【摘要】 目的　观察再灌注时犬在体心肌早期后除极 (EAD)的起源。方法　 12只健康犬 ,阻断左前降支主干 30 min后恢复前降支血流制备再灌注模型。应用单相动作电位记录技术 ,同步记录犬在体心肌再灌注时心外膜、中层和心内膜心肌 MAP及体表心电图 ,分析其相关参数的变化。结果　再灌注 30 m in内 ,12只犬中有 9只出现了 EAD(75 % ) ,Epi、Mid及 Endo的 EAD振幅 (EADA)分别为 3.44± 1.6 3m V、5 .49± 1.2 4m V、3.88± 1.40 m V ,Mid较Epi及 Endo的 EADA高 ,差异有显著性 (P<0 .0 1) ;Epi、Mid及 Endo的 EAD耦联间期 (EAD- CI)分别为 131.6 3± 17.43ms,12 5 .2 9± 2 3.6 4m s和 130 .0 5± 19.38ms,Mid较 Epi及 Endo的 EAD- CI小 ,差异有显著性 (P<0 .0 5 ) ,中层心肌的 EAD振幅最高 ,且出现时程最早。12只犬中有 7只出现了恶性室性心律失常 ,均发生于出现 EAD的犬中。再灌注心律失常发生率为 5 8.3%。结论　犬在体心肌再灌注时出现明显 EAD,且 EAD起源于中层心肌细胞 ,由其介导的触发活动可能是再灌注性心律失常发生的主要机制更多还原

【Abstract】 Objective To observe the origin of early afterdepolarization in intact canine during reperfusion. Methods 12 dogs were reperfused after 30min acute ischemia. With MAP recording technique, MAPs of Epi, Mid and Endo were recorded simultaneously during reperfusion; the changes of MAPD 90, EAD and reperfusion arrhythmias were observed and analyzed. Results Compared with the duration of ischemia ,MAPD had no significant changes in the period of 30 min reperfusion. During reperfusion, EAD developed in 9 dogs, the EADA (EAD amplitude) in Epi, Mid and Endo was 3.44±1.63mV, 5.49±1.24mV and 3.88±1.40mV and the EAD-CI(coupling interval) in Epi, Mid and Endo was 131.63±17.43ms, 125.29±23.64ms and 130.05±19.38 ms respectively. EAD in the Mid was the biggest and the earliest. Reperfusion arrhythmias developed in 7 dogs among the 9 dogs in which EAD developed. Conclusions These findings show that EAD originates from the Mid during myocardial reperfusion in intact canine and may be one of the mechanisms of reperfusion arrhythmia.更多还原