Reactive Oxygen Species Production in the Early and Later Stage of Chronic Ventilatory Hypoxia
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11130%2F12%3A8183" target="_blank" >RIV/00216208:11130/12:8183 - isvavai.cz</a>
Výsledek na webu
<a href="http://www.biomed.cas.cz/physiolres/pdf/prepress/932206.pdf" target="_blank" >http://www.biomed.cas.cz/physiolres/pdf/prepress/932206.pdf</a>
DOI - Digital Object Identifier
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Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
Reactive Oxygen Species Production in the Early and Later Stage of Chronic Ventilatory Hypoxia
Popis výsledku v původním jazyce
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 chronichypoxia. In our study Wistar rats were kept for 1, 4 and 21 days in an isobaric hypoxic chamber (F-iO2=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 theproduction 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.
Název v anglickém jazyce
Reactive Oxygen Species Production in the Early and Later Stage of Chronic Ventilatory Hypoxia
Popis výsledku anglicky
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 chronichypoxia. In our study Wistar rats were kept for 1, 4 and 21 days in an isobaric hypoxic chamber (F-iO2=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 theproduction 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.
Klasifikace
Druh
J<sub>x</sub> - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)
CEP obor
ED - Fyziologie
OECD FORD obor
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Návaznosti výsledku
Projekt
Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.
Návaznosti
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)
Ostatní
Rok uplatnění
2012
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Physiological Research
ISSN
0862-8408
e-ISSN
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Svazek periodika
61
Číslo periodika v rámci svazku
2
Stát vydavatele periodika
CZ - Česká republika
Počet stran výsledku
7
Strana od-do
145-151
Kód UT WoS článku
000306507400003
EID výsledku v databázi Scopus
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