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

Undernutrition may exacerbate hyperoxia-induced lung injury, a finding that may be of significance in the early clinical management of the premature human infant. Addressing this specific problem, we found that 72 h of food restriction in guinea pig pups delivered 3 days preterm increased mortality rates among pups exposed to 95% oxygen (8/18) and yet had no effect on 21% oxygen (air)-exposed pups (0/10). Reduced tolerance of hyperoxic conditions was not, however, associated with increased lung injury, assessed as pulmonary microvascular leakage. Pulmonary antioxidant enzyme activities [Cu,Zn superoxide dismutase (SOD), Mn SOD, glutathione peroxidase, and catalase] were unaltered by starvation or hyperoxia. Lung glutathione concentration was slightly decreased after food restriction, whereas hyperoxic exposure did not change either lung or bronchoalveolar lavage fluid glutathione concentrations or lung antioxidant enzyme activities. Increased susceptibility to the lethal effects of oxygen in the starved preterm guinea pig pup could not be attributed to a deficiency of pulmonary antioxidant defenses.
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PMID:Effect of food restriction on hyperoxia-induced lung injury in preterm guinea pig. 141 61

The objectives of this study were to investigate whether oral supplementation of L-2-oxothiazolidine-4-carboxylate (OTC) is effective for increasing tissue glutathione (GSH) concentrations in rats fed a diet very low (0.5%) in protein-a model of wasting malnutrition-and to determine the efficacy of OTC for protection against pulmonary oxygen toxicity. Weanling rats, fed a 0.5 or 15% protein diet for 2 wk, were given an oral supplement of OTC, and tissue GSH concentrations were measured over a 24 h period. OTC supplementation to rats fed 0.5% protein significantly increased GSH concentrations in liver and lung, but not in kidney and blood, when compared with the 0.5% protein unsupplemented group. The liver GSH concentration in the 0.5% protein OTC-supplemented group was higher than the 15% control group. Daily supplementation of OTC protected rats from pulmonary oxygen toxicity during 4 days of 85% oxygen exposure as determined by lung-to-body weight ratios and in vivo proton magnetic resonance imaging. Although hyperoxia exposure increased lung GSH concentrations in all groups, OTC supplementation was effective for increasing lung GSH concentration in rats fed the 0.5% protein diet. This study demonstrated that oral administration of OTC to wasting malnourished rats is an effective procedure to increase GSH concentration rapidly in target organs such as lung, and that daily supplementation of a low dose of OTC has a sustained effect to protect against pulmonary oxygen toxicity during 4 days of hyperoxia exposure.
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PMID:Elevation of lung glutathione by oral supplementation of L-2-oxothiazolidine-4-carboxylate protects against oxygen toxicity in protein-energy malnourished rats. 152 40

As a test of the hypothesis that hyperoxia might hinder the growth of nascent lung macrophages, term newborn rabbits were treated with room air or increasing oxygen concentrations (40%, 80%, or greater than or equal to 95%) for 96 hours after birth. After 24, 48, 72, and 96 hours of environmental exposure, pulmonary alveolar macrophage population kinetics were determined by three methods: (1) bronchoalveolar lavage cell yields, (2) thymidine incorporation by macrophages, and (3) assessment of macrophage cell division by mitotic indices. Newborn rabbits kept in room air or 40% inspired O2 showed a steady increase of macrophages in lung lavage, but pups treated with 80% or greater than or equal to 95% oxygen showed no rise of macrophage yield in lung washings after 96 hours of exposure (P less than 0.02). The diminished macrophage yield noted in pups treated with 80% or greater than or equal to 95% oxygen was explained by rates of thymidine uptake and macrophages replication (mitotic indices) that were greater than 12-fold lower than values seen in rabbit pups housed in room air or 40% inspired O2 for 96 hours (P less than 0.05). These findings could not be attributed to malnutrition caused by oxygen toxicity because all groups appeared well and gained weight equally during the period of exposure. We conclude that acute hyperoxia impedes the intraalveolar proliferation of lung macrophages, an observation that may have implications regarding host defense and for repair and growth of the lung in neonates needing respiratory support.
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PMID:Prevention of pulmonary alveolar macrophage proliferation in newborn rabbits by hyperoxia. 336 92

Undernutrition was found to compromise the tolerance of newborn rat pups to hyperoxia (greater than 95% O2 for 7 days). Survival rate for the normally nourished pups (11 pups/dam) was 56 of 77 (73%) but only 47 of 108 (44%) for the undernourished (18 pups/dam) group (P less than 0.005). Body growth, lung growth, and lung DNA content were significantly reduced by undernutrition. Hyperoxia inhibited these same parameters in both groups of pups. The growth inhibitory effects of O2 and undernutrition were additive, with an especially marked depression of lung DNA content (decreases 65%). Lung maturation was also markedly inhibited by O2 but to a similar extent in both nutrition groups. Despite the disparity in their O2 tolerance, 18/litter and 11/litter pups in O2 responded with equivalent increases in lung antioxidant enzymes. We suggest that the additive depressive effects of neonatal undernutrition and hyperoxia on lung DNA may compromise repair of ongoing O2-induced lung damage and help account for the compromised O2-tolerance we consistently observed even in the presence of significantly elevated antioxidant enzyme defenses.
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PMID:Oxygen toxicity in newborn rats: the adverse effects of undernutrition. 717 19

Continuous maternal hyperoxygenation treatment (2.5 l/min by means of a nasopharyngeal cannula) was given in four patients presenting with intrauterine growth-retarded (IUGR) fetuses and decelerative fetal heart rate (FHR) patterns at 27-28 weeks of gestation. The effect of maternal hyperoxia was studied longitudinally. Neither the incidence of generalized fetal movements (FGM%) nor the pulsatility index of the internal carotid artery increased under hyperoxia. In fact, both variables decreased progressively. FHR variation was abnormal prior to the start of hyperoxygenation and showed a slight but transient increase. On average, maternal hyperoxygenation 'resulted' in a prolongation of the duration of pregnancy of 9 days. The neonatal mortality was similar in the study group as compared to a control group of IUGR infants. However, hypoglycemia, thrombocytopenia and disseminated intravascular coagulation at birth were found more frequently in the study group. Conversely, blood gas abnormalities were less frequent in the fetuses of mothers that were treated with oxygen. We conclude that positive effects of oxygen therapy in IUGR fetuses remain uncertain and that detrimental effects due to prolongation of intrauterine malnutrition have not as yet been sufficiently excluded.
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PMID:Continuous maternal hyperoxygenation in the treatment of early fetal growth retardation. 1279 38

Several factors are associated with bronchopulmonary dysplasia. Among them, hyperoxia and lung immaturity are considered to be fundamental; however, the effect of malnutrition is unknown. Our objective was to evaluate the effects of 7 days of postnatal malnutrition and hyperoxia on lung weight, volume, water content, and pulmonary morphometry of premature rabbits. After c-section, 28-day-old New Zealand white rabbits were randomized into four groups: control diet and room air (CA, N = 17), control diet and > or = 95% O2 (CH, N = 17), malnutrition and room air (MA, N = 18), and malnutrition and > or = 95% O2 (MH, N = 18). Malnutrition was defined as a 30% reduction of all the nutrients provided in the control diet. Treatments were maintained for 7 days, after which histological and morphometric analyses were conducted. Lung slices were stained with hematoxylin-eosin, modified orcein-resorcin or picrosirius. The results of morphometric analysis indicated that postnatal malnutrition decreased lung weight (CA: 0.83 +/- 0.19; CH: 0.96 +/- 0.28; MA: 0.65 +/- 0.17; MH: 0.79 +/- 0.22 g) and water content, as well as the number of alveoli (CA: 12.43 +/- 3.07; CH: 8.85 +/- 1.46; MA: 7.33 +/- 0.88; MH: 6.36 +/- 1.53 x 10-3/mm) and elastic and collagen fibers. Hyperoxia reduced the number of alveoli and increased septal thickening and the mean linear intercept. The reduction of alveolar number, collagen and elastic fibers was intensified when malnutrition and hyperoxia were associated. These data suggest that dietary restriction enhances the magnitude of hyperoxia-induced alveolar growth arrest and lung parenchymal remodeling. It is interesting to consider the important influence of postnatal nutrition upon lung development and bronchopulmonary dysplasia.
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PMID:Effect of postnatal malnutrition on hyperoxia-induced newborn lung development. 1957 40

Bronchopulmonary dysplasia (BPD) is an important lung developmental pathophysiology that affects many premature infants each year. Newborn animal models employing both premature and term animals have been used over the years to study various components of BPD. This review describes some of the neonatal rabbit studies that have contributed to the understanding of BPD, including those using term newborn hyperoxia exposure models, premature hyperoxia models, and a term newborn hyperoxia model with recovery in moderate hyperoxia, all designed to emulate aspects of BPD in human infants. Some investigators perturbed these models to include exposure to neonatal infection/inflammation or postnatal malnutrition. The similarities to lung injury in human premature infants include an acute inflammatory response with the production of cytokines, chemokines, and growth factors that have been implicated in human disease, abnormal pulmonary function, disordered lung architecture, and alveolar simplification, development of fibrosis, and abnormal vascular growth factor expression. Neonatal rabbit models have the drawback of limited access to reagents as well as the lack of readily available transgenic models but, unlike smaller rodent models, are able to be manipulated easily and are significantly less expensive than larger animal models.
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PMID:Animal models of bronchopulmonary dysplasia. The preterm and term rabbit models. 2532 82

Extremely low birth weight and reduced caloric intake have significant adverse effects on lung development and are risk factors for bronchopulmonary dysplasia. Vascular endothelial growth factor (VEGF) is highly involved in lung microvascular development, and may be affected by nutritional status. To test the hypothesis that suboptimal nutrition decreases VEGF signaling in formula-fed neonatal rats, and to determine whether supplementation with probiotics, prebiotics, or synbiotics ameliorate the effects, rat pups at birth (P0) were placed in room air (RA) or intermittent hypoxia (12%) during hyperoxia (50% O2) from birth to P3. The pups were either maternally-fed; or formula-fed with or without supplementation. Formula-fed pups were separated from their mothers at birth and hand-gavaged every 3 hours. Lung VEGF signaling was determined on P3. In RA, all formula-fed groups were significantly growth suppressed with decreased lung weights. Hyperoxia had a less remarkable effect on body weight; and mean lung weight was lower only in the unsupplemented formula-fed group. Lung VEGF was decreased in all formula-fed RA and hyperoxia groups, except the probiotics group. In RA, sVEGFR-1 levels were elevated in all formula-fed groups except the synbiotics group. However in hyperoxia, sVEGFR-1 levels were higher in the unsupplemented formula group. All genes involved in angiogenesis were downregulated in the formula-fed groups compared to maternally-fed. Formula feeding results in significant malnutrition associated with decreased lung size and lung VEGF levels in neonatal rat pups. Probiotic supplementation prevented the adverse effects of combined hyperoxia and suboptimal nutrition on lung VEGF suggesting preservation of angiogenesis.
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PMID:Benefits of pre-, pro- and Syn-biotics for lung angiogenesis in malnutritional rats exposed to intermittent hypoxia. 2536 Feb 12