Fig. 5. Postischemic treatment of intralipid increases mitochondrial calcium retention capacity (CRC) after ischemia-reperfusion injury as cyclosporine-A in a cychlophilin-D-dependent manner. (A , B ) Typical recordings of the mitochondrial permeability transition pore opening in isolated mitochondria from control group, 1% intralipid, and 1.5 μM cyclosporine-A groups subjected to 20 min of global ischemia followed by 10 min of reperfusion as well as sham hearts before (A ) and after addition of 1.5 μM cyclosporine-A directly in the cuvette (B ). (C ) Calcium retention capacity in the absence of cyclosporine-A (red bars ) and after addition of cyclosporine-A in the cuvette (black bars ). **P < 0.001 versus  CTRL; ##P < 0.001 versus  sham+ cyclosporine-A group; ∧∧P < 0.001 versus  sham (n = 6). CsA = cyclosporine-A; CTRL = control; ILP = intralipid; mPTP = mitochondrial permeability transition pore.

Fig. 5. Postischemic treatment of intralipid increases mitochondrial calcium retention capacity (CRC) after ischemia-reperfusion injury as cyclosporine-A in a cychlophilin-D-dependent manner. (A , B ) Typical recordings of the mitochondrial permeability transition pore opening in isolated mitochondria from control group, 1% intralipid, and 1.5 μM cyclosporine-A groups subjected to 20 min of global ischemia followed by 10 min of reperfusion as well as sham hearts before (A ) and after addition of 1.5 μM cyclosporine-A directly in the cuvette (B ). (C ) Calcium retention capacity in the absence of cyclosporine-A (red bars ) and after addition of cyclosporine-A in the cuvette (black bars ). **P < 0.001 versus  CTRL; ##P < 0.001 versus  sham+ cyclosporine-A group; ∧∧P < 0.001 versus  sham (n = 6). CsA = cyclosporine-A; CTRL = control; ILP = intralipid; mPTP = mitochondrial permeability transition pore.

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