Fig. 1 | Scientific Reports

Fig. 1

From: Chronic administration of ivabradine improves cardiac Ca handling and function in a rat model of Duchenne muscular dystrophy

Fig. 1

Ca handling properties of ventricular cardiomyocytes derived from from wt, control DMDmdx, and IVA-treated DMDmdx rats. (a) Original trace example of an intracellular Ca measurement showing the event sequence. Ca transients were first elicited by electrical stimulation at 0.1 Hz frequency. Thereafter, a Ca transient was induced by caffeine application. After caffeine washout, electrical stimulation was started again, and isoprenaline was applied. (b) Representative single electrically-evoked Ca transients of a wt, control DMDmdx, and IVA-treated DMDmdx myocyte at an enlarged time scale in standard extracellular solution. The decay of the electrically-induced Ca signal following the rapid initial rise was fitted with a single exponential function to derive τ-values. (c) left: Comparison of mean Ca peak fluorescence relative to baseline (F/F0) between wt, DMDmdx and IVA-treated DMDmdx myocytes. Each data point represents a single cell, and values are expressed as median, interquartile range, and minimum/maximum. [107 cells for wt (5 animals); 97 cells for DMDmdx (6 animals) and 177 cells for IVA-treated DMDmdx (6 animals) myocytes]. (c) middle: Comparison of the Ca transient decay kinetics in wt, DMDmdx and IVA-treated DMDmdx myocytes. (c) right: Comparison of mean Ca peak fluorescence, elicited by caffeine application, relative to baseline (F/F0) between wt, DMDmdx and IVA-treated DMDmdx myocytes [82 cells for wt (5 animals); 81 cells for DMDmdx (5 animals) and 167 cells for IVA-treated DMDmdx (6 animals) myocytes]. *p < 0.05, **p < 0.01, ***p < 0,001, ****p < 0,0001; ns, not significant.

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