Introduction: Recent studies have shown acute cardioprotective effects of cyclosporine. The aim of the present study was to determine the protective role of cyclosporine on the model simulated the rotational nodal arrhythmia (AVNRT) by using extracellular field potential recordings of isolated atrioventricular-node (AV-node) of rabbit. Methods: This study was performed on isolated double-perfused AV-node of male New Zealand rabbits (1.5-2.5 kg) in one group (n=7). Basic and rate-dependent stimulation protocols (recovery, facilitation, fatigue) and arrhythmia threshold (index of refractoriness) and % Gap incidence were measured for assessment of electrophysiological properties of the AVnode. All stimulation protocols were repeated in control step and in the presence of various cumulative concentrations of cyclosporine (0.5 10 μm). Results: Cyclosporine prolonged the effective refractory period from 114.3±7.9 to 142±7.3 msec at the concentration of 10 μm. It also prolonged the functional refractory period from 162±3.3 to 178.6±5 msec and increased the time of Wenckebach at the concentrations of 5 10 μM. Various concentrations of cyclosporine increased fatigue and reached a significant level at 10 μm. Gap incidence was 82%, 16.6% and 20% in the control and treatments with 0.5 and 10 μm of cyclosporine, respectively. Conclusion: Block of MPTP by cyclosporine caused inhibition of basic and rate-dependent properties of atrioventricular node. Cyclosporine, by raising the threshold of arrhythmia, could be possibly considered as an antiAVNRT drug.