 to 100%. NADPH-dependent O-2 generation increased similarly in liver nuclei (from 0.20 +/- 0.09 to 1.20 +/- 0.12 nmol/min per mg protein), while lung nuclei produced only 0.45 +/- 0.09 nmol/min per mg protein at 100% oxygen. NADH and NADPH had an additive effect on O-2 generation by liver nuclei, yielding 2.58 +/- 0.21 nmol/min per mg protein at 100% oxygen. Very little or no superoxide dismutase activity was present in washed nuclear preparations. The oxygen-dependence of nuclear O-2 generation shows that nuclear-derived partially reduced species of oxygen may affect nuclear function during hyperoxia or other metabolic situations where overproduction of oxygen radicals is problematic.
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PMID:Hyperoxia enhances lung and liver nuclear superoxide generation. 632 74

In order to elucidate that which are the factors that may influence the direction of brain activation-induced changes in the redox state of oxidized/reduced nicotinamide adenine dinucleotide (NAD/NADH), the brain cortex was electrically stimulated during arterial hypotension and following reinfusion of the shed blood, during arterial hyper- and hypoxia, and during the second phase of spreading cortical depression (SD). Cerebrocortical NADH fluorescence and vascular volume ( CVV ) of cats, anaesthetized by chloralose, were measured with a microscope fluororeflectometer . Under physiologically normal conditions electrical stimulation resulted in pronounced cortical NAD reduction and increase in CVV . These reactions were not altered by arterial hyperoxia and continuous superfusion of the brain cortex with oxygenated artificial cerebrospinal fluid (mock CSF). Arterial hypotension and SD (in phase II) increased NAD reduction and CVV markedly, and the superimposed electrical stimulation brought about NADH oxidation and greatly depressed CVV responses. Reinfusion of the shed blood did not restore NAD/NADH redox state and CVV to their reference levels, and electrical stimulation under this condition led to NADH oxidation and negligible vascular reactions. Since under physiologically normal conditions electrical activation of the brain cortex resulted in NAD reduction and marked increase in CVV and the magnitude of these reactions were not altered by arterial hyperoxia or by superfusion of the brain cortex with oxygenated CSF, it is very unlikely that the brain cortex became hypoxic during stimulation. Because when the steady NAD/NADH redox state of the brain cortex was shifted toward reduction by arterial hypotension and reinfusion and SD, electrical stimulation led to NADH oxidation, it is suggested that the prestimulatory steady redox state has great importance in determining the direction of NAD/NADH redox reactions evoked by activation of the brain cortex.
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PMID:Determinants of brain activation-induced cortical NAD/NADH responses in vivo. 632 66

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

In order to evaluate the relationship between brain oxygen supply and demand (O2 balance) in real time, it is necessary to use a multiparametric monitoring approach. Cerebral blood flow (CBF) is a representative parameter of O2 supply. The extracellular level of K+ is a reliable indicator of O2 demand since more than 60% of the energy consumed by the brain is utilized by active transport processes. Mitochondrial NADH redox state can represent the balance between O2 supply and demand. In order to monitor the brain of experimental animals or patients, we constructed the multiparametric assembly (MPA) and the following parameters were monitored simultaneously and in real time: CBF, CBV, NADH redox state, extracellular K+, DC potential, EEG, tissue temperature and ICP. Animals were exposed to hypoxia, ischemia, hypercapnia, hyperoxia and spreading depression (SD) and the relative changes in CBF and NADH were calculated and found to be significant indicators of brain energy state. Monitoring these two parameters increases the possibility of differentiating between various pathophysiological states. Each added parameter increases the power of diagnosis and determination of the functional state of the brain. Preliminary results obtained in patients monitored in the ICU or in the OR show that the responses to hypercapnia, spreading depression or ischemia are similar to those measured in experimental animals.
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PMID:Multiparametric monitoring of brain oxygen balance under experimental and clinical conditions. 958 30

The generation of reactive oxygen species (ROS) is a steady-state cellular event in respiring cells. Their production can be grossly amplified in response to a variety of pathophysiological conditions such as inflammation, immunologic disorders, hypoxia, hyperoxia, metabolism of drug or alcohol, exposure to UV or therapeutic radiation, and deficiency in antioxidant vitamins. Uncontrolled production of ROS often leads to damage of cellular macromolecules (DNA, protein, and lipids) and other small antioxidant molecules. A number of major cellular defense mechanisms exist to neutralize and combat the damaging effects of these reactive substances. The enzymic system functions by direct or sequential removal of ROS (superoxide dismutase, catalase, and glutathione peroxidase), thereby terminating their activities. Metal binding proteins, targeted to bind iron and copper ions, ensure that these Fenton metals are cryptic. Nonenzymic defense consists of scavenging molecules that are endogenously produced (GSH, ubiquinols, uric acid) or those derived from the diet (vitamins C and E, lipoic acid, selenium, riboflavin, zinc, and the carotenoids). These antioxidant nutrients occupy distinct cellular compartments and among them, there are active recycling. For example, oxidized vitamin E (tocopheroxy radical) has been shown to be regenerated by ascorbate, GSH, lipoic acid, or ubiquinols. GSH disulfides (GSSG) can be regenerated by GSSG reductase (a riboflavin-dependent protein), and enzymic pathways have been identified for the recycling of ascorbate radical and dehydroascorbate. The electrons that are used to fuel these recycling reactions (NADH and NADPH) are ultimately derived from the oxidation of foods. Sickle cell anemia, thalassemia, and glucose-6-phosphate-dehydrogenase deficiency are all hereditary disorders with higher potential for oxidative damage due to chronic redox imbalance in red cells that often results in clinical manifestation of mild to serve hemolysis in patients with these disorders. The release of hemoglobin during hemolysis and the subsequent therapeutic transfusion in some cases lead to systemic iron overloading that further potentiates the generation of ROS. Antioxidant status in anemia will be examined, and the potential application of antioxidant treatment as an adjunct therapy under these conditions will be discussed.
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PMID:Interaction of antioxidants and their implication in genetic anemia. 1060 86

Exposure of adult male rats to hyperoxia (O(2) > 95%) resulted in a tendency for all of the components of the pulmonary cytochrome P450 (P450) system to increase at 48 h after the exposure. However, the most pronounced effect of hyperoxia was observed on pulmonary ethoxycoumarin O-deethylase and ethoxyresorufin O-deethylase activities which were induced 4- and 25-fold respectively after 48 h. In the liver, P450 and NADH b(5) reductase were increased after 48 h, while other components of the monooxygenase system remained unchanged. In the hepatic microsomes, contrary to the lungs, aminopyrine N-demethylase activity was decreased after 24 h of hyperoxic exposure (P < 0.05) and returned to the control level by 48 h. Similar changes were observed in benzphetamine N-demethylase activity. Aniline hydroxylase activity was decreased after 8 h of hyperoxic exposure (P < 0.01) and remained decreased at 24 h (P < 0. 01) and 48 h (P < 0.05). The level of induction of ethoxycoumarin O-deethylase and ethoxyresorufin O-deethylase activities, however, was almost similar in the liver to that observed in the lungs.
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PMID:Effect of hyperoxia on rat pulmonary and hepatic cytochrome P450 monooxygenases. 1066 85

The hyperoxia-improved tolerance to maximal aerobic performance was studied in relation to exercising muscle metabolic state. Five students were submitted to four different tests on a cycle ergometer, each being conducted under normoxia and hyperoxia (60% FiO2) on separate days: Test 1, a progressive exercise until exhaustion to determine the maximal work load (Wmax) which was unchanged by hyperoxia; Test 2, an exercise at Wmax (287 +/- 12 W) until exhaustion to determine the performance time (texh) which was elevated by 38% under hyperoxia but exhaustion occurred at the same arterial proton and lactate concentrations; Test 3 (S-Exercise test) consisted of cycling at Wmax for 90% normoxic-texh (4.8 +/- 0.5 min under both O2 conditions) then followed by a 10-s sprint bout during which the total work output (Wtot) was determined; Wtot was elevated by 15% when exercising under hyperoxia; Test 4 (M-Exercise test) consisted also of cycling at Wmax for 4.8 +/- 0.5 min with blood and muscle samples taken at rest and at the end of the exercise to compare the level of different metabolites. During hyperoxic M-Exercise test, glycogen was twice more depleted whereas glucose-6-phosphate and lactate were less accumulated when compared with normoxia. No significant differences were observed for pyruvate, phosphocreatine and muscle/blood lactate ratio between the two conditions. Conversely to normoxia, levels of ATP, ADP and total NADH were maintained at their resting level under 60% FiO2. These data lead us to suppose a higher oxidation rate for pyruvate and NADH in mitochondria, thereby lowering the metabolic acidosis and allowing a better functioning of the glycolytic and contractile processes to delay the time to exhaustion.
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PMID:Effect of hyperoxia on aerobic and anaerobic performances and muscle metabolism during maximal cycling exercise. 1071 78


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