AI Article Synopsis
- The study investigates how nitric oxide (NO) and high oxygen levels (hyperoxia) affect lung edema and the expression of a protein called Na,K-ATPase in newborn piglets.
- Exposure to NO in regular air showed minimal effect on Na,K-ATPase levels, whereas hyperoxia alone raised both the mRNA and protein levels of Na,K-ATPase and worsened lung conditions.
- When NO was given with hyperoxia, it reduced the rise of Na,K-ATPase but did not improve lung damage, suggesting NO might disrupt the body's defense against high oxygen toxicity.
Article Abstract
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 exposed to NO in room air experienced only a slight decrease in Na,K-ATPase alpha subunit protein level. Hyperoxia, in the absence of NO, induced both the mRNA and the protein level of Na,K-ATP-ase alpha subunit and significantly increased wet lung weight, extravascular lung water, and alveolar permeability. NO in hyperoxia decreased the hyperoxic-mediated induction of Na,K-ATPase alpha subunit mRNA and protein while wet lung weight, extravascular lung water, and alveolar permeability remained elevated. These results suggest that 50 ppm of inhaled NO may not improve hyperoxic-induced lung injury and may interfere with the expression of Na,K-ATPase which constitutes a part of the cellular defense mechanism against oxygen toxicity.
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| http://dx.doi.org/10.1159/000014096 | DOI Listing |
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