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Страница 1 од 265 резултати
Dopamine restores lung ability to clear edema in rats exposed to hyperoxia.
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Exposure to hyperoxia causes lung injury, decreases active sodium transport and lung edema clearance in rats. Dopamine (DA) increases lung edema clearance by stimulating vectorial Na+ flux and Na, K-ATPase function in rat alveolar epithelium. This study was designed to test whether DA (10(-)5 M)
MRI detection of hyperoxia-induced lung edema in Zn-deficient rats.
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In a pioneering application of proton Magnetic Resonance Imaging (MRI), lung edema has been monitored in vivo in Zn-deficient rats exposed to 85% oxygen. Dietary Zn appears to play a role in protecting against hyperoxia-induced lung damage.
Influence of inhaled nitric oxide and hyperoxia on Na,K-ATPase expression and lung edema in newborn piglets.
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This study was undertaken to examine the combined effect of nitric oxide (NO) and hyperoxia on lung edema and Na,K-ATPase expression. Newborn piglets were exposed to room air (FiO2 = 0.21), room air plus 50 ppm NO, hyperoxia (FiO2 >/= 0.96) or to hyperoxia plus 50 ppm NO for 4-5 days. Animals
Acute respiratory failure induced by bleomycin and hyperoxia: pulmonary edema, cell kinetics, and morphology.
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The acute manifestations of experimental bleomycin- and hyperoxia-induced lung damage were examined. Hamsters were treated with 5 U/kg bleomycin intratracheally followed by exposure to 80% oxygen (O2). As little as 12 hr of O2 exposure potentiated the bleomycin injury; however, the onset of
[Relationship between expression of aquaporin-1, -5 and pulmonary edema in hyperoxia-induced lung injury in newborn rats].
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OBJECTIVE
Aquaporin (AQP) is a group of cell membrane transporting proteins. The study was designed to investigate the changes of AQP1 and AQP5 in the lung tissue under hyperoxia and their roles in pulmonary edema.
METHODS
Two hundred newborn rats were randomized into different oxygen concentrations
Isoproterenol improves ability of lung to clear edema in rats exposed to hyperoxia.
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Exposure of adult rats to 100% O(2) results in lung injury and decreases active sodium transport and lung edema clearance. It has been reported that beta-adrenergic agonists increase lung edema clearance in normal rat lungs by upregulating alveolar epithelial Na(+)-K(+)-ATPase function. This study
Novel peptide for attenuation of hyperoxia-induced disruption of lung endothelial barrier and pulmonary edema via modulating peroxynitrite formation.
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Pulmonary damages of oxygen toxicity include vascular leakage and pulmonary edema. We have previously reported that hyperoxia increases the formation of NO and peroxynitrite in lung endothelial cells via increased interaction of endothelial nitric oxide (eNOS) with β-actin. A peptide (P326TAT) with
Recombinant human VEGF treatment transiently increases lung edema but enhances lung structure after neonatal hyperoxia.
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Recent studies suggest that VEGF may worsen pulmonary edema during acute lung injury (ALI), but, paradoxically, impaired VEGF signaling contributes to decreased lung growth during recovery from ALI due to neonatal hyperoxia. To examine the diverse roles of VEGF in the pathogenesis of and recovery
[Pathomechanism of brain edema in normobaric hyperoxia].
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[Expression of high mobility group protein-B1 in mice with hyperoxia-induced bronchopulmonary dysplasia].
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OBJECTIVE
To study the effect of hyperoxia exposure on high mobility group protein-B1 (HMGB1) expression in neonatal mice and the role of HMGB1 in the pathogenesis of bronchopulmonary dysplasia (BPD).
METHODS
C57BL/6 mice were randomly exposed to 60% O2 or air 1 day after birth. BPD was induced by
[The expression of α-smooth muscle actin during the lung injury induced by hyperoxia].
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OBJECTIVE
To explore the expression of α-smooth muscle actin (α-SMA) during the lung injury induced by hyperoxia in infantile rats.
METHODS
Sixty-four male Sprague-Dawley (SD) rats about 3 weeks were randomly assigned into normal control group which exposured to room air [fraction of inspired oxygen
Inactivation of exogenous surfactant by pulmonary edema fluid.
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Modified natural porcine surfactant was mixed with edema fluid sampled from the airways of hyperoxia-exposed adult rabbits. By varying the concentration of surfactant lipids (10, 25, and 50 mg/mL) and edema fluid proteins (0-280 mg/mL), we obtained a series of preparations with protein to surfactant
Pulmonary lymphatics and edema accumulation after brief lung injury.
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In a past study of hyperoxia-induced lung injury, the extensive lymphatic filling could have resulted from lymphatic proliferation or simple lymphatic recruitment. This study sought to determine whether brief lung injury could produce similar changes, to show which lymphatic compartments fill with
Reduction of the edema of acute hyperoxic lung injury by granulocyte depletion.
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Increased numbers of granulocytes are found in lungs acutely injured by hyperoxia, but their contribution to lung injury remains unknown. We found that circulating granulocytes markedly increased (P less than 0.01) in rabbits exposed to hyperoxia for 72 h and that the numbers of granulocytes in lung
Granulocytes and hyperoxia act synergistically in causing acute lung injury.
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Various indirect methods have implicated the polymorphonuclear leukocyte (PMN) as being an important, but not an absolutely necessary, factor in hyperoxia-associated pulmonary edema. By utilizing the cell free isolated perfused rabbit lung model, we demonstrated that the addition of purified,
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