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目的:观察心悸宁(XJN)浸膏粉溶液对豚鼠单个心室肌细胞动作电位的影响。方法:使用Langendorff灌流系统离体灌流心脏,急性酶解法分离获得心肌细胞。全细胞膜片钳技术电流钳模式记录动作电位。结果:0.25%XJN使静息电位(RP)从用药前的(-70.62±7.02)mV上升至(-66.99±8.29)mV(P<0.05),动作电位0相除极幅度(APA)从用药前(114.24±12.30)mV减小至(107.40±13.56)mV(P<0.05);动作电位0相最大除极速率(Vmax)从用药前(117.49±32.89)V/s减慢至(84.99±25.61)V/s(P<0.01);复极至50%时动作电位时程(APD50)从用药前(282.94±41.76)ms缩短至(232.10±26.93)ms(P<0.05);动作电位3相复极速率(V3)从用药前(-3.08±0.69)V/s减慢至(-2.06±1.07)V/s(P<0.05)。0.5%XJN使RP,APA,Vmax和V3的变化与0.25%XJN的变化趋势一致,但APD50和复极至90%时动作电位时程(APD90)延长更显著。结论:体外应用XJN引起心室肌细胞RP上升,APA减小,Vmax和V3减慢。0.25%浓度组引起APD50缩短,0.5%浓度组引起APD50和APD90延长。以上影响可能是XJN在临床上具有广谱抗心律失常作用的电生理学机制。
Objective: To observe the effect of XJN extract powder on action potentials of guinea pig single ventricular myocytes. METHODS: The Langendorff perfusion system was used to perfuse the heart, and the myocardial cells were isolated by acute enzymatic hydrolysis. Whole cell patch clamp technique current clamp mode recording action potentials. RESULTS: 0.25% XJN increased the resting potential (RP) from (-70.62±7.02) mV before treatment to (-66.99±8.29) mV (P<0.05). Action potential 0 phase depolarization amplitude (APA) from medication The first (114.24±12.30) mV was reduced to (107.40±13.56) mV (P<0.05); the maximum depolarization rate (Vmax) of the action potential 0 phase was slowed from (117.49±32.89) V/s before (84.99±) 25.61)V/s (P<0.01); action potential duration (APD50) was shortened from (282.94±41.76) ms to (232.10±26.93) ms (P<0.05) after repolarization to 50%; action potential 3 The rate of repolarization (V3) slowed from (-3.08±0.69) V/s before treatment to (-2.06±1.07) V/s (P<0.05). The changes of RP, APA, Vmax and V3 in 0.5% XJN were consistent with the trend of 0.25% XJN, but the extension of APD90 and APD90 was more significant at APD50 and repolarization to 90%. CONCLUSIONS: In vitro application of XJN increased RP in ventricular myocytes, decreased APA, and decreased Vmax and V3. In the 0.25% group, the APD50 was shortened, and in the 0.5% group, APD50 and APD90 were prolonged. The above effects may be an electrophysiological mechanism in which XJN has a broad-spectrum antiarrhythmic effect in clinic.