Summary
To study the effect of of lidocaine and amiodarone on the transmural heterogeneity of ventricular repolarization in isolated rabbit hearts model of sustained global ischemia and to explore the mechanisms underlying the antiarrhythmic activity of lidocaine and amiodarone, rabbits were randomly divided into 4 groups: control group, ischemia group, lidocaine group and amiodarone group. By the monophasic action potential (MAP) recording technique, MAPs of epicardium, midmyocardium and endocardium were simultaneously recorded across the left ventricular free wall in rabbit hearts perfused by low-flow ischemia (2.5 mL/min) in Langendorff method to study the transmural dispersion of repolarization (TDR) and arrhythmic induced by ischemia. Our results showed that TDR of three myocardial layers in ischemia group were significantly lengthened after ischemia. TDR was increased from 17.5±3.9 ms to 31.2±4.6 ms at the time that concided with the onset of sustained ventricle arrhythmic. Amiodarone could decrease TDR, but lidocaine could increase TDR at initial ischemia, and no significant difference was found at other ischemia time points. 5 cases had ventriclar arrhythmia in ischemia group (62.5%), but no case in lidocaine group (P<0.01) and only 1 case in amiodarone group had ventrilar arrhythmia (P<0.01). No significant difference was found between amiodarone group and lidocaine group. It is concluded that TDR of of three myocardial layers increases significantly at ischemia and it is closely associated with development of ventricular arrhythmia, and amiodarone could decrease TDR, but lidocaine could increase TDR at initial ischemia and has no effects at other ischemia time points.
Similar content being viewed by others
References
Naccarelli G V, Wolbrette D L, Patel H Met al. Amiodarone: clinical trial. Curr Opin Cardiol, 2000,15:64
Antman E M, Lau J, Kupelnick Bet al. A comparison of results of meta-analyses of randomized control trials and recommendations of clinical experts: treatments for myocardial infarction. JAMA, 1992,268:240
Sicouri S, Antzelevitch C. A subpopulation of cells with unique electrophysiological properties in the deep subepicardium of the canine ventricle. Circ Res, 1991, 68:1729
Yan G X, Kowey P R. ST segment elevation and sudden cardiac death: from the Brugada syndrome to acute myocardial ischemia. J Cardiovasc Electrophysiol, 2000,11:1330
Li Y T, Zhang C T, Lu Z Yet al. Experimental observation on genesis of U wave in ECG in rabbits. Chin J Cardiol (Chinese), 2000,28:124
Spear J F, Moore E N. Effects of acute global low-flow ischemia on triggered arrhythmias in d-sotalol-induced long Q-T intervals in perfused rabbit hearts. J Cardiovasc Pharmacol, 2001,37:196
Zhang C T, Xu D W, Li Yet al. Experimental study of the effect of autonomic nervous system on the transmural dispersion of ventricular repolarization under acute myocardial ischemiain vivo. J Huazhong Uni Sci Technol [Med Sci], 2002,22:96
Opthof T, Coronel R, Vermeulen J Tet al. Dispersion of refractoriness in normal and ischaemic canine ventricle: effects of sympathetic stimulation. Cardiovasc Res, 1993,27:1954
Wu J, Zipes D P. Transmural reentry during acute global ischemia and reperfusion in canine ventricular muscle. Am J Physiol Heart Circ Physiol, 2001,280: H2717
Antzelevitch C, Sicouri S. Clinical relevance of cardiac arrhythmias generated by afterdepolarizations: The role of M cells in the generation of U waves, triggered activity and torsade de pointes. JACC, 1994,23:259
Barrett T D, Hayes E S, Walker M J A. Lack of selectivity for ventricular and ischaemic tissue limits the antiarrhythmic actions of lidocaine, quinidine and flecanide against ischaemia-induced arrhythmias. Eur J Pharmacol, 1995,285:229
Cardinal R, Janse M J, Van Eeden Iet al. The effects of lidocaine on intracellular and extracellular potentials, activation, and ventricular arrhythmias during acute regional ischemia in the isolated porcine heart. Circ Res, 1981,49:792
Campbell T J, Hemsworth P D. Selective depression of maximum rate of depolarization of guinea-pig ventricular action potentials by amiodarone and lidocaine in simulated ischaemia: comparison with encainide. Clin Exp Pharmacol Physiol, 1990,17:135
Sicouri S, Moro S, Elizari M V. d-Sotalol induces marked action potential prolongation and early afterdepolarizations in M but not epicardial or endocardial cells of the canine ventricle. J Cardiovasc Pharmacol Ther, 1997,2:27
Author information
Authors and Affiliations
Additional information
You Binquan, male, born in 1970, M. D., Ph. D.
Rights and permissions
About this article
Cite this article
Binquan, Y., Jun, P., Nian, L. et al. Effect of lidocaine and amiodarone on transmural heterogeneity of ventricular repolarization in isolated rabbit hearts model of sustained global ischemia. J. Huazhong Univ. Sci. Technol. [Med. Sci.] 25, 400–403 (2005). https://doi.org/10.1007/BF02828207
Received:
Issue Date:
DOI: https://doi.org/10.1007/BF02828207