慢性充血性心力衰竭时K_(ATP)通道与心室肌电生理特性变化的关系

The Relation Between K_ ATP Channel and the Electrophysiologic Changes of Ventricular Myocytes in Chronic Heart Failure.

探讨慢性充血性心力衰竭 (CHF)时三磷酸腺苷敏感性钾通道 (KATP通道 )在心室肌电生理特性改变和室性心律失常发生中的意义。采用阿霉素制作CHF兔模型。 2 9只兔分为健康对照组 (HC组 )和CHF实验组 ,后者包括CHF对照组 (CHFC组 )、CHF +KATP通道开放剂组 (P组 )、CHF +KATP通道阻断剂组 (G组 )、CHF +KATP通道开放剂和阻断剂组 (P +G组 )四个亚组。每组均予心房快速起搏 30min ,分别测定起搏前后 90 %单相动作电位时程(MAPD90 )、心室有效不应期 (VERP)及其离散度和兴奋时间 (AT)离散度 ,测定毕程序刺激诱发室性心动过速或心室颤动。结果 :快速起搏使MAPD90 、VERP延长 ,在CHFC组较HC组显著 (11.82± 10 .2 0vs 8.18± 6 .97ms,P <0 .0 5和14 .95± 12 .82vs 9.0 7± 8.79ms,P <0 .0 1) ,而G组和P +G组的MAPD90 、VERP延长更明显。各组快速起搏均未引起MAPD90 、VERP离散度变化 ,但CHFC组和P组都有AT离散度显著增大 (2 8.5 3± 8.6 3vs 36 .80± 6 .97ms ,P <0 .0 1和 2 6 .33± 5 .82vs 33.80± 9.5 0ms,P <0 .0 5 ) ,阻断剂可对抗AT离散度的增大。结论 :快速心房起搏可开放CHF心室肌KATP通道 ,一方面阻止MAPD90 、VERP的延长 ,另一方面又加大AT的非同步性 ,使室性心动过速易于诱发。

Abnormality of ventricular repolarization has been revealed,but,in chronic heart failure(CHF),the effects of K ATP channel on electrophysiologic parameters of ventricular myocytes and ventricular tachycadia is unclear.CHF model was produced by adriamycin(2 mg/kg weight/week×8 weeks iv)in Japanese white rabbits.Twenty nine rabbits were divided into 5 groups,including health control,CHF control,CHF plus pinacidil (K ATP channel opener) treated,CHF plus glibenclamide(K ATP channel blocker)-treated and CHF plus pinacidil and glibenclamide treated group.All groups subjected to 30 min of atrial pacing at 260 beats per minute,and electrophysiologic parameters[90% monophasic action potential duration(MAPD 90 ),effective refractory period(ERP),activated time(AT) and their dispersions] were measured pre and post pacing in ventricle.Ventricular tachycardia(VT) and fibrillation(VF) was provoked by S 1S 2S 3 programmed stimulation after measurements.Results:Thirty minutes of atrial pacing resulted in prolongation of MAPD 90 and ERP.The prolongation was more distinct in CHF control group than in health control group(11.82±10.20 vs 8.18±6.97 ms, P <0.05 and 14.95±12.82 vs 9.07±8.79 ms, P <0.01),and glibenclamide brought about extra prolongation.Both CHF control and iv pinacidil enlarged AT dispersion (28.53±8.63 vs 36.80±6.97 ms, P <0.01 and 26.33±5.82 vs 33.80±9.50 ms, P <0.05),which was reduced by glibenclamide.In CHF control group and CHF plus pinacidil treated group,2 and 4 hearts,respectively,experienced episodes of VT or VF pre or in S 1S 2S 3 programmed stimulation.Conclusions:Opening K ATP channel,which was resulted from rapid atrial pacing,would inhibit prolongation of MAPD 90 and ERP,exacerbate inhomogeneity of conduction,and facilitate provocation of VT or VF in CHF.