摘要
为比较胺碘酮和奎尼丁在缺血条件下的细胞电生理效应，给临床研究提供实验依据。采用常规细胞内微电极法观察到，在模拟缺血液中，加入胺碘酮能延缓和减轻缺血引起的电生理改变，表现为ＲＰ、ＡＰＡ、Ｖｍａｘ、ＡＰＤ和ＳＰＴＲ各指标都有改善（Ｐ＜０．０５）；相反，加入奎尼丁使ＰＲ进一步除极、ＡＰＡ、Ｖｍａｘ、ＳＰＴＲ进一步减小，加剧了模拟缺血的电生理效应（Ｐ＜０．０５）。而且，胺碘酮对缺血心肌电活动的恢复作用优于奎尼丁（Ｐ＜０．０５）。结论：胺碘酮较奎尼丁更易缓解缺血心肌的电不稳定。
Tocomparetheelectrophysiologicefectsofamiodaronewiththoseofquinidineonis-chemicventricularmyocardiumtoprovideanexperimentalbasisforclinicalstudywasdone.Conven-tionalintracelularmicroelectrodetechniqueswereused.Addingamiodaronetothemimicischemicsolutioncoulddelayandattenuatetheelectrophysiologicchangesinducedbyischemia,whichamelio-ratedsuchelectrophysiologicalparametersasRP,APA,Vmax,APDandSPTR(P<0.05).Incon-trast,addingquinidineexertedfurtherdepolarizationofRP,furtherreductioninAPA,VmaxandSPTR,whichaggravatedtheelectrophysiologicefectsofischemia(P<0.05).Inaddition,amio-daronewasbeterthanquinidinefortherecoveryofelectricalactivityfromischemia(P<0.05).Amidaroneissuperiortoquinidineinstabilizingtheelectricalactivityofischemicmyocardium.Thisresultmaybepartofthemechanismforexplanationofthediferentefectsofthetwodrugsonelec-tricalinstabilityofpatientswithmyocardialinfarction.
出处
《中华心血管病杂志》
CAS
CSCD
北大核心
1996年第6期411-415,共5页
Chinese Journal of Cardiology
关键词
胺碘酮
奎尼丁
心肌缺血
电生理学
amiodaronequinidinemyocardialischemiaelectrophysiology
