Ventricular anti-arrhythmic effects of heptanol in hypokalaemic, langendorff-perfused mouse hearts

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.3C;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, 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 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 and CI to control values (P.0.05). Antiarrhythmic effects of heptanol during hypokalaemia were explicable by ERP changes, scaling and CI.