【摘要】 目的:探讨急性心肌缺血过程中肥厚左心室跨壁复极离散度变化及与室性心律失常关系。方法:分别记录肥厚及正常对照心室肌标本在模拟缺血过程中、不同刺激周长下内外膜动作电位及跨壁复极离散度变化;对比室性心律失常发生率、分析机制。结果:①和对照组相比,肥厚组在缺血各个时段跨壁复极离散度均显著升高,且随缺血时间、刺激周长的延长逐步递增。②肥厚组在缺血过程中早后除极、延迟后除极发生率显著高于对照组,且多次形成跨壁折返性心律失常。对照组虽有延迟后除极,但未能形成跨壁折返。结论:肥厚心室跨壁复极离散度存在缺血时间、刺激周长的双重依赖;在此基础上早后除极、延迟后除极诱发跨壁折返是缺血肥厚心室心律失常的主要机制之一。更多还原

【Abstract】 Objective:To study the transmural dispersion of repolarization(TDR) in hypertrophied left ventricles(LVH) of rabbits during acute ischemia and to probe the mechanism of ventricular arrhythmia.Method:We recorded the transmembrane action potential in endocardium,epicardium and compared the TDRs of LVH and normal left ventricles respectively during acute ischemia at different basic cycle length(BCL).We also compared the ratio of LVH and control group during ischemia.Result:①Compared to control group,the TDRs of LVH group were significantly elevated depending on the prolongation of ischemic duration and BCL.②The ratio of early after-depolarization(EAD) and delayed after-depolarization(DAD) in LVH group was much higher than that in control group,and then caused tranmural-reentry ventricular arrhythmia in most preparations.It did not happen in control group although DAD occurred in endocardium.Conclusion:TDRs of LVH are dependent on both ischemic duration and BCL;EAD and DAD induced transmural reentry underlies one of the crucial mechanism of hyperthophied left ventricles during ischemia.更多还原