Cardioprotective Effect of Chronic Hypoxia Involves Inhibition of Mitochondrial Permeability Transition Pore Opening
Jazyk angličtina Země Česko Médium print
Typ dokumentu časopisecké články
PubMed
39560196
PubMed Central
PMC11629960
DOI
10.33549/physiolres.935427
PII: 935427
Knihovny.cz E-zdroje
- MeSH
- chronická nemoc MeSH
- cyklosporin * farmakologie MeSH
- hypoxie * metabolismus MeSH
- infarkt myokardu metabolismus patologie prevence a kontrola MeSH
- krysa rodu Rattus MeSH
- potkani Wistar * MeSH
- přechodový pór mitochondriální permeability * metabolismus MeSH
- reperfuzní poškození myokardu * metabolismus prevence a kontrola patologie MeSH
- srdeční mitochondrie metabolismus účinky léků patologie MeSH
- transportní proteiny mitochondriální membrány metabolismus MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- cyklosporin * MeSH
- přechodový pór mitochondriální permeability * MeSH
- transportní proteiny mitochondriální membrány 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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