Wang Yuhua, Fu Lijia, Wang Lihong, Xu Lianqin, Yang Baofeng
Daqing Oilfield General Hospital, Daqing 163001, China.
Zhonghua Xin Xue Guan Bing Za Zhi. 2014 Aug;42(8):675-9.
To explore the antiarrhythmic mechanism of ampelopsin through electrophysiological study in rats.
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.
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.
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.
通过大鼠电生理研究探讨蛇葡萄素的抗心律失常机制。
体内实验组如下：对照组、低剂量组、中剂量组和高剂量组。通过注射乌头碱诱导大鼠心律失常，然后研究蛇葡萄素的抗心律失常作用。此后从大鼠分离心肌细胞。采用全细胞膜片钳技术记录心肌细胞动作电位时程（APD）、钠电流（INa）、钙电流（ICa）、瞬时外向钾电流（Ito）和内向整流钾电流（IK1）。
体内实验表明，低、中、高剂量蛇葡萄素组乌头碱诱导的实验性心律失常发生率显著低于对照组（每组n = 5，均P < 0.05）。体外全细胞膜片钳实验表明，低、中、高剂量组的动作电位时程显著短于对照组，且低、中、高剂量蛇葡萄素组的动作电位幅度也显著低于对照组，对照组、低、中、高剂量组分别为（101.8 ± 5.1）、（113.2 ± 9.0）、（120.1 ± 7.4）、（134.1 ± 6.9）mV（每组n = 9，均P < 0.05）。进一步研究表明，低、中、高剂量蛇葡萄素使心肌细胞钠电流从（-36.75 ± 3.60）降至（-31.03 ± 2.61）、（-26.63 ± 3.72）和（-17.55 ± 4.43）pA/pF（每组n = 9，均P < 0.05），但峰值电位的激活电压不受蛇葡萄素影响。此外，高剂量蛇葡萄素组的内向整流钾电流也高于对照组（P < 0.05）。四组之间钙电流和瞬时外向钾电流相似。
蛇葡萄素在该大鼠模型中发挥抗心律失常作用，其潜在的电生理机制部分与抑制INa、增强IK1及延长APD有关。
