@article{oai:hama-med.repo.nii.ac.jp:00001850,
 author = {Matsunaga, Masaki and Saotome, Masao and Satoh, Hiroshi and Katoh, Hideki and Terada, Hajime and Hayashi, Hideharu},
 issue = {9},
 journal = {Circulation Journal},
 month = {Aug},
 note = {Background Mitochondrial Ca2+ overload is a major cause of irreversible cell injury during various metabolic stresses. The protective effects of various agents that affect mitochondrial function against Ca2+ overload during Ca2+ paradox were investigated in rat ventricular myocytes. Methods and Results On Ca2+ repletion following Ca2+ depletion, [Ca2+]i increased rapidly, and 90 of 210 cells (43%) died. In viable cells, the increase in [Ca2+]i was lower than in dead cells. KB-R7943 prevented the increase in [Ca2+]i, and completely inhibited cell death. Ruthenium red (RuR), diazoxide (Dz) or cyclosporin A (CsA) prevented cell death (15%, 26% and 17%, respectively; p<0.05), and the protective effect of Dz was abolished by 5- hydroxydecanoate. These agents did not reduce the increase in [Ca2+]i in viable cells or the rate of initial increase in [Ca2+]i in all cells. RuR and Dz decreased [Ca2+]m in skinned myocytes, but CsA did not affect [Ca2+]m. Dz reduced NADH fluorescence, whereas RuR and CsA did not. Conclusions The protective effects of RuR and Dz could be ascribed to altered Ca2+ regulation by decreasing [Ca2+]m, and Dz could have an additional effect on oxidative phosphorylation. The protective effect of CsA could be directly associated with the mitochondrial permeability transition pore.},
 pages = {1132--1140},
 title = {Different Actions of Cardioprotective Agents on Mitochondrial Ca2+ Regulation in a Ca2+ Paradox-Induced Ca2+ Overload},
 volume = {69},
 year = {2005}
}