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

Persons with chronic mountain sickness (CMS) hypoventilate and are more hypoxemic than normal individuals, but the cause of the hypoventilation is unclear. Studies of 14 patients with CMS and 11 healthy age-matched control subjects residing in Lhasa, Tibet, China (3,658 m) were conducted to test the hypothesis that hypoventilation, blunted hypoxic ventilatory responsiveness (HVR), and hypoxic ventilatory depression of CMS were due to increased endogenous opioid production. Patients with CMS compared with control subjects exhibited hypoventilation (end-tidal carbon dioxide pressure [PETCO2] = 36.6 +/- 1.0 versus 31.5 +/- 0.5 mm Hg, p less than 0.05), lower tidal volume (VT = 0.54 +/- 0.02 versus 0.61 +/- 0.02 ml BTPS, p less than 0.05), blunted HVR (shape parameter A = 17 +/- 8 versus 114 +/- 22 mm Hg/L BTPS/min, p less than 0.05), and a depressant effect of ambient hypoxia on ventilation (delta PETCO2 with acute hyperoxia = -3.5 +/- 0.5 versus -1.0 +/- 0.6 mm Hg, p less than 0.05). Reduced forced expiratory volume in 1 s to vital capacity ratios (FEV1/VC) and a higher proportion of cigarette smokers in the group of patients with CMS compared with control subjects suggested that at least some patients with CMS had mild airway obstructive lung disease. Naloxone infusion (0.14 mg/kg) to six patients with CMS did not change resting VT, PETCO2, HVR, or SaO2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Decreased ventilation and hypoxic ventilatory responsiveness are not reversed by naloxone in Lhasa residents with chronic mountain sickness. 225 47

Freshly isolated rat hepatocytes suspensions were incubated under an atmosphere of 95% O2/5% CO2 or 95% air/5% CO2 for 10 h. Cell injury and death were observed between the 6th and 10th hour of incubation, only in 95% O2-treated hepatocytes. Oxygen-induced injury was preceded by marked lipid peroxidation and rapid depletion of cellular alpha tocopherol content. The exogenous administration of unesterified alpha tocopherol (T, 25 microM) resulted in a 20-fold increase in cellular T levels (4.2 nmol/10(6) cells) but failed to protect these hepatocytes from the toxic effects of oxygen. In contrast, hepatocytes incubated with 25 microM of the succinate ester of alpha tocopherol (TS) contained both TS (3.0 nmol/10(6) cells) and T (1.4 nmol/10(6) cells) and were completely protected from the toxic effects of oxygen, including the induction of lipid peroxidation. These findings suggest that TS cytoprotection results not from the cellular accumulation of T but rather, from cellular TS accumulation. The data also indicate that the depletion of cellular T is not the critical cellular event that is responsible for hyperoxia (reactive oxygen intermediate)-induced injury. Instead, it appears that TS possesses unique cytoprotective properties that intervene in the critical cellular events that lead to oxygen toxicity. Thus, vitamin E succinate and our hyperoxic hepatocyte preparation provide a promising new model system for the study and prevention of tissue damage resulting from the toxic effects of hyperoxia and reactive oxygen intermediates.
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PMID:Oxygen toxicity: unique cytoprotective properties of vitamin E succinate in hepatocytes. 228 88

We studied the effects of metabolic and respiratory acidosis (pH 7.20) and alkalosis (pH 7.60) on pulmonary vascular tone in 32 pentobarbital-anesthetized dogs ventilated with hyperoxia (inspired oxygen fraction, FIO2 0.40) and with hypoxia (FIO2 0.10). Ventilation, pulmonary capillary wedge pressure (Ppw), and cardiac output (3 l.min-1.m-2) were maintained constant to prevent passive changes in pulmonary arterial pressure (Ppa). Metabolic acidosis and alkalosis were induced with HCl (2 mmol.kg-1.h-1) and NaHCO3-Na2CO3 (5 mmol.kg-1.h-1) infusions, respectively, and respiratory acidosis and alkalosis by modifying the inspiratory CO2 fraction. The hypoxia-induced rise in Ppa-Ppw gradient increased from 5 to 9 mmHg in metabolic acidosis (P less than 0.001), decreased from 6 to 1 mmHg in metabolic alkalosis (P less than 0.001), remained unchanged in respiratory acidosis, and decreased from 5 to 2 mmHg in respiratory alkalosis (P less than 0.001). Linear relationships were found between pH and Ppa-Ppw gradients. These data indicate that in intact anesthetized dogs, metabolic acidosis and alkalosis, respectively, enhance and reverse hypoxic pulmonary vasoconstriction (HPV). Respiratory acidosis did not affect HPV and respiratory alkalosis blunted HPV, which suggests an pH-independent vasodilating effect of CO2.
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PMID:Effects of acidosis and alkalosis on hypoxic pulmonary vasoconstriction in dogs. 230 2

Continuous exposure of Chinese hamster ovary (CHO) cells to an atmosphere of 98% O2, 2% CO2 (normobaric hyperoxia) leads within a period of several days to cytostasis and clonogenic cell death. Here we report respiratory failure as an important early symptom of oxygen intoxication in CHO cells, resulting in a more than 80% inhibition of oxygen consumption within 3 days of hyperoxic exposure. This inhibition appeared to be correlated with selective inactivation of three mitochondrial key enzymes, NADH dehydrogenase, succinate dehydrogenase, and alpha-ketoglutarate dehydrogenase. The latter enzyme controls the influx of glutamate into the Krebs cycle and is particularly critical for oxidative ATP generation in most cultured cells, which depends on exogenous glutamine rather than glucose as a carbon source. As expected, the inactivation of alpha-ketoglutarate dehydrogenase was correlated with a fall in cellular glutamine utilization, which became apparent from the first day of hyperoxic exposure. Thereafter, glucose utilization and lactate excretion started to increase, up to 3-fold, indicating a cellular response to respiratory failure aimed at increased ATP generation from glycolysis. However, in spite of this response, the cellular ATP level progressively decreased, up to 2.5-fold. Thus, killing of CHO cells by normobaric hyperoxia seems to be due to a severe disturbance of mitochondrial metabolism eventually leading to a depletion of cellular ATP pools.
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PMID:Respiratory failure and stimulation of glycolysis in Chinese hamster ovary cells exposed to normobaric hyperoxia. 235 58

The purpose of this study is to examine effects of hyperoxic gas mixtures on changes of blood indices during bicycle exercise of human. Oxygen-enriched gases (30% O2) were inspired during the ramp load exercise of 25 watt/min. Changes of blood indices were analyzed with Sequential Multiple Analyzer with the computer (SMAC). The improvement of exercise performance were discussed about relationship between function of hyperoxic gas and physiological mechanism. Three experimental conditions were set as follows (I) 30% O2 +N2 gases balance, (II) air (21% O2), and (III) 30% O2 +2% CO2 +N2 gases balance. Arterial blood were sampled from the radial artery of the forearm in order to analyze following items; 1) pH level, PaO2, PaCO2, and HCO3 of these blood gases, 2) Blood sugar, TG, and F-CH of the blood contents, 3) red blood corpuscle, white blood corpuscle, Hb, and Ht values, 4) LDH, CK, GOT, and GPT of the blood enzymes, 5) TP, ALB, Na, K, Ca and Cl of the electric ions. In the case of inspiring hyperoxic gases, the recovery rate of blood indices increased after this ramp load exercise remarkably, and the whole exercise metabolism were removed from acidosis tendency to alkalosis value of the resting condition significantly. At hyperoxic experimental conditions, the blood sugar and oxygen consumption were much more decreased than these at normal oxygen content one during both states of exercise and recovery times. These data of the blood indices would support strongly to the hypothesis that improvement of oxygen delivery should be depended upon the enhanced performance with the hyperoxic gases. There might be effects of the hyperoxia on the cellular metabolism and on function of the vascular muscle during those aerobic exercise.
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PMID:[Effects of breathing high concentrations of oxygen on changes in blood indices during bicycle exercise]. 238 13

Seven human spinal cord-lesioned subjects (SPL) underwent electrically induced muscle contractions (EMC) of the quadriceps and hamstring muscles for 10 min: 5 min control, 2 min with venous return from the legs occluded, and 3 min postocclusion. Group mean changes in CO2 output compared with rest were +107 +/- 30.6, +21 +/- 25.7, and +192 +/- 37.0 (SE) ml/min during preocclusion, occlusion, and postocclusion EMC, respectively. Mean arterial CO2 partial pressure (PaCO2) obtained from catheterized radial arteries at 15- to 30-s intervals showed a significant (P less than 0.05) hypocapnia (36.2 Torr) during occlusion and a significant (P less than 0.05) hypercapnia (38.1 Torr) postocclusion relative to a group mean preocclusion EMC PaCO2 of 37.5 Torr. Relative to preocclusion EMC, expired ventilation (VE) decreased during occlusion and increased after release of occlusion. However, changes in VE always occurred after changes in end-tidal PCO2 (mean 41 s after occlusion and 10 s after release of occlusion). In the two subjects investigated during hyperoxia, the VE and PaCO2 responses to occlusion and release did not differ from normoxia. We conclude that the data do not support mediation of the EMC hyperpnea in SPL by humoral mechanisms that others have proposed for mediation of the exercise hyperpnea in spinal cord-intact humans.
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PMID:Ventilatory response of spinal cord-lesioned subjects to electrically induced exercise. 238 11

Pulmonary diffusing capacities (DL) of NO and CO were determined simultaneously from rebreathing equilibration kinetics in anesthetized paralyzed supine dogs (mean body wt 20 kg) after denitrogenation (replacement of N2 by Ar). During rebreathing the dogs were ventilated in closed circuit with a gas mixture containing 0.06% NO, 0.06% 13C18O, and 1% He in Ar for 15 s, with tidal volume of 0.5 liter and frequency of 60/min. The partial pressures of NO, 13C18O, 16O18O, N2, Ar, CO2, and He in the trachea were continuously analyzed by mass spectrometry. Measurements were performed at various O2 levels characterized by the mean end-expired PO2 during rebreathing (PE'O2). In control conditions ("normoxia," PE'O2 = 67 +/- 8 Torr) the following mean +/- SD values were obtained (in ml.min-1.Torr-1): DLNO = 52.4 +/- 11.0 and DLCO = 15.4 +/- 2.9. In hypoxia (PE'O2 = 24 +/- 7 Torr) DLNO increased by 11 +/- 8% and DLCO by 19 +/- 10%, and in hyperoxia (PE'O2 = 390 +/- 26 Torr) DLNO decreased to 87 +/- 3% and DLCO to 56 +/- 8% with respect to values in normoxia. DLNO/DLCO of 3.24 +/- 0.06 (hypoxia), 3.38 +/- 0.31 (normoxia), and 5.54 +/- 1.04 (hyperoxia) were significantly higher than the NO/CO Krogh diffusion constant ratio (1.92) predicted for simple diffusion through aqueous layers. With increasing O2 uptake elicited by 2,4-dinitrophenol, DLNO and DLCO increased and DLNO/DLCO remained close to unchanged. The results suggest that the combined effects of diffusion and chemical reaction with hemoglobin limit alveolar-capillary transport of CO. If it is assumed that reaction kinetics of NO with hemoglobin (known to be extremely fast) are not rate limiting for NO uptake, the contribution of the slow chemical reaction with hemoglobin to the total CO uptake resistance (= 1/DLCO) was estimated to be 38% in hypoxia, 41% in normoxia, and 64% in hyperoxia. The various factors expected to restrict the validity of this analysis are discussed, in particular the effects of functional inhomogeneity.
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PMID:Pulmonary diffusing capacities for nitric oxide and carbon monoxide determined by rebreathing in dogs. 238 15

Fluosol-DA 20% (FDA), an emulsion of fluorocarbons in a glucose electrolyte solution can deliver physiologically significant amounts of oxygen (O2) to the tissues and improve ischaemic hypoxia. To investigate its effect on critical oxygen delivery level (QO2c), four groups of six phenobarbitone anaesthetised air-ventilated splenic clamped mongrel dogs were haemodiluted to a haematocrit (Hct) of 25%; two groups with FDA and two with 6% dextran solution. Oxygen consumption (VO2) was derived from expired gas measurement and analysis, or by using a spirometer and carbon dioxide absorption. Whole body O2 flux (QO2) was calculated from mixed venous and arterial O2 contents and the Fick-derived cardiac output. QO2 was progressively decreased by haemorrhaging in steps of 1.5-2.5 ml per kg. Hct was kept at 25% using packed cells. VO2/QO2 pairs were calculated at each step and QO2c was determined for each animal by least squares fitting of data with 2 straight lines. Analyses of variance were performed. QO2c was significantly less in the FDA and O2 (F+O) group than either the dextran and O2 (D+O) or dextran and air (D+A) groups. Analysis of O2 extraction at QO2c, which effectively normalized results for differences in resting, VO2, had significantly better extraction in the FDA and air (F+A) than the D+A group. When fluorocarbon- and plasma-dissolved oxygen was subtracted, the O2 extraction in the F+A group was significantly better than in the D+A and F+O groups. The results imply that normoxic FDA haemodilution in animals respiring air can improve O2 delivery and that hyperoxia interferes with this process.
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PMID:Critical oxygen delivery levels during shock following normoxic and hyperoxic haemodilution with fluorocarbons or dextran. 244 79

A pulse oximeter (Ohmeda Biox 3700) and two transcutaneous systems (Radiometer TCM3) were applied simultaneously to 18 newborn infants with respiratory insufficiency. All infants had either an umbilical catheter placed in the mid thoracic aorta or a radial artery catheter. The average monitoring time was 2 hours. Arterial blood pO2, pCO2 and pH (Radiometer ABL300), arterial sO2, HbCO and metHb (Radiometer OSM3), erythrocyte 2,3 DPG concentration, and fetal hemoglobin fraction (alkali denaturation kinetic method) were measured. Using arterial sO2 and pO2 as reference, the analytical bias of pulse oximetry (-0.5 +/- 1.0%, mean +/- 1 SD) corresponded in magnitude, when converted to pO2, to that of transcutaneous - pO2 (0.6 +/- 1.4 kPa for combined O2-CO2 electrode and -0.1 +/- 2.3 kPa for single O2 electrode). Transcutaneous pCO2 showed the smallest bias (0.3 +/- 0.3 kPa). Both pulse oximetry and transcutaneous pO2 electrodes were good as trend monitors detecting rapid changes in the infants' oxygenation status. The pulse oximeter offers certain advantages in not requiring calibration or heating. The variations in the levels of fetal hemoglobin fraction (44 to 97%), pH (7.27 to 7.49), pCO2 (3.3 to 6.8 kPa) and 2,3 diphosphoglycerate concentration (1.6 to 5.9 mmol/l) between the infants studied, resulted in a variable pO2-sO2 relation (p50 2.5 to 3.5 kPa). This presents difficulties in interpreting sO2 values in sick newborn infants, and we therefore recommend caution in using a pulse oximeter to apply strict limits for avoiding hypoxia and hyperoxia in this population.
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PMID:Pulse oximetry versus transcutaneous pO2 in sick newborn infants. 245 78

Counter-current arrangement of afferent and efferent blood flow in tissues is commonly considered to be detrimental to tissue oxygenation, since O2 diffusion would shunt O2 away from the tissue. We have investigated the combined effects of counter-current CO2 and O2 exchange in a simple model, paying particular attention to the Bohr effect. We have obtained the following main results. (1) Back-diffusion of CO2 leads to increasing CO2 partial pressure (PCO2) and CO2 content along the afferent vessel. This is enhanced when fixed acid is released by the tissue into the venous blood, e.g. during hypoxia, which leads to a further PCO2 increase therein. (2) The increasing PCO2, with concomitant decrease in pH, in the afferent blood leads to a decrease in blood O2 affinity (Bohr effect) and thus results in increased PO2. (3) The resulting O2 diffusion shunt diminishes the O2 content in afferent blood, but for most conditions its PO2 remains higher than without the Bohr effect. (4) During hypoxia, both the PO2 in blood reaching the tissue (Pta) as well as in that leaving it (Ptv) are significantly elevated above the level without the Bohr effect. Moreover, with fixed acid release both Pta and Ptv for O2 can be higher than the arterial PO2 value. (5) During hyperoxia, O2 diffusion shunt prevents the tissue PO2 levels from increasing to levels that might be regarded as toxic. It is concluded that a diffusion shunt in tissues stabilizes the O2 partial pressure at the tissue when it varies in arterial blood (hypoxia or hyperoxia).
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PMID:Significance of the Bohr effect for tissue oxygenation in a model with counter-current blood flow. 250 42


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