Wolk R, Cobbe S M, Hicks M N, Kane K A
Department of Medical Cardiology, Royal Infirmary, Glasgow, Scotland.
J Cardiovasc Pharmacol. 1998 Feb;31(2):253-61. doi: 10.1097/00005344-199802000-00011.
The aims of this study were to establish a working rabbit heart model of regional myocardial ischaemia in which electrophysiologic parameters and arrhythmogenesis could be correlated and to explore the mechanisms underlying the antiarrhythmic activity of lignocaine. Monophasic action-potential duration (MAPD90), effective refractory period (ERP), and conduction delay were measured at three ventricular sites in isolated hearts paced at 3.3 Hz. The hearts were treated before and throughout 30 min of ischaemia and 15 min of reperfusion with a vehicle or 20 microM lignocaine. In both groups, ischaemia produced a similar shortening in MAPD90. Lignocaine decreased ERP shortening during ischaemia from -56+/-4 to -32+/-6 ms. An ischaemia-induced increase in conduction delay was greater in the lignocaine than the control group (49+/-7 vs. 11+/-2 ms). Ischaemia-induced dispersion of repolarisation was reduced by lignocaine from 66+/-4 to 32+/-7 ms, and dispersion of refractoriness was decreased from 57+/-6 to 16+/-3 ms. Lignocaine decreased inducibility of ventricular fibrillation (VF) during ischaemia from 86 to 25%. We conclude that, in this model, the antiarrhythmic activity of lignocaine during regional ischaemia is associated with an increase in ischaemia-induced conduction delay and reduced dispersion of repolarisation and refractoriness.
本研究的目的是建立一个局部心肌缺血的家兔心脏工作模型，在此模型中电生理参数与心律失常的发生机制可相互关联，并探索利多卡因抗心律失常活性的潜在机制。在3.3 Hz起搏的离体心脏的三个心室部位测量单相动作电位时程（MAPD90）、有效不应期（ERP）和传导延迟。在缺血30分钟和再灌注15分钟之前及整个过程中，用赋形剂或20微摩尔利多卡因处理心脏。在两组中，缺血均使MAPD90出现类似程度的缩短。利多卡因减少了缺血期间ERP的缩短，从-56±4毫秒降至-32±6毫秒。缺血诱导的传导延迟增加在利多卡因组比对照组更明显（49±7毫秒对11±2毫秒）。利多卡因使缺血诱导的复极离散度从66±4毫秒降至32±7毫秒，不应期离散度从57±6毫秒降至16±3毫秒。利多卡因使缺血期间心室颤动（VF）的诱导率从86%降至25%。我们得出结论，在此模型中，局部缺血期间利多卡因的抗心律失常活性与缺血诱导的传导延迟增加以及复极和不应期离散度降低有关。
