[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.


CONCLUSIONS
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.
Daqing Oilfield General Hospital, Daqing 163001, China.
Yuhua
Y
Wang
Daqing Oilfield General Hospital, Daqing 163001, China.
Lijia
L
Fu
Daqing Oilfield General Hospital, Daqing 163001, China.
Lihong
L
Wang
Daqing Oilfield General Hospital, Daqing 163001, China.
Lianqin
L
Xu
Daqing Oilfield General Hospital, Daqing 163001, China.
Baofeng
B
Yang
D000200:Action Potentials; D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology*; D001145:Arrhythmias, Cardiac; D005419:Flavonoids / Q000494:pharmacology*; D032383:Myocytes, Cardiac; D018408:Patch-Clamp Techniques; D015221:Potassium Channels; D051381:Rats
D000889:Anti-Arrhythmia Agents; D005419:Flavonoids; D015221:Potassium Channels; C106407:ampelopsin