Fig. 6. Isoflurane opens mitochondrial potassium adenosine-5′-triphosphate-sensitive (mitoKATP) channels to the greatest extent in nondiabetic induced pluripotent stem cell-derived cardiomyocytes (N-iPSC-CMs). Mitochondrial membrane potential was monitored in dissociated iPSC-CMs. Representative signal traces from the addition (arrow ) of isoflurane alone or in the presence of mitoKATPblocker 5-hydroxydecanoate (5-HD) in N-iPSC-CMs in 11 mM glucose (A ). Isoflurane opened mitoKATPchannels and caused a loss of tetramethylrhodamine ethyl ester fluorescence indicative of a mitochondrial depolarization. 5-hydroxydecanoate partly blocked the isoflurane-induced mitochondrial depolarization. Diazoxide depolarized the mitochondria in both N-iPSC-CMs and DM-iPSC-CMs in a 5 mM, 11 mM, and 25 mM glucose environment. Isoflurane induced the greatest mitochondrial depolarization in N-iPSC-CMs in a 5 mM glucose environment. 5-hydroxydecanoate partly attenuated the isoflurane-induced mitochondrial depolarization (B ). Isoflurane-induced mitochondrial depolarization was reduced in DM-iPSC-CMs compared with N-iPSC-CMs in their respective glucose conditions (C ). *P < 0.05 versus baseline; †P < 0.05 versus isoflurane treatment. 5-HD = 5-hydroxydecanoate; DM-iPSC-CMs = type 2 diabetic induced pluripotent stem cell-derived cardiomyocytes; N-iPSC-CMs = nondiabetic induced pluripotent stem cell-derived cardiomyocytes; TMRE = tetramethylrhodamine ethyl ester.