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

Rabbits were exposed to 100% oxygen at pressures of 256 to 1520 mm Hg for up to 5 d and the blood and erythrocytes of these animals were examined for changes that could be related to hyperoxia. Glutathione reductase activity of erythrocytes was reduced 5 to 29% by hyperoxia, whereas that of the plasma was not significantly altered. Significant changes in red and white cell counts, including differential leukocyte count, could not be detected. Electrophoretic analysis of the proteins and esterases derived from plasma and membranes and cytoplasmic fractions of erythrocytes did not reveal changes attributable to hyperoxia.
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PMID:Effects of hyperoxia on glutathione reductase activity, membrane proteins, and esterases of rabbit erythrocytes. 88 26

Prolonged exposure to hyperoxia can result in significant lung injury and has been associated with the development of bronchopulmonary dysplasia. Leukotrienes (LT) recruit polymorphonuclear leukocytes (PMN) to the lung, increase vascular permeability, and have therefore been postulated to play a role in the pathogenesis of hyperoxic lung injury. This study investigates ICI 198,615 (ICI), an LTD4 and LTE4 receptor antagonist in preventing hyperoxic lung injury in newborn rabbits. Matched littermates of 7-day-old rabbits received ICI (0.1 or 1.0 microM/kg/h) or vehicle alone, were exposed to greater than 95% O2, and sacrificed after 48, 72, 84 and 96 h of exposure. Bronchoalveolar alveolar lavage fluid (BAL) of the left lung was analyzed for white cell count, differential, absolute number of PMNs, total protein, and cyclooxygenase products 6-keto-PGF1 alpha, and thromboxane B2. Lung water was quantified utilizing the right lung. Results demonstrated no significant differences between the ICI groups or between the ICI groups and controls. In conclusion, the administration of the LTD4 and LTE4 receptor antagonist ICI 198,615 was insufficient to reduce the formation of pulmonary edema, reduce mortality or attenuate hyperoxic lung injury. These experiments suggest that a number of other mediators may be involved in the hyperoxic lung injury process and that the functional inhibition of a portion of the arachidonic acid cascade was not sufficient to either prevent or attenuate hyperoxic lung injury in newborn rabbits.
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PMID:Evaluation of a leukotriene receptor antagonist in prevention of hyperoxic lung injury in newborn rabbits. 131 78

We hypothesized that inhaled nitric oxide (iNO), a selective vasodilator for pulmonary hypertension, may exacerbate hyperoxia-related lung inflammatory injury by alteration of phosphatidylcholine (PC) synthesis in mature lungs. Healthy adult rats were allocated to 4 groups and exposed to: 95% oxygen, or 20ppm iNO, or both (ONO), or room air, all for 48h. (3)H-choline chloride was injected i.v. at 10min, 8, 16, and 24h prior to the end of 48h exposure and the animal lungs were processed. In oxygen group, oxidative damage and inflammation were significantly induced compared to the room air group. In ONO group there were significantly elevated glutathione, attenuated malondialdehyde, myeloperoxidase, and wet-to-dry lung weight ratio in lung parenchyma, decreased white cell counts and vascular-to-alveolar leakage of albumin in bronchoalveolar lavage fluid. In both oxygen and ONO groups both total phospholipids and surfactant protein-A were significantly increased compared with the room air group. Newly synthesized (3)H-PC was low in the lungs of NO group but high over time in both oxygen and ONO groups. Morphologically, lung injury was mild in ONO, but moderate in both oxygen and NO groups. We conclude that iNO alleviated oxidative damage and inflammation, and reduced alveolar leakage in hyperoxic injury of the mature lungs. Hyperoxia enhanced production of surfactant, whereas iNO did not attenuate this effect.
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PMID:Inhaled nitric oxide attenuates hyperoxic and inflammatory injury without alteration of phosphatidylcholine synthesis in rat lungs. 1648 Sep 8