Moller R A, Covino B G
Department of Anesthesia, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115.
Anesth Analg. 1988 Feb;67(2):107-14.
The cardiac electrophysiologic effects of bupivacaine (B) and lidocaine (L) were evaluated in an isolated rabbit Purkinje fiber-ventricular muscle model to determine the effects of a) progressively increasing and b) decreasing concentrations of B and L on transmembrane action potentials. Bupivacaine (3 and 5 micrograms/ml) significantly decreased diastolic resting potential, maximum rate of depolarization, and action potential amplitude. Lidocaine (10-20 micrograms/ml) also decreased maximum rate of depolarization and action potential amplitude, but the decreases were significantly different from those produced by B. High concentrations of B (30 micrograms/ml) and L (100 micrograms/ml) resulted in delayed conduction between Purkinje fibers and ventricular muscle cells and, ultimately, conduction blockade. The duration of conduction blockade was significantly longer with B than with L. The results of this study indicate that B produces electrophysiologic changes in cardiac tissue that may produce ventricular arrhythmias of a reentrant type.
在离体兔浦肯野纤维 - 心室肌模型中评估了布比卡因（B）和利多卡因（L）的心脏电生理效应，以确定：a）B和L浓度逐渐增加以及b）浓度逐渐降低时对跨膜动作电位的影响。布比卡因（3和5微克/毫升）显著降低舒张期静息电位、最大去极化速率和动作电位幅度。利多卡因（10 - 20微克/毫升）也降低最大去极化速率和动作电位幅度，但这些降低与B所产生的降低有显著差异。高浓度的B（30微克/毫升）和L（100微克/毫升）导致浦肯野纤维与心室肌细胞之间的传导延迟，并最终导致传导阻滞。B导致的传导阻滞持续时间显著长于L。本研究结果表明，B在心脏组织中产生的电生理变化可能导致折返型室性心律失常。
