目的:研究家兔心肌肥厚时三层心肌细胞延迟整流钾电流rn慢激活成分异质性的改变及长期应用咪达普利(Imi)对此变化rn的作用.方法:缩窄兔单侧腹主动脉制备心肌肥厚模型，rn同时设Imi治疗组和假手术组.采用全细胞膜片箝技术记录rn兔心肌细胞动作电位和钾电流.结果:(1)肥厚心肌细胞的rn膜电容明显高于假手术组和Imi治疗组；其动作电位时程rn(APD)显著延长，尤其是中层细胞(M)延长最为显著；应用rnImi后可逆转此延长效应；(2)肥厚心肌细胞上IKs,tail密度rn均不同程度的降低，外膜和内膜细胞分别降低25.3％±2.9％rn和20.3％±4.7％，而M降低最为显著为38.0％±3.7％；rn用Imi后电流密度降低程度明显被缓解，该电流的跨室壁异rn质性减少.(3)在三层心肌细胞上IKr,tail的差异不明显，且rnIKr,tail密度在三组也改变较小.结论:长期应用Imi可以减rn少兔肥厚心肌细胞延迟整流钾电流慢激活成分的跨室壁异质rn性改变.%AIM: To investigate the transmural heterogeneous change of slow component of delayed rectifying potassiumcurrent in rabbit left ventricular hypertrophic myocytes and the effect of long-term treatment with imidapril (Imi).METHODS: Rabbits were divided into hypertrophy group (left ventricular hypertrophy induced by partial ligationof abdominal aorta), Imi-treated group (surgical treatment as hypertrophy group was treated with Imi), and Sham-operated group as control. Whole-cell patch-clamp technique was used to record potassium currents. RESULTS:(1) Membrane capacitance was larger in hypertrophic cells than in sham-operated and Imi-treated cells. Actionpotential durations (APD) of epicardium (Epi), midmyocardium (M), and endocardium (Endo) were remarkablylonger in hypertrophic cells than those in Imi-treated and sham-operated cells. The prolongation of APD90 of M wasthe most pronounced in three layer myocytes of hypertrophic group. (2) The densities of IKs,tail of hypertrophic cellswere reduced by Epi 25.3 %±2.9 %, M 38.0 %±3.7 % and Endo 20.3 %±4.7 % compared with those of sham-operated cells. The decrease of IKs,tail density was more pronounced in M than in Epi and Endo (n = 13, P＜0.01 vsEpi or Endo). (3) The density of IKr,tail in Imi-treated cells was not different from that in sham-operated cellssignificantly (n =10). CONCLUSION: Imi reduced prolongation of APD and inhibited the heterogeneous changeof IKs.tail in rabbit left ventricular hypertrophic myocytes.
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