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. 2014 Jul 16;5:264. doi: 10.3389/fphys.2014.00264

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Copyright © 2014 Xie, Kauffman and Akar.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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CsA delays OS-induced mitochondrial and contractile dysfunction. (A) Model of acute OS. Continuous 200 μM H₂O₂ perfusion for 30 min leads to ΔΨ_m depolarization and initiation of VF. (B) Sequences of isopotential contour maps depicting the spatio-temporal distribution of ΔΨ_m in representative control (untreated) and CsA-treated hearts following challenge with H₂O₂ (200 μM) for 30 min. (C) Average ΔΨ_m response to acute OS in all control and CsA treated hearts.