Hyperoxia has been shown to attenuate the increase in pulmonary artery (PA) pressure associated with immersed exercise in thermoneutral water, which could serve as a possible preventive strategy for the development of immersion pulmonary edema (IPE). We tested the hypothesis that the same is true during exercise in cold water. Six healthy volunteers instrumented with arterial and PA catheters w...

Pulmonary expression of granulocyte/macrophage colony-stimulating factor (GM-CSF) is critically important for normal functional maturation of alveolar macrophages. We found previously that lung GM-CSF is dramatically suppressed in mice exposed to hyperoxia. Alveolar epithelial cells (AEC) are a major source of GM-CSF in the peripheral lung, and in vivo hyperoxia resulted in greatly reduced expr...

background: an increased oxidative stress in patients under treatment with high concentrations of oxygen (hyperoxia) is considered to be one of the major mechanisms of lung injury. between different mediators, transition metal ions especially iron, by generation of very reactive free radicals play an important role in oxidative stress process. disruption of normal iron hemostasis has been repor...

RATIONALE The underlying pathophysiology of bronchopulmonary dysplasia includes a macrophage-mediated host response orchestrated by anti-inflammatory peroxisome proliferator-activated receptor gamma (PPARγ) and anti-oxidant nuclear factor (erythroid-derived 2)-like 2 (Nrf2). These have not yet been studied in combination. This study tested the hypothesis that combined inflammatory and oxidative...

Das KC. Thioredoxin-deficient mice, a novel phenotype sensitive to ambient air and hypersensitive to hyperoxia-induced lung injury. Am J Physiol Lung Cell Mol Physiol 308: L429–L442, 2015. First published December 24, 2014; doi:10.1152/ajplung.00285.2014.— Pulmonary oxygen toxicity is a major clinical problem for patients undergoing supplemental oxygen therapy. Thioredoxin (Trx) is an endogenou...

Exposure of pulmonary artery endothelial cells (PAECs) to hyperoxia results in a compromise in endothelial monolayer integrity, an increase in caspase-3 activity, and nuclear translocation of apoptosis-inducing factor (AIF), a marker of caspase-independent apoptosis. In an endeavor to identify proteins involved in hyperoxic endothelial injury, we found that the protein expression of heat-shock ...

Hyperoxic acute lung injury (HALI) is characterized by inflammation and epithelial cell death. CLOCK genes are master regulators of circadian rhythm also implicated in inflammation and lung diseases. However, the relationship of CLOCK genes in hyperoxia-induced lung injury has not been studied. This study will determine if HALI alters CLOCK gene expression. To test this, wild-type and NALP3(-/-...

The purpose of this study was to examine the behavior of Glutathione Peroxidase (GPx) activity and Free Radicals (FR) production in the brain during graded hyperoxia exposure with and without selenium preventive intake. Forty two adult male rats were assigned to seven groups, six animals each. The first group served as control and the second, third and fourth groups were exposed to hyperoxia fo...

Hyperoxia can lead to a myriad of deleterious effects in the lung including epithelial damage and diffuse inflammation. The specific mechanisms by which hyperoxia promotes these pathological changes are not completely understood. Activation of ion channels has been proposed as one of the mechanisms required for cell activation and mediator secretion. The two-pore-domain K(+) channel (K2P) Trek-...

Hyperoxia is known to injure tissues and cells (1) . In a series of papers the quantitative influence of hyperoxia on some aspects of lung ultrastructure was elucidated (2-4) . These studies revealed that hyperoxia resulted in rapid destruction of the pulmonary capillaries, a thickening of the air-blood barrier, and, eventually, a repopulation of the alveolar epithelium by granular pneumocytes ...