Extracellular Cl-free-induced cardioprotection against hypoxia/reoxygenation is associated with attenuation of mitochondrial permeability transition pore.

The isotonic substitution of extracellular chloride by gluconate (extracellular Cl-free) has been demonstrated to elicit cardioprotection by attenuating ischaemia/reperfusion-induced elevation of intracellular chloride ion concentration ([Cl]). However, the downstream mechanism underlying the cardioprotective effect of extracellular Cl-free is not fully established. Here, it was investigated whether extracellular Cl-free attenuates mitochondrial dysfunction after hypoxia/reoxygenation (H/R) and whether mitochondrial permeability transition pore (mPTP) plays a key role in the extracellular Cl-free cardioprotection.