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目的:观察交泰丸(JTW)浸膏粉溶液对豚鼠心室肌细胞膜电位的影响。方法:使用Langendorff灌流系统离体灌流心脏,急性酶解法分离获得单个心室肌细胞。全细胞膜片钳技术电流钳模式记录膜电位。结果:0.2%交泰丸浸膏粉使静息电位(RP)从用药前(-85.91±6.24)mV下移至(-99.64±6.62)mV(n=8,P<0.01),0相除极幅度(APA)从用药前(128.91±1.39)mV上升至(139.74±2.67)mV(n=8,P<0.01),复极至50%时动作电位时程(APD50)从用药前(505.49±30.97)ms缩短至(329.94±44.32)ms(n=8,P<0.01),复极至90%时动作电位时程(APD90)从用药前(524.96±30.99)ms缩短至(358.41±43.51)ms(n=8,P<0.01),复极至50%到复极至90%的动作电位时程(APD50-90)从用药前(16.56±1.48)ms延长至(27.31±3.62)ms(n=8,P<0.01),动作电位3相复极速率(V3)从用药前(-2.93±0.33)V/s减慢至(-1.95±0.28)V/s(n=8,P<0.01)。0.1%,0.4%交泰丸浸膏粉对各项指标的影响与0.2%交泰丸浸膏粉的变化趋势一致。结论:交泰丸浸膏粉引起心室肌细胞RP下移,APA上升,APD50缩短,APD90缩短,APD50-90延长和V3减慢。以上影响可能是其在临床上具有抗心律失常作用的电生理学机制。
Objective: To observe the effect of Jiaotai Pills (JTW) extract powder solution on the membrane potential of guinea pig ventricular myocytes. Methods: Perfused heart was isolated by Langendorff perfusion system and single ventricular myocytes were isolated by acute enzymatic method. Whole cell patch clamp technique Current clamp mode to record membrane potential. Results: 0.2% JiaoTai Pills extract powder could reduce resting potential (RP) from (-85.91 ± 6.24) mV to (-99.64 ± 6.62) mV (n = 8, P <0.01) The amplitude of APA increased from (128.91 ± 1.39) mV to (139.74 ± 2.67) mV (n = 8, P <0.01) before treatment and from 50.49 (APD90) was shortened from (524.96 ± 30.99) ms to (358.41 ± 43.51) ms after repolarization to 90% with the mean time (± 30.97) ms to (329.94 ± 44.32) ms (APD50-90) increased from (16.56 ± 1.48) ms to (27.31 ± 3.62) ms before repolarization to 50% repolarization to 90% repolarization (P <0.01) (n = 8, P <0.01). The bipolar rate (V3) of action potential decreased from -2.93 ± 0.33 V / s to -1.95 ± 0.28 V / s before treatment (n = 8, P <0.01). 0.1%, 0.4% Zhaotai Pills extract powder on the impact of indicators and 0.2% Zhaotai Pills extract powder the same trend. CONCLUSION: Jiaotai Pills extract powder causes RP of ventricular myocytes down, APA rise, APD50 shortening, APD90 shortening, APD50-90 prolongation and V3 slowing down. The above effect may be its electrophysiological mechanism of clinical anti-arrhythmic effect.