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<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 (lambda, CV x VERP) from 7.9+/-1.1 to 5.1+/-0.3 mm (P<0.05) while increasing critical intervals (CI, APD(90)-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). Anti-arrhythmic effects of heptanol during hypokalaemia were explicable by ERP changes, scaling. and CI.