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

We measured ventilation in nine young adults while they breathed pure O2 after breathing room air and after 5 and 25 min of hypoxia. With isocapnic hypoxia (arterial O2 saturation 80 +/- 2%) mean ventilation increased at 5 min and then declined, so that at 25 min values did not differ from those on room air. After 3 min of O2 breathing, ventilation was greater than that on room air or after 25 min of isocapnic hypoxia, whether the hyperoxia had been preceded by hypoxia or normoxia. During transitions to pure O2 breathing, ventilation was analyzed breath by breath with a moving average technique, searching for nadirs before and after increases in PO2. After both 5 and 25 min of hypoxia, O2 breathing was associated with transient depressions of ventilation, which were greater after 25 min than after 5 min. Significant depressions were not observed when hyperoxia followed room air breathing, and O2-induced nadirs after hypoxia were lower than those observed during room air breathing. O2 transiently depressed ventilation after hypoxia but not after room air breathing. These results suggest that the normal ventilatory response to isocapnic hypoxia has two components, an excitatory one from peripheral chemoreceptors, which is turned off by O2 breathing, and a slower inhibitory one, probably of central origin, which is affected less promptly by O2 breathing.
J Appl Physiol (1985) 1988 Sep
PMID:Effect of 100% O2 on hypoxic eucapnic ventilation. 318 86

The oxygen dependence of aquatic oxygen consumption was measured in active and anesthetized stage XVIII Discoglossus pictus tadpoles (Amphibia, Anura). The active tadpoles are good oxygen regulators in moderate hyperoxia and moderate hypoxia, whereas they are oxygen conformers in acute hypoxia. Critical oxygen pressure was 52 mmHg O2. Anesthetizing the larvae changes them to perfect oxygen conformers between moderate hyperoxia and moderate hypoxia (249-63 mmHg O2). At stage XVIII the aquatic respiratory organs are still capable of producing oxygen regulation when free access to air is denied. The marked capacity for oxygen regulation in D. pictus tadpoles is concordant with the strong hypoxic environments in which these animals usually live in nature.
Rev Esp Fisiol 1988 Sep
PMID:Oxygen regulation capacity in Discoglossus pictus tadpoles between moderate hyperoxia and acute hypoxia in water. 323 86

Immaturity, pulmonary barotrauma, and oxygen toxicity have been implicated in the pathogenesis of bronchopulmonary dysplasia (BPD). Although the physiologic and biochemical consequences of oxygen toxicity have been described in newborn and adult animals, there have been no controlled observations in prematures. We compared the physiologic and morphologic effects of prolonged hyperoxia with those of clinically appropriate oxygen in premature baboons with hyaline membrane disease (HMD) supported with conventional positive pressure ventilation and continuous distending airway pressure (PPV/PEEP). Twenty-one premature baboons were delivered at 140 days gestation, intubated and resuscitated, and supported with PPV/PEEP and standard NICU techniques for 11 days. The FIO2, PaO2, PaCO2, pHa, ventilator and airway pressures, and blood pressure were intermittently measured and recorded. The physiologic observations could be divided into 3 distinct phases. During Phase 1 (0 to 42 h) there were no significant intergroup differences, and (a/A)PO2 and IO2 (oxygenation index; (a/A)PO2/Paw) remained stable. In Phase 2 (43 to 96 h) there was a rapid improvement in (a/A)PO2 and IO2 in both groups, but the response in the hyperoxic animals was significantly dampened. During Phase 3 (97 to 264 h) there was continued improvement in the "prn" animals, which contrasted with progressive deterioration in those exposed to FIO2 1.0. Five of 11 "prn" and 3 of 10 FIO2 1.0 baboons developed air leaks during Phase 1 or early Phase 2. Four of 10 of the hyperoxic animals died after the late onset of air leak. Pathologic changes of BPD were found in all FIO2 1.0 animals surviving more than 6 days but in none of the "prn" long-term survivors.(ABSTRACT TRUNCATED AT 250 WORDS)
Am Rev Respir Dis 1987 Sep
PMID:Oxygen toxicity in the premature baboon with hyaline membrane disease. 330 71

Glutathione concentrations were measured in rat bronchoalveolar lavage fluid (BALF) obtained from normal rats and rats exposed to a fraction of inspired oxygen (FiO2) of 0.8 for up to 5 days. We also perturbed rat lung glutathione concentrations by administering the compound diisopropylidene acetone (phorone) to a separate group of animals and correlated changes in BALF glutathione with changes in lung tissue glutathione. We found that reduced glutathione is present in normal rat BALF but glutathione disulfide is extremely low. Increases in lung tissue glutathione concentration and in BALF glutathione concentration occurred after 5 days of exposure to hyperoxia. Animals treated with phorone exhibited decreases in lung glutathione concentration two hours after dosing and increases in lung glutathione concentration 24 hours after dosing. Rat BALF obtained from phorone-treated animals at 2 or 24 hours after administration revealed that changes in BALF glutathione concentrations reflected changes in lung tissue glutathione concentration. The presence of glutathione in lung lavage fluid suggests that the compound could be playing an extracellular role in the lung, either as an antioxidant or as a coenzyme for other glutathione-related enzymatic reactions.
J Lab Clin Med 1988 Sep
PMID:Glutathione concentrations in rat lung bronchoalveolar lavage fluid: effects of hyperoxia. 341 Nov 97

Injury to the lung during in vivo exposure to hyperoxia results in vascular restructuring and pulmonary hypertension. This study reports the pattern of cellular proliferation that occurs in proximal intrapulmonary arteries over time during vessel wall injury and adaptation to increased partial pressures of oxygen. Although the remodeling of the capillary bed has been emphasized particularly during oxygen injury to the lung, this report identifies significant proliferative changes within the vessel wall of proximal arterial segments isolated from rats exposed to 85% oxygen. An increased incorporation of 3H-thymidine by endothelial cells is the earliest and most dramatic vessel wall response. The labeling index of these cells is increased more than tenfold by the end of 7 days in hyperoxia. Proliferation of medial smooth muscle cells and adventitial fibroblasts is also significantly increased. The increased cell number within these compartments is noted especially for its contribution to the overall vessel wall hypertrophy observed in chronic hyperoxic pulmonary hypertension. This general proliferative response is accompanied by specific shifts in the relative percentages of different actin protein isoforms as identified by two-dimensional gel electrophoresis. Changes in the distribution of actin isoforms are discussed as potential markers of a phenotypic modulation among vascular smooth muscle cells that occurs during the progression of pulmonary vessel wall remodeling.
Am J Pathol 1988 Sep
PMID:Proliferative changes in the pulmonary arterial wall during short-term hyperoxic injury to the lung. 341 83

Prostanoid formation in human umbilical vessels perfused in vitro was assessed at different oxygen tensions. At an atmosphere of 5% oxygen the production rate of prostacyclin (measured as 6-keto-PGF1 alpha) was higher, while those of thromboxane A2 (measured as TXB2), PGE2 and PGF2 alpha were lower than with 20%, 50% and 95% oxygen. The stimulatory effect of angiotensin II on prostanoid production was found to be independent on the prevailing oxygen tension. Vascular formation of prostanoids thus seems to be at least partially affected by the ambient oxygen tension. Though altered oxygen tension does not seem to affect angiotensin induced prostanoid formation, the action of other vasoactive agents influencing vascular formation of prostanoids may respond differently to hypoxia or hyperoxia.
Prostaglandins 1987 Sep
PMID:Altered prostanoid formation in human umbilical vasculature in response to variations in oxygen tension. 343 54

Healthy adult baboons exposed to 100% oxygen for 5 to 7 days maintained on continuous mechanical ventilation develop severe bilateral noncardiogenic pulmonary edema that resembles in many aspects the human adult respiratory distress syndrome (ARDS). In the present study, we evaluated the effects of hyperoxia for 5 to 6 days in 8 baboons to compare changes in abnormalities in bronchoalveolar lavage fluid (BALF) biochemical markers, hemodynamic measurements, and pulmonary function tests in order to find early predictors of lung injury. All animals had bilateral alveolar infiltrates, severe hypoxemia, and progressive deterioration of pulmonary function tests. Diffuse alveolar damage and mild-moderate pneumonias were found and were associated with low-grade bacterial infection. Total lung capacity, diffusing capacity for carbon monoxide, pulmonary static compliance, and oxygenation were significantly impaired after Day 5; BALF proteins, elastase, and total polymorphonuclear leukocytes increased significantly at least 24 h before (Day 4) any abnormalities in chest radiographs, pulmonary function tests, and hemodynamic measurements were detected. We conclude that exposure to 100% oxygen in this model causes marked gas exchange, hemodynamic, biochemical, cytologic, radiographic, and pathologic changes similar to those noted in patients with ARDS. Bronchoalveolar lavage abnormalities precede hemodynamic and gas exchange abnormalities.
Am Rev Respir Dis 1987 Sep
PMID:One hundred percent oxygen lung injury in adult baboons. 363 38

The influence of arterial O2 and CO2 tensions on electroconvulsive seizure duration was investigated in five mongrel dogs under consistent anaesthetic conditions. Seizure durations were measured in a randomized protocol of nine possible combinations of arterial gas tension spanning increased, normal or decreased levels of PaO2 and PaCO2. Seizure duration was directly related to PaO2 (p less than 0.00001) and inversely related to PaCO2 (p less than 0.0001). A significant synergism was evident at the extremes of PaO2 and PaCO2, with seizure duration being greater than predicted for hyperoxia-hypocapnia and hypoxia-hypercapnia and shorter than predicted for hypoxia-hypocapnia and hyperoxia-hypercapnia. We conclude that arterial gas tensions strongly influence ECT-induced seizure duration and through this may influence the therapeutic efficacy of electroconvulsive therapy.
Can J Anaesth 1987 Sep
PMID:Arterial PaO2 and PaCO2 influence seizure duration in dogs receiving electroconvulsive therapy. 366 9

Oxygen toxicity in the non-ischemic and non-hypoxic heart has not been reported. In an experiment on isolated rat heart lung preparation, the effects of superoxide dismutase (SOD) on oxygen toxicity during hyperoxic perfusion were evaluated with intramyocardial high energy phosphates and the release of creatine phosphokinase (CPK) in the perfusate blood. Although there were no significant differences in high energy phosphates between SOD-treated and untreated hearts, the CPK release from the SOD-treated hearts was significantly less than from the untreated hearts. SOD increased the oxygen pressure of perfusate blood, too. These results indicate that hyperoxia induced cardiac and lung cell damage which was protected by SOD.
Jpn Circ J 1987 Sep
PMID:Protective effects of superoxide dismutase against oxygen toxicity in rat's heart lung preparation. 369 65

The effects of hyperoxia on lung tumor development were examined in mice and rats. In mice, exposure to 70% O2 prevented the development of urethan- or 3-methylcholanthrene-induced lung tumors. Dietary antioxidants [butylated hydroxytoluene (BHT) and butylated hydroxyanisole (BHA)] were unable to prevent the inhibition of tumor development by oxygen, although BHT retained its capability to enhance tumor development in mouse lung. In visible-size tumors, oxygen did not depress DNA synthesis. Oxygen also reduced the number of pulmonary metastatic nodules after i.v. injection of mammary gland-derived carcinoma cells, but failed to inhibit growth of murine lung carcinoma or murine melanoma-derived cell lines. Rats treated with one single intratracheal instillation of 3-methylcholanthrene developed multiple lung lesions; their growth could be prevented by exposure of the animals to 40 or 70% O2. It is concluded that hyperoxia prevents development of transformed cells in vivo in the lung and may affect adversely the growth of selected cell lines metastatic to the lung.
Carcinogenesis 1986 Sep
PMID:Modification of lung tumor growth by hyperoxia. 374 30


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