胺碘酮、索他洛尔与d-索他洛尔对犬心室肌细胞电生理作用的实验研究

EFFECTS OF AMIODARONE,D,L-SOTALOL AND D-SOTALOL ON APD_(90) AND TRANSMURAL DISPERSION OF REPOLARIZATION(TDR) IN CANINE LEFT VENTRICLE

目的 分析胺碘酮、索他洛尔与d -索他洛尔对犬心室肌细胞电生理作用。方法 采用标准玻璃微电极技术 ,观察胺碘酮、d ,l-索他洛尔 (即索他洛尔 )与d -索他洛尔对犬心室肌细胞动作电位时程 (APD)及跨壁复极离散(TDR)的作用 ,以研究三种药物不同的促心律失常发生率的机制。结果 胺碘酮 (5 μM)对心室壁三层细胞APD作用不一 ,使M细胞的APD90 缩短 ,而内、外膜的APD90 延长 ,TDR降低。索他洛尔 (10 0 μM)使心室壁三层细胞APD90均延长 ,对M细胞APD延长更明显 ,使TDR增加。d -索他洛尔 (10 0 μM)使心室壁三层细胞APD90 均增加 ,但以M细胞APD90 增加最为显著 ,而且随着d -索他洛尔诱发早期后除极、APD交替变异发生 ,而在心室肌内、外膜细胞则未见上述变化。结论 胺碘酮、索他洛尔及d -索他洛尔三种药物的不同促心律失常作用与其对心室TDR的作用不同有关。

Objective To investigate the effects of amiodarone,d,l-sotalol and d-sotalol on APD_ 90 and transmural dispersion of repolarization(TDR) in canine left ventricle. Methods The effects of drugs on APD_ 90 and transmural dispersion of repolarization(TDR) in canine left ventricle were investigated by using standard glass microelectrode techniques. Results ①amiodarone(5μM)shortened APD_ 90 in M cell,prolonged APD_ 90 in epicardium and endocardium,and reduced TRD.②d,l-sotalol (100μM)prolonged APD_ 90 in three type myocardium,most in M cell(P<0.05).At BCL 5 000ms,TDR was enhanced from (86.1±14.6)ms to (96.0±15.1)ms(P<0.05).③d-sotalol (100μM)prolonged APD_ 90 markedly in M cell,and significantly enhanced TDR from (88.4±10.4)ms to ( 435.2 ±86.8)ms(P<0.01).In M cell,d-sotalol induced early after depolarizations(EADs) and APD alternans,not in epicardium and endocardium. Conclusion The different risks of proarthythmia are associated with the different effects of drugs on TDR.