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Fig. 2 | BMC Pharmacology and Toxicology

Fig. 2

From: Histone deacetylase inhibition by Entinostat for the prevention of electrical and structural remodeling in heart failure

Fig. 2

Effects of Entinostat on key electrophysiological parameters in control and rapidly paced rabbit hearts. a Cycle lengths-dependent effects on monophasic action potential (MAP90) in sham-operated hearts (light blue) and failing hearts (dark blue) treated with 0.5 ml/d DMSO and in sham-operated hearts (orange) and failing hearts (red) treated with 0.01 g/d Entinostat (One-way ANOVA p(CL400–900) = 0.030, 0.034, 0.035, 0.041, 0.030, 0.027 (*)). b Cycle lengths-dependent effects on QT-interval in sham-operated rabbit hearts as compared to failing hearts. c A representative Western blot analysis demonstrating an increase of histone H3 acetylation in Entinostat (E) treated hearts compared to vehicle (C). d Proportion of rabbit hearts showing early afterdepolarizations (EADs) while the extracellular K+ concentration was lowered to 1.5 mM. e Number of non-sustained ventricular tachyarrhythmias (nsVT) per rabbit heart in the presence of low extracellular K+ concentration. On average, 7 episodes of non-sustained polymorphic tachycardias were observed in failing hearts treated with DMSO compared to 4 non-sustained ventricular tachyarrhythmia episodes in the non-stimulated control group and 2.5 non-sustained ventricular tachyarrhythmia episodes in failing hearts treated with Entinostat

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