Fig. 6.

a Sequence of a calcein-loaded mouse cardiomyocyte with rigor contracture during the first 5 min of reperfusion (60 × magnification). Because calcein is entrapped in mitochondria, the decay of green fluorescence reflects mitochondrial permeabilization. b Quantification of total mitochondrial calcein release at 15 min reperfusion, with respect to maximal mitochondrial calcein release achieved after the addition of atractyloside (ATR), in isolated cardiomyocytes from wild-type (WT) and cyclophilin-D knock-out (CyD-KO) mouse hearts, previously submitted to either 15 or 25 min ischemia. The inset shows mitochondrial calcein kinetics [changes in fluorescence with respect to the initial value, F/F₀)] throughout reperfusion, indicating mitochondrial permeability transition pore (mPTP) opening in the different groups of cells. Maximal mitochondrial calcein release was induced in WT cardiomyocytes treated with 20 µmol/L atractyloside. Data are expressed as mean ± SEM of 5–6 cardiomyocytes per group. Modified from [358]