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

Chronic sequelae of neonatal hyperoxia was studied in male rats exposed to 0.96-1.0 FiO2 for the first 8 days of life. At 58 days of age functional and morphologic cardiopulmonary changes were compared with controls. Right ventricular systolic pressure was measured percutaneously under anesthesia and was increased in the O2 group (29.5 mm Hg +/- 3.1 versus 23.2 mm Hg +/- 3.5, p less than 0.001). Lung and heart weights were similar between groups. Right ventricular weights however were increased in the O2 group (0.197 g +/- 0.023 versus 0.175 g +/- 0.020, p less than 0.001). Air pressure-volume curves were similar but in the O2 rats saline deflation curves were shifted left and maximal fluid lung volumes were greater (14.1 +/- 1.2 versus 12.0 +/- 0.7 ml, p less than 0.001). Pulmonary arteries were perfused at 100 cm H2O with a barium-gel mixture and lungs were fixed at 25 cm H2O with formalin. Microscopic examination of lungs revealed dysplastic changes of alveolar architecture which included irregularly enlarged alveoli and incomplete alveolar septation. Morphometric studies of the lungs showed that the O2 rats had an increased volume proportion of parenchyma (0.865 +/- 0.020 versus 0.850 +/- 0.019, p less than 0.05), increased mean linear intercept (72.3 microns +/- 9.5 versus 53.6 microns +/- 5.0, p less than 0.001), decreased number of alveoli per mm2 (207 +/- 34 versus 319 +/- 39, p less than 0.001) and fewer small arteries (20-200 microns) per mm2 (8.7 +/- 1.3 versus 14.9 +/- 2.4, p less than 0.001). The number of small arteries/100 alveoli was similar.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic vascular pulmonary dysplasia associated with neonatal hyperoxia exposure in the rat. 364 29

The aim of this study was to determine if resuscitation from hypopnea when breathing oxygen resulted in a slower recovery than that seen when breathing room air. Hyperoxia, in preterm human neonates and lambs, decreases minute ventilation (Vl), but no study has shown this effect during recovery from apnea or hypopnea, a common clinical setting. Thus, recovery from hypopnea was studied in eight unanesthesized preterm lambs, breathing spontaneously via an endotracheal tube placed into a tracheostomy. Hypopnea, defined here as a decrease in Vl from baseline greater than 50%, was induced by instillation of distilled water onto the larynx. After a baseline 30 sec when Vl, heart rate, and arterial blood gas were measured, a standard hypopnea stimulus was given over 30 sec. The lambs then breathed air or oxygen during a 2-min recovery period, which started with 15 sec of artificial ventilation. The degree of recovery at 2 min was less in the oxygen (O2) breathing group: Vl (ml/kg/min) = 381 +/- 27 in air and 270 +/- 18 in O2, P less than 0.01; pH = 7.38 +/- 0.005 in air and 7.34 +/- 0.008 in O2, P less than 0.01; arterial carbon dioxide tension (PaCO2, mmHg) = 45.0 +/- 1.3 in air and 49 +/- 1.3 in O2, P less than 0.01; base excess = 2.1 +/- 0.6 in air and 1.1 +/- 0.5 oxygen, P less than 0.01. By 2 min a return to baseline values of Vl, pH, and PaCO2 was noted only in the air breathing group, where the arterial oxygen tension also returned to normal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Recovery from hypopnea in preterm lambs: effects of breathing air or oxygen. 367 Sep 6

Interactions between internal and external O2 stimulus levels were assessed by measuring the ventilatory and cardiovascular responses to varying water (PWO2) and air bladder (PabO2) O2 levels and intravascular NaCN in anesthetized spontaneously ventilating Lepisosteus osseus. As PWO2 fell, air-breathing frequency (fab) increased. Buccal pressure amplitude (Pb) also increased as PWO2 fell from hyperoxia to normoxia, but hypoxic water depressed Pb. The PO2 in the ventral aorta (VA) fell as PabO2 fell, which stimulated fab and Pb when the gar was in normoxic or hyperoxic water. Thus gill ventilation and air breathing were normally controlled by both internal and external O2 levels, but aquatic hypoxia uniformly depressed gill ventilation regardless of changes in PabO2 levels. Heart rate and blood pressure were unaffected by these changes. NaCN stimulated hypoxic reflexes and bradycardia more quickly when given into the VA or conus than when given into the dorsal aorta. The animals appear to possess internal chemoreceptors that set the level of hypoxic drive and external chemoreceptors that inhibit gill ventilation and shift the ventilatory emphasis from water to air breathing.
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PMID:Chemoreflexive responses to hypoxia and NaCN in longnose gar: evidence for two chemoreceptor loci. 372 1

The partition of O2 uptake between gills and skin was examined in the freshwater eel (Anguilla anguilla L.) at ambient PO2 ranging from hyperoxia (PO2 = 400 Torr) to severe hypoxia (PO2 = 10 Torr), using a technique of open-flow respirometry. All the expired water was collected, and the ventilatory flow and the mixed expired water PO2 were directly measured. The ventilatory water flow decreased moderately in hyperoxia, increased markedly between normoxia and 40 Torr, and below 40 Torr, hyperventilation was gradually reduced. Between PO2 400 and 70 Torr, the total O2 uptake was constant and the skin O2 uptake was lower than gill O2 uptake (32% of total uptake in normoxia). Between 70 and 10 Torr, the skin contribution to the total O2 uptake progressively increased, and was higher than gill O2 uptake in severe hypoxia. A possible facilitation of cutaneous O2 uptake in hypoxia is discussed from estimates of the O2 diffusing capacity of the skin.
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PMID:Cutaneous and gill O2 uptake in the European eel (Anguilla anguilla L.) in relation to ambient PO2, 10-400 Torr. 379 48

In dogs acutely immersed in cold water (8-13 degrees C) oxygen uptake increased and rapidly reached a maximum value (CV02 Max). A few minutes after the start of immersion colonic temperature began to fall more or less rapidly depending on the dog but always in a linear fashion. Twenty min. after the start of immersion the inspired air was switched from air to a 60% O2/40% N2 gas mixture. The switch to the hyperoxia gas mixture slowed down or even stopped the fall in colonic temperature. Concomitantly a lowering of plasma lactate concentration was observed. It may be concluded that hyperoxia improves the cold tolerance of dogs exposed to a severe cold stress. This improvement may be due to a direct effect of hyperoxia on cellular metabolism. However other effects induced by hyperoxia cannot be ruled out.
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PMID:Increased tolerance to cold induced by hyperoxia in hypothermic dogs. 384 37

We did two studies to see if severe neutropenia might reduce the severity or delay development of O2-induced lung microvascular injury. First, we treated 11 rabbits with nitrogen mustard until their circulating neurophil count decreased to less than 50/microliters of blood, after which the rabbits breathed pure O2 until death; nine other rabbits received no nitrogen mustard and had normal numbers of circulating neutrophils during O2 breathing. All rabbits died of respiratory failure with pulmonary edema, and although chemotherapy decreased the number of neutrophils in the lungs by greater than 90%, it did not influence survival time or extravascular lung water content. To see if severe neutropenia might slow the development of O2-induced lung microvascular injury, we assessed the effects of sustained hyperoxia on lung fluid balance in unanesthetized lambs treated with hydroxyurea, so that their absolute neutrophil count was less than 50/microliters of blood. We measured pulmonary arterial and left atrial pressures, cardiac output, lung lymph flow, and concentrations of protein in lymph and plasma during a 2- to 4-h control period and then daily for 2 to 4 h as the lambs continuously breathed pure O2. After 3 days of hyperoxia, lymph flow doubled and the concentration of protein in lymph increased from 3.3 +/- 0.5 to 4.2 +/- 0.3 g/dl. Tracer studies with 125I-albumin before and 3 days after the start of O2 breathing confirmed the development of increased lung vascular permeability to protein. All lambs died of respiratory failure with pulmonary edema after 3-5 days in O2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Oxygen-induced lung microvascular injury in neutropenic rabbits and lambs. 398 Mar 93

The effects of exposure to CdCl2 aerosols followed by hyperoxia were studied in mouse lung. Special emphasis was placed on analysis of cell proliferation following injury. Male Balb/c mice were exposed to aerosols of 4.9 micrograms Cd/liter for 1 hr while controls were exposed to water aerosols. Immediately after, half of each group was placed in 80% O2 for 6 days, while the rest were left in room air. Three endpoints were used to assess lung injury; measurement of hydroxyproline, [14C]thymidine incorporation into DNA, and histopathology. Parenchymal and bronchiolar labeling indices were determined following autoradiography. A 1-hr exposure to CdCl2 aerosols caused marked cell proliferation in the lung with the peak of cell labeling occurring at Day 5. In animals exposed to both CdCl2 + 80% O2, the cell labeling peak was delayed until Day 9. Cell differentiation studies showed a delay in the peak of type II epithelial cell and endothelial cell division when CdCl2 exposure was followed by the 80% O2 treatment. On Day 15 most of the labeled cells were identified as interstitial cells in both treated groups. Bronchiolar cell labeling was suppressed at the early time period in the Cd + O2 group. With time, the histologically visible lung lesions tended to resolve in animals exposed to CdCl2 or CdCl2 and 80% O2, whereas total pulmonary hydroxyproline remained at all times (3, 6, and 12 months) significantly higher in Cd-treated animals when compared to controls. It was concluded that acute lung injury by a toxic inhalant can be amplified if there is an initial delay in pulmonary cell proliferation following an acute insult.
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PMID:Cadmium-induced lung injury: cell kinetics and long-term effects. 402 12

Daily resting and exercise electrocardiograms from 81 healthy subjects taking part in eight different air saturation chamber experiments at depths of 2-132 ft sea water gauge (fswg) were recorded and interpreted. Scalar and planar characteristics were measured and analyzed in addition to noting changes in rhythm. Of the measured variables, only the heart rate and QT-interval changed significantly in the majority of exposures. Heart rate decrements of 14%-23% were observed, generally with normalization after several days at depth, and in some cases a rebound immediately postexposure. The observed increase in QT-interval can be explained entirely by the bradycardia, which seems to be due to a combination of pressure, hyperoxia, and a chamber effect. Further distinction among these factors was not possible. Associated with the decrements in heart rate were asymptomatic supraventricular arrhythmias, generally AV-nodal escape rhythms or beats, in 10% of the subjects. One incident of symptomatic ventricular tachycardia was noted 20 h after surfacing during an exercise test. Otherwise, only infrequent, isolated premature ventricular beats were detected at depth, but were not more frequent than in the predive periods. These findings are consistent with the premise that exposure to hyperbaric air and other nitrogen-oxygen mixtures causes an increase in parasympathetic tone of sufficient magnitude to cause cardiac arrhythmias. That autonomic imbalance in diving activities may cause more malignant arrhythmias is discussed.
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PMID:Cardiac arrhythmias and heart rate changes in prolonged hyperbaric air exposures. 608 26

Progressive hyperoxia caused a gradual increase in arterial blood oxygen tension (PaO2). Initially there was no change in venous O2 tension (PvO2) but in extreme hyperoxia (PO2 650 mmHg) it increased to 2.5 times the normoxic (PO2 150 mmHg) level (Table 1). Ventilation frequency gradually decreased down to 73% of the normoxic value as PO2 rose towards a maximum at 700 mmHg (Fig. 1). In moderately hyperoxic water (mean PO2 233 mmHg) heart rate (fH) increased significantly above the normoxic level. Further increases in ambient PO2 caused a progressive reduction in fH to a level significantly below the normoxic rate in extreme hyperoxia (Fig. 2). Injection of atropine abolished these changes, and the atropinized fH was similar to that measured during moderate hyperoxia. The initial increase in fH during progressive hyperoxia is attributed to release of vagal tone, due to removal of normoxic stimulation of peripheral oxygen receptors; whereas, the secondary bradycardia is attributed to the stimulation of oxygen receptors located in the venous system. Injection of 5 ml of hyperoxaemic blood into the venous system of normoxic fish caused a transient bradycardia (Fig. 3), lasting a mean of 73 sec, which is the approximate time for passage of the blood volume of the venous system through the heart. This bradycardia was neither pH dependent nor a pressor response and provides supporting evidence for the existence of a venous oxygen receptor.
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PMID:Changes in heart rate during progressive hyperoxia in the dogfish Scyliorhinus canicula L.: evidence for a venous oxygen receptor. 614 44

Increased concentrations of angiotensin converting enzyme (ACE) were found in lung lavages from rabbits exposed to hyperoxia for 72 h and the concentrations of ACE were correlated with ratios of extravascular lung water to body weight (r = 0.69, p less than 0.05) and albumin concentrations in lung lavages (r = 0.89, p less than 0.01). In parallel studies, rabbits treated with nitrogen mustard in which granulocytopenia was maintained throughout the 72-h hyperoxic exposure period had less evidence of edematous lung injury and lower concentrations of ACE in their lung lavages than similarly treated rabbits in which granulocytopenia was not maintained. The results suggested that granulocytes contribute to acute edematous lung injury from hyperoxia and that ACE concentrations in lung lavages reflect this process.
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PMID:Angiotensin converting enzyme concentrations in the lung lavage of normal rabbits and rabbits treated with nitrogen mustard exposed to hyperoxia. 626 99


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