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Reactive oxygen species production in the early and later stage of chronic ventilatory hypoxia
D. Hodyc, E. Johnson, A. Skoumalová, J. Tkaczyk, H. Maxová, M. Vízek, J. Herget
Jazyk angličtina Země Česko
Typ dokumentu práce podpořená grantem
NLK
Directory of Open Access Journals
od 1991
Free Medical Journals
od 1998
ProQuest Central
od 2005-01-01
Medline Complete (EBSCOhost)
od 2006-01-01
Nursing & Allied Health Database (ProQuest)
od 2005-01-01
Health & Medicine (ProQuest)
od 2005-01-01
ROAD: Directory of Open Access Scholarly Resources
od 1998
- MeSH
- arteria pulmonalis metabolismus MeSH
- hypoxie komplikace metabolismus MeSH
- krysa rodu rattus MeSH
- kyselina peroxydusitá metabolismus MeSH
- oxid dusnatý biosyntéza krev MeSH
- peroxid vodíku metabolismus MeSH
- plicní hypertenze etiologie MeSH
- potkani Wistar MeSH
- reaktivní formy kyslíku metabolismus MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- práce podpořená grantem MeSH
Pulmonary hypertension resulting from chronic hypoxia is at least partly caused by the increased production of reactive oxygen species (ROS). The goal of the presented study was to investigate the dynamics and the site of production of ROS during chronic hypoxia. In our study Wistar rats were kept for 1, 4 and 21 days in an isobaric hypoxic chamber (FiO2=0.1), while controls stayed in normoxia. We compared NO production in expired air, plasma and perfusate drained from isolated rat lungs and measured superoxide concentration in the perfusate. We also detected the presence of superoxide products (hydrogen peroxide and peroxynitrite) and the level of ROS-induced damage expressed as the concentration of lipid peroxydation end products. We found that the production and release of ROS and NO during early phase of chronic hypoxia has specific timing and differs in various compartments, suggesting the crucial role of ROS interaction for development of hypoxic pulmonary hypertension.
Citace poskytuje Crossref.org
Literatura
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