Fig. 1

Traces showing monophasic action potentials (MAPs) recorded from the epicardium of a representative heart during regular 8 Hz pacing at different time points (A–D). MAPs recorded 120 s before the introduction of 2 mM heptanol (A). MAPs recorded immediately after introduction of 2 mM heptanol (B). MAPs recorded 120 s after introduction of 2 mM heptanol (C). MAPs recorded 900 s after withdrawal of 2 mM heptanol (D). Activation latency (trace a) and APD₉₀ (trace b) plotted as a function of time (E). The time at which 2 mM heptanol was introduced is indicated by an arrow. Before introduction of 2 mM heptanol, activation latency was 13.1 ms. 120 s after introduction of 2 mM heptanol, this was increased to 29.5 ms. In contrast, APD₉₀ was 44.9 ms before and 46.1 ms after introduction of heptanol. Epicardial activation latencies (white bars), obtained before (n = 8) and 120 s after introduction of 0.1 (n = 8), 0.5 (n = 7), 1 (n = 9), and 2 mM (n = 7) heptanol during regular 8 Hz pacing (F). Endocardial activation latencies (black bars) before (n = 9) and 120 s after introduction of 0.1 (n = 5), 0.5 (n = 10), 1 (n = 5), and 2 mM (n = 5) heptanol, obtained during regular 8 Hz pacing. Asterisks indicate the epicardial activation latencies that were significantly increased by heptanol (ANOVA, P < 0.05). Daggers indicate the endocardial activation latencies that were significantly increased by heptanol (ANOVA, P < 0.05). Hashes indicate that endocardial activation latencies were significantly larger than the corresponding epicardial activation latencies at a given heptanol concentration (ANOVA, P < 0.05)