Objective: To investigate the mechanism of α-allocryptopine-induced inhibition of the transient outward potassium current ( I<sub>to</sub>) in rabbit left-ventricular myocytes. Methods: We used the whole-cell patch-clamp technique to record the I<sub>to</sub> in the myocytes, which were isolated from the rabbit left ventricle by a Langendorff-perfusion device. Results: Allocryptopine decreased the amplitude and the density of the I<sub>to</sub> in a concentration-dependent (range from 1 to 100 µ M with an IC<sub>50</sub> value of 37 ± 8 µ M) and frequency- or use-independent manner. At a test potential of +50 mV, the peak current density of I<sub>to</sub> was decreased from 21.56 ± 3.24 to 13.37 ± 2.86 pA/pF by 30 µ M allocryptopine. The fast time constant of I<sub>to</sub> inactivation was reduced from 9.8 ± 1.8 to 5.7 ± 0.7 ms and the slow time constant of I<sub>to</sub> was reduced from 50.8 ± 9.0 to 32.2 ± 12.7 ms by 30 µ M allocryptopine. The inactivated curve slope was changed from –19.2 ± 7.1 to –7.5 ± 0.6 mV, while the half-activated voltage and activated curve slope and half-inactivated voltage values were not affected by allocryptopine. Transmural heterogeneity of the I<sub>to</sub> was decreased in the presence of allocryptopine. At a test potential of +50 mV, the densities of I<sub>to</sub> were reduced by 28.6% (epimyocardium), 50.3% (midmyocardium) and 20.1% (endocardium) after expoure to 30 µ M allocryptopine.Transmural dispersion of the I<sub>to</sub> was reduced from 11.2 ± 1.2 to 4.7 ± 0.6 pA/pF by 30 µ M allocryptopine. Conclusion: Allocryptopine produced a blocking effect on the I<sub>to</sub> in cardiac myocytes, which may be an important mechanism in its antiarrhythmic effect.