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. 2014 Jun 9;18(8):1540–1548. doi: 10.1111/jcmm.12329

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© 2014 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.

This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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Fig. 6 — Effects of KN93 (0.1 μM) and ranolazine (0.1 μM) on ouabain-induced ventricular tachycardia (VT). (A) Upper and middle panels show the examples of ouabain (1 μM)-induced ventricular tachycardia (VT) in right ventricular apex (RVA) and right ventricular out-flow tract (RVOT). The lower panels show that ouabain (1 μM) induced higher incidences of total or sustained VT with a faster beating rates in the RVOT (n = 18) than in the RVA (n = 18). (B) Upper and middle panels show the examples that KN93 (0.1 μM) or ranolazine (0.1 μM) can terminate ouabain (1 μM)-induced sustained VT in RVOT preparations. Lower panels show that the superfusing time was longer for KN-93 (but not for ranolazine) to terminate ouabain-induced ventricular arrhythmias in the RVOT (n = 5) than in the RVA (n = 4). Arrows (↑) indicate electrical stimuli. *P < 0.05, ***P < 0.005 versus RVOT.