Effects of therapeutic concentrations of procainamide on transmembrane action potentials of normal and infarct zone Purkinje fibers and ventricular muscle cells.
Effects of therapeutic concentrations of procainamide on transmembrane action potentials of normal and infarct zone Purkinje fibers and ventricular muscle cells.
复制标题
普鲁卡因酰胺治疗浓度对正常和梗死区浦肯野纤维和心室肌细胞跨膜动作电位的影响。
DOI：
10.1097/00005344-198906000-00006
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发表时间：
1989
影响因子：
3
通讯作者：
Miura,DS
中科院分区：
文献类型：
--
作者：
Dangman,KH;Miura,DS
普鲁卡因胺是一类抗心律失常药物。大多数关于普鲁卡因胺细胞电生理效应的研究都是在远高于治疗范围的浓度下进行的。我们研究了药物治疗浓度（10mg /L）对犬离体心脏组织跨膜动作电位的影响。在最大舒张电位（MDPs）为- 93±1 mV的正常假肌腱浦肯野纤维中，普鲁卡因胺使动作电位持续时间（APD）减少- 20mV，并略微延长APD 100%。最大dV/dt值没有降低。在MDPs为- 92±1 mV的正常心内膜下浦肯野纤维中，普鲁卡因胺10 mg/L显著降低了dV/dt max，但对APD - 20mV没有影响。在左室心内膜正常肌细胞中，普鲁卡因胺10 mg/L仅使APD升高100%。普鲁卡因胺对部分去极化浦肯野纤维的影响不同。在正常的心内膜下浦肯野纤维制剂中，与7.5 mM KCl-Tyrode溶液混合后，平均最大舒张电位为- 73±2 mV，普鲁卡因胺10 mg/L轻微降低动作电位振幅（APA），增加APD - 60mV。相反，在MDPs为−75±4 mV的24小时梗死区浦肯野纤维中，普鲁卡因胺10 mg/L可使APA和dV/dt max降低100%，延长APD。在一项梗死制剂实验中，普鲁卡因胺在短于400 ms的周期长度下也诱导2:1阻滞。这些实验结果表明，治疗浓度的普鲁卡因胺对梗死心脏部分去极化区的动作电位有选择性影响。这一作用可以解释为什么普鲁卡因胺可以消除一些再入性心律失常。
Procainamide is a class I antiarrhythmic drug. Most studies of the cellular electrophysiologic effects of procainamide have been done with concentrations well above the therapeutic range. We studied the effects of therapeutic concentrations (10 mg/L) of the drug on transmembrane action potentials recorded from isolated canine cardiac tissues. In normal false tendon Purkinje fibers with maximal diastolic potentials (MDPs) of− 93±1 mV, procainamide decreased action potential duration (APD)− 20mV and slightly prolonged APD 100%. The dV/dt max was not decreased. In normal subendocardial Purkinje fibers with MDPs of− 92±1 mV, procainamide 10 mg/L significantly decreased dV/dt max but did not affect APD− 20mV. In normal muscle cells from left ventricular endocardium, procainamide 10 mg/L increased only APD 100%. The effects of procainamide on partially depolarized Purkinje fibers varied. In normal subendocardial Purkinje fiber preparations superfused with 7.5 mM KCl-Tyrode's solution, the mean maximal diastolic potentials were− 73±2 mV, and procainamide 10 mg/L slightly decreased action potential amplitude (APA) and increased APD− 60mV. In contrast, in 24-h infarct zone Purkinje fibers with MDPs of− 75±4 mV, procainamide 10 mg/L decreased APA and dV/dt max and prolonged APD 100%. In one experiment on an infarct preparation, procainamide also induced 2: 1 block at cycle lengths shorter than 400 ms. The results of these experiments indicate that therapeutic concentrations of procainamide exert selective effects on action potentials in partially depolarized zones of infarcted hearts. This action may explain why procainamide can abolish some reentrant arrhythmias.