Does heptanol prevent ventricular arrhythmias and alter electrophysiological properties in hypokalaemic Langendorff-perfused mouse hearts?
Heptanol exerts anti-arrhythmic effects during hypokalaemia in mouse hearts by restoring effective refractory period and scaling excitation wavelengths and critical intervals.
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 (P0.05), reducing excitation wavelengths (λ, CV x VERP) from 7.9±1.1 to 5.1±0.3 mm (P0.001). 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 (P0.05), 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.
Tse et al. (Thu,) studied this question.
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