[Electrophysiological study on the antiarrhythmic mechanism of ampelopsin in rats].

Objective: To explore the antiarrhythmic mechanism of ampelopsin through electrophysiological study in rats.

Methods: The in vivo experimental groups were as follows:control group, low-dose, middle-dose and high-dose group. Arrhythmia in rats was induced by aconitine injection, and then the antiarrhythmic effects of ampelopsin were studied. Cardiomyocytes were isolated from rats therafter. The whole-cell patch-clamp technique was used to record action potential duration (APD), sodium currents (INa), calcium current (ICa), transient outward potassium currents (Ito) and inward rectifier potassium currents (IK1) in cardiomyocytes.

Results: In vivo experiments showed that the incidence of aconitine-induced experimental arrhythmias in low, middle and high-dose ampelopsin group was significantly lower than that in control group (n = 5 each group, all P < 0.05). In vitro whole-cell patch clamp experiments showed that action potential duration in low, middle and high-dose groups was significantly shorter than that in control group, and amplitude of action potential was also significantly lower in low, middle and high-dose ampelopsin groups than in control group (134.1 ± 6.9), (120.1 ± 7.4), (113.2 ± 9.0), and (101.8 ± 5.1) mV for control, low, middle and high-dose group (n = 9 each group, all P < 0.05).Further research revealed that sodium currents in cardiomyocytes were decreased by low, middle and high-dose ampelopsin from (-36.75 ± 3.60) to (-31.03 ± 2.61), (-26.63 ± 3.72), and (-17.55 ± 4.43) pA/pF (n = 9 each group, all P < 0.05), but the activation voltage for peak potential was not affected by ampelopsin. Moreover, the inward rectifier potassium current was also higher in high-dose ampelopsin group than in control group (P < 0.05). Calcium current and transient outward potassium current were similar among four groups.

Conclusion: Ampelopsin exerts anti-arrhythmic effects in this rat model, and the underlying electrophysiological mechanism is partly associated with the inhibition of INa and enhancement of IK1, and prolongation of APD.