Ware D L, Atkinson J B, Brooks M J, Echt D S
Vanderbilt University, Nashville, Tennessee.
Pacing Clin Electrophysiol. 1993 Feb;16(2):337-46. doi: 10.1111/j.1540-8159.1993.tb01585.x.
Prior studies in dogs with normal hearts have demonstrated that lidocaine increases but procainamide does not change the energy required for successful defibrillation. Because many postinfarct patients receiving implantable cardioverter defibrillator devices require adjunctive antiarrhythmic therapy, we have studied the effects of lidocaine and procainamide on the relationship between delivered voltage and defibrillation success in mongrel dogs 21 +/- 3 days following ligation of the left anterior descending and first diagonal coronary arteries. Internal defibrillation testing using a patch-patch electrode configuration was performed before and during the administration of saline controls (n = 10), lidocaine (n = 10) and procainamide (n = 10). The mean infarct size as determined by staining with tetrazolium was 13.4% +/- 8.3% of right and left ventricles, and did not differ significantly between groups. The 50% effective defibrillation (ED50) voltage increased with infusions of saline (16% +/- 15%), lidocaine (40% +/- 22%), and procainamide (13% +/- 15%) and the ED50 energy increased 41% +/- 44%, 104% +/- 62%, and 35% +/- 36%, respectively. However, the increase in ED50 voltages and energies were significantly greater in animals receiving lidocaine compared to those receiving either saline control or procainamide (P < 0.01). There were trends toward change of hemodynamic parameters in all animals following baseline defibrillation testing; stroke volume declined 21% +/- 16%; and mean pulmonary artery and aortic pressure increased by 22% +/- 25% and 11% +/- 15%, respectively. In conclusion, unlike our previous studies in dogs with normal hearts, in this model hemodynamic deterioration occurred with repeated fibrillation and defibrillation, and defibrillation voltage requirements increased in the control series. Taking into consideration the increase in defibrillation voltage requirements over the duration of the experiments, lidocaine increases and procainamide does not change ED50; thus, their effects are similar in normal and infarcted canine hearts.
先前对心脏正常的犬类进行的研究表明，利多卡因会增加成功除颤所需的能量，而普鲁卡因酰胺则不会改变这一能量。由于许多接受植入式心脏复律除颤器装置的心肌梗死后患者需要辅助抗心律失常治疗，我们研究了利多卡因和普鲁卡因酰胺对杂种犬在左前降支和第一对角冠状动脉结扎21±3天后除颤成功与输送电压之间关系的影响。在给予生理盐水对照（n = 10）、利多卡因（n = 10）和普鲁卡因酰胺（n = 10）之前及期间，使用贴片-贴片电极配置进行体内除颤测试。通过四氮唑染色确定的平均梗死面积为左右心室的13.4%±8.3%，各组之间无显著差异。随着生理盐水（16%±15%）、利多卡因（40%±22%）和普鲁卡因酰胺（13%±15%）的输注，50%有效除颤（ED50）电压升高，ED50能量分别增加41%±44%、104%±62%和35%±36%。然而，与接受生理盐水对照或普鲁卡因酰胺的动物相比，接受利多卡因的动物ED50电压和能量的增加显著更大（P < 0.01）。在基线除颤测试后，所有动物的血流动力学参数均有变化趋势；每搏量下降21%±16%；平均肺动脉压和主动脉压分别升高22%±25%和11%±15%。总之，与我们先前对心脏正常犬类的研究不同，在该模型中，反复的颤动和除颤会导致血流动力学恶化，且对照组的除颤电压需求增加。考虑到实验过程中除颤电压需求的增加，利多卡因会增加而普鲁卡因酰胺不会改变ED50；因此，它们在正常和梗死犬心的作用相似。
