Laboratory of Developmental Cardiology, Institute of Physiology of the Czech Academy of Sciences, Prague, Czech Republic.
Physiol Res. 2024 Nov 19;73(5):881-884. doi: 10.33549/physiolres.935427.
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.
本研究旨在探讨线粒体通透性转换孔（mPTP）在慢性持续低氧（CH）对急性心肌缺血/再灌注（I/R）损伤的保护作用中的潜在作用。成年雄性 Wistar 大鼠适应 CH 3 周，而对照组保持在常氧条件下。随后，在给予 mPTP 抑制剂环孢菌素 A（CsA）的同时，对其进行 I/R 损伤。测定梗死面积和缺血再灌注心律失常的发生率。我们的结果表明，与相应的对照组相比，适应 CH 以及 CsA 的给药减少了心肌梗死面积。然而，CsA 的给药并没有放大 CH 的有益作用，这表明抑制 mPTP 的开放有助于 CH 的保护作用。
