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Cardioprotective Effect of Chronic Hypoxia Involves Inhibition of Mitochondrial Permeability Transition Pore Opening
P. Alanova, L. Alan, J. Neckar, B. Ostadal, F. Kolar
Status minimal Language English Country Czech Republic
Document type Journal Article
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- MeSH
- Chronic Disease MeSH
- Cyclosporine * pharmacology MeSH
- Hypoxia * metabolism MeSH
- Myocardial Infarction metabolism pathology prevention & control MeSH
- Rats MeSH
- Rats, Wistar * MeSH
- Mitochondrial Permeability Transition Pore * metabolism MeSH
- Myocardial Reperfusion Injury * metabolism prevention & control pathology MeSH
- Mitochondria, Heart metabolism drug effects pathology MeSH
- Mitochondrial Membrane Transport Proteins metabolism MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
The aim of the study was to examine the potential role of mitochondrial permeability transition pore (mPTP) in the cardioprotective effect of chronic continuous hypoxia (CH) against acute myocardial ischemia/reperfusion (I/R) injury. Adult male Wistar rats were adapted to CH for 3 weeks, while their controls were kept under normoxic conditions. Subsequently, they were subjected to I/R insult while being administered with mPTP inhibitor, cyclosporin A (CsA). Infarct size and incidence of ischemic and reperfusion arrhythmias were determined. Our results showed that adaptation to CH as well as CsA administration reduced myocardial infarct size in comparison to the corresponding control groups. However, administration of CsA did not amplify the beneficial effect of CH, suggesting that inhibition of mPTP opening contributes to the protective character of CH.
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