Wald R W, Waxman M B, Downar E
Circ Res. 1980 May;46(5):612-9. doi: 10.1161/01.res.46.5.612.
We studied the effect of therapeutic concentrations of lidocaine, procainamide, quinidine, propranolol, and diphenylhydantoin on two models of depressed conduction and unidirectional block produced by asymmetric focal cooling and crushing in sheep Purkinje fibers. All drugs were shown to induce reversible deterioration of conduction. Unidirectional block was converted to bidirectional block with each drug. Improvement of conduction was rare and conversion of unidirectional block to bidirectional conduction never was observed. These experiments suggest that all five drugs may act by a uniform mechanism of action in some reentrant ventricular arrhythmias involving a zone of depressed conduction or unidirectional block within the Purkinje network.
我们研究了利多卡因、普鲁卡因胺、奎尼丁、普萘洛尔和苯妥英钠的治疗浓度对两种由不对称局灶性冷却和挤压绵羊浦肯野纤维所产生的传导抑制和单向阻滞模型的影响。所有药物均显示可诱导传导的可逆性恶化。每种药物均可使单向阻滞转变为双向阻滞。传导改善情况罕见,且从未观察到单向阻滞转变为双向传导。这些实验表明,在某些涉及浦肯野网络内传导抑制区或单向阻滞的折返性室性心律失常中,所有这五种药物可能通过统一的作用机制发挥作用。