Abstract:

Objective To investigate the influence of citalopram on the fast response action potential, slow response action potential, in vitro electrocardiogram (ECG) and in vivo ECG of cardiac myocytes, and explore its mechanism of  adverse cardiac effects. Methods Conventional microelectrode technique was employed to record the fast and slow response action potentials of the isolated papillary muscles of guinea pigs. In vivo and in vitro ECG were recorded from anesthetized animals and Langendorff-perfused hearts, respectively. Results Citalopram could prolong the RR interval and QRS duration of in vivo ECG. The premature ventricular contraction and atrial ventricular block were induced by 12.5×10^-6 mol/L citalopram. The maximum ascending velocity of 0 phase (Vmax), action potential amplitude (APA) and action potential duration (APD50 and APD90) were dosedependently decreased by citalopram in the fast and slow response action potentials of guinea pigs, respectively. Conclusion Citalopram can inhibit sodium and calcium channels effectively, which may be the ionic mechanism that citalopram induces arrhythmia in the clinical practice.

Key words: citalopram, fast response action potential, slow response action potential, Langendoff perfusion,
in vitro electrocardiogram, guinea pig