Fig. 6. Inhibition of the mitochondrial permeability transition pore opening by isoflurane postconditioning in wild-type (WT) hearts but not in endothelial nitric oxide synthase knockout (eNOS −/−) hearts subjected to 30 min of ischemia followed by 30 min of reperfusion. (A ) The amount of in vitro Ca2+overload necessary to open the mitochondrial permeability transition pore in WT hearts and in eNOS −/−hearts; (B ) representative tracings showing the changes in membrane potential (Δψm) of mitochondria isolated from WT hearts after in vitro Ca2+loading; (C ) tracings showing the changes in Δψmof mitochondria isolated from the eNOS −/−hearts after in vitro Ca2+loading. Opening of the mitochondrial permeability transition pore was assessed after in vitro Ca2+overload by following changes in Δψmusing the fluorescent dye rhodamine 123. Carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone (FCCP) was added at the arrows to depolarize mitochondria. *P < 0.05 versus sham; # P < 0.05 versus control (n = 10/group).