Liu B, Hu D Y, Gao Y, Liu X L
Heart Center, Beijing Red Cross Chaoyang Hospital affiliated to Capital University of Medical Sciences, China.
Zhongguo Yao Li Xue Bao. 1997 Jul;18(4):333-6.
To study the direct effect of enalapril on cellular electrophysiology of myocardium.
Conventional microelectrodes technique was used to record the action potentials (AP) of guinea pig papillary muscles.
Enalapril caused an increase of the AP amplitude (APA) and the resting potential (RP) in a concentration-dependent manner without any significant change of AP duration, Vmax and overshoot of AP. Superfusion of ouabain 0.5 mumol.L-1 reduced APA and RP, induced stable delayed after-depolarizations (DAD) at different basic cycle lengths (BCL) in a frequency-dependent manner. At BCL 200 ms, the amplitude of DAD was large enough to induce nonsustained triggered activity (TA). In additional presence of enalapril 10 mumol.L-1, the DAD amplitude at 500, 400, 300, and 200 ms were decreased from 5.3 +/- 2.3, 5.9 +/- 2.8, 7.4 +/- 2.1, and 8.9 +/- 1.3 to 2.6 +/- 0.7, 3.1 +/- 1.0, 3.7 +/- 1.5, and 5.3 +/- 1.1 (mV) respectively, all P < 0.01. The compensation intervals were increased in a similar frequency-dependent manner. The number of TA induced at BCL 200 ms was decreased from 3.6 +/- 0.7 to 0.8 +/- 0.2 (P < 0.05).
Enalapril directly inhibits DAD and TA induced by ouabain through increasing RP and APA, which may contribute to its anti-arrhythmic effect.
研究依那普利对心肌细胞电生理的直接作用。
采用常规微电极技术记录豚鼠乳头肌的动作电位(AP)。
依那普利可使动作电位幅度(APA)和静息电位(RP)呈浓度依赖性增加,而动作电位时程、最大上升速率和动作电位超射无明显变化。用0.5 μmol·L-1哇巴因灌流可降低APA和RP,并以频率依赖性方式在不同基础周期长度(BCL)诱导出稳定的延迟后去极化(DAD)。在BCL为200 ms时,DAD幅度大到足以诱发非持续性触发活动(TA)。在加入10 μmol·L-1依那普利后,500、400、300和200 ms时的DAD幅度分别从5.3±2.3、5.9±2.8、7.4±2.1和8.9±1.3降至2.6±0.7、3.1±1.0、3.7±1.5和5.3±1.1(mV),均P<0.01。代偿间期也以类似的频率依赖性方式增加。在BCL为200 ms时诱发的TA次数从3.6±0.7降至0.8±0.2(P<0.05)。
依那普利通过增加RP和APA直接抑制哇巴因诱导的DAD和TA,这可能是其抗心律失常作用的机制之一。