Ventricular arrhythmic and electrophysiological properties were examined during normokalaemia (5.2 mM [K+]), hypokalaemia (3 mM [K+]) or hypokalaemia in the presence of 0.1 or 2 mM heptanol in Langendorff‑perfused mouse hearts. Left ventricular epicardial or endocardial monophasic action potential recordings were obtained during right ventricular pacing. Hypokalaemia induced ventricular premature beats (VPBs) in 5 of 7 and ventricular tachycardia (VT) in 6 of 7 hearts (P<0.01), prolonged action potential durations (APD90) from 36.2±1.7 to 55.7±2.0 msec (P<0.01) and shortened ventricular effective refractory periods (VERPs) from 44.5±4.0 to 28.9±3.8 msec (P<0.01) without altering conduction velocities (CVs) (0.17±0.01 m/sec, P>0.05), reducing excitation wavelengths (λ, CV x VERP) from 7.9±1.1 to 5.1±0.3 mm (P<0.05) while increasing critical intervals (CI, APD90‑VERP) from ‑8.3±4.3 to 26.9±2.0 msec (P>0.001). Heptanol (0.1 mM) prevented VT, restored effective refractory period (ERP) to 45.2±2.9 msec without altering CV or APD, returning λ to control values (P>0.05) and CI to 8.4±3.8 msec (P<0.05). Heptanol (2 mM) prevented VPBs and VT, increased ERP to 67.7±7.6 msec (P<0.05), and reduced CV to 0.11±0.1 m/sec (P<0.001) without altering APD (P>0.05), returning λ and CI to control values (P>0.05). Anti‑arrhythmic effects of heptanol during hypokalaemia were explicable by ERP changes, scaling λ and CI.

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