The aim of this study was to explore the mechanism of racemic higenamine in the treatment of sick sinus syndrome (SSS). A total of 40 New Zealand rabbits were randomly divided into normal sinus node and damaged sinus node (SND) groups, and each group was randomly divided into treatment and control groups (n=10). The SND model was established by formaldehyde wet dressing of the sinus node area. The treatment groups were administered an intravenous infusion of 0.04 mg/kg racemic higenamine via the marginal ear vein within 5 min. The electrophysiological indicators of sinoatrial function, including the sinus node recovery time (SNRT), corrected sinus node recovery time (CSNRT), total sinoatrial conduction time (TSACT) and sinus cycle length (SCL), were determined before and 20 min after medication and the changes in these indicators were evaluated. The two control groups were administered 10 ml physiological saline. Following the administration of racemic higenamine, the SNRT, CSNRT, TSACT and SCL in the normal sinus node and SND groups were significantly shortened compared with those in the control groups (P<0.01). The electrophysiological influence of racemic higenamine on sinoatrial function in the SND group was significantly greater than that in the normal sinus node group (P<0.01), and its effect in the treatment of arrhythmia caused by a damaged sinus node was statistically significant (P<0.05). The main electrophysiological mechanism of racemic higenamine in the treatment of SSS was the enhancement of sinus node self-discipline and improvement of sinoatrial and atrioventricular conduction function.