目的　观察罗哌卡因和布比卡因对豚鼠心室乳头肌纤维动作电位的影响。方法　用含罗哌卡因和布比卡因 1、3、5 μg·ml-1的台氏液分别灌流豚鼠心室乳头肌 ,记录用药前、用药后及药物洗脱后动作电位各参数的改变 :动作电位幅值 (APA)、动作电位 0时相最大上升速度 (Vmax)、动作电位5 0 %复极时程 (APD50 )及动作电位 90 %复极时程 (APD90 )。结果　各浓度局麻药均抑制Vmax,罗哌卡因 5 μg·ml-1抑制程度 (下降 2 7 4% )与布比卡因 3μg·ml-1(下降 2 8 4% )相似 ,与等浓度布比卡因 (下降42 6 % )相比呈显著性降低 (P <0 0 5 )。罗哌卡因和布比卡因 5 μg·ml-1均明显抑制APA ,分别下降2 5 6 %和 5 98%。罗哌卡因 5 μg·ml-1使APD50 和APD90 分别缩短 1 86 %和 1 6 % ,明显小于等浓度布比卡因 (7 2 3%和 4 96 % )。结论　罗哌卡因对心室乳头肌动作电位的影响较布比卡因小 ,其心肌毒性机制主要与抑制钠离子通道而降低心肌的兴奋性与传导有关 Objective To observe the effects of ropivacaine and bupivacaine on the action potentials of guinea pig papillary muscles. Methods Guinea pig ventricular papillary muscles were perfused with 1, 3, 5 μg · ml-1 Tyrode ’s solution containing ropivacaine and bupivacaine. The changes of action potentials before treatment, after treatment and after drug elution were recorded. Action potential amplitude (APA), action potential zero maximum phase velocity (Vmax), action potential 50% repolarization duration (APD50) and action potential 90% repolarization duration (APD90). Results The local anesthetics were inhibited by Vmax at each concentration. The inhibitory effect of ropivacaine 5 μg · ml-1 (decreased by 27.4%) was similar to that of bupivacaine 3 μg · ml-1 (decreased by 28.4%), Bupivacaine (42 6% decrease) was significantly lower (P <0 05). Ropivacaine and bupivacaine 5 μg · ml-1 significantly inhibited APA, decreased by 25.6% and 588%, respectively. Ropivacaine 5 μg · ml-1 shortened APD50 and APD90 by 86% and 16%, respectively, which was significantly lower than that of bupivacaine (72.3% and 496%). Conclusion The effect of ropivacaine on the action potential of ventricular papillary muscle is less than that of bupivacaine. The mechanism of myocardial toxicity is mainly related to the inhibition of sodium channel and the decrease of cardiac excitability and conduction