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up-regulation and cardioprotection induced by chronic intermittent hypoxia
1 Institute of Physiology, Academy of Sciences of the Czech Republic, Prague , Czech Republic; Centre for Cardiovascular Research, Prague , Czech Republic
2 Department of Animal Physiology, Faculty of Science, Charles University, Prague, Czech Republic; Centre for Cardiovascular Research, Prague , Czech Republic
3 Prague, Czech Republic; Department of Animal Physiology, Faculty of Science, Charles University, Prague, Czech Republic
4 Department of Biochemistry, Faculty of Science, Charles University, Prague, Czech Republic
5 Prague, Czech Republic; Institute of Physiology, Academy of Sciences of the Czech Republic, Prague , Czech Republic; Centre for Cardiovascular Research, Prague , Czech Republic
6 Prague, Czech Republic; Department of Biochemistry, Faculty of Science, Charles University, Prague, Czech Republic
7 Prague, Czech Republic; Centre for Cardiovascular Research, Prague , Czech Republic; Department of Animal Physiology, Faculty of Science, Charles University, Prague, Czech Republic
8 2nd Faculty of Medicine, Charles University, Prague, Czech Republic; Centre for Cardiovascular Research, Prague , Czech Republic
9 Prague, Czech Republic; Centre for Cardiovascular Research, Prague , Czech Republic; 2nd Faculty of Medicine, Charles University, Prague, Czech Republic
* To whom correspondence should be addressed. E-mail: kolar{at}biomed.cas.cz.
The aim was to determine whether increased oxidative stress during the adaptation to chronic intermittent hypoxia (CIH) plays a role in the induction of improved cardiac ischemic tolerance. Adult male Wistar rats were exposed to CIH in a hypobaric chamber (7000 m, 8 h/day, 5 days/wk, 24-30 exposures). Half of the animals received antioxidant N-acetylcysteine (NAC; 100 mg/kg) daily before the exposure; the remaining rats received saline. Controls were kept under normoxia and treated in a corresponding manner. One day after the last exposure (and/or NAC injection), anesthetized animals were subject to 20-min coronary artery occlusion and 3-h reperfusion for infarct size determination. In parallel subgroups, biochemical analyses of the left ventricular myocardium were performed. Adaptation to CIH reduced infarct size from 56.7±4.5 % of the area at risk in the normoxic controls to 27.7±4.9 %. NAC treatment decreased the infarct size in the controls to 42.0±3.4 % but it abolished protection provided by CIH (to 41.1±4.9 %). CIH decreased the reduced-to-oxidized glutathione ratio and increased the relative amount of protein kinase C (PKC) isoform-
in the particulate fraction; NAC prevented these effects. The expression of PKC-
was decreased by CIH and not affected by NAC. Activities of superoxide dismutase, catalase and glutathione peroxidase were affected by neither CIH nor NAC treatment. It is concluded that oxidative stress associated with CIH plays a role in the development of increased cardiac ischemic tolerance. The infarct size-limiting mechanism of CIH seems to involve the PKC--dependent pathway but apparently not the increased capacity of major antioxidant enzymes.
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