贝那普利对扩张型心肌病中层心肌细胞动作电位时程的影响

目的探讨贝那普利对扩张型心肌病（DCM）中层心肌细胞动作电位时程的影响及其抑制莹性心律失常。方法制作DCM家兔模型，并给予贝那普利干预，然后测定其室颤阈值（VFT）以及心外膜、中层心肌和心内膜心肌细胞的单相动作电位复极90％时程（APD90）、跨室壁复极离散度（TDR）。结果DCM治疗组（DCM＋贝那普利）与DCM对照组相比，治疗组VFT阈值升高，三层心肌APD90均缩短，以中层心肌APD90缩短更为明显，TDR减小。结论贝那普利能抑制DCM室性心律失常的发生，间接地减小三层心肌跨室壁复极不均一性是重要机制。

Effect of benazepril on action potential duration of midmyocardial cell in rabbit models with dilated cardiomyopathy

Objective] To test the effect of oral benazepril on action potetial duration of midmyocardial cel in rabbit models of dilated cariomyopathy (DCM) and find whether this effect plays an important role in suppressing ventricular arrhythmias. Methods] Adriamycin was used to induce rabbit models with DCM. The rabbits were divided into DCM group, Benazepril DCM group and control group. In benazepril DCM group the oral benazepril was given per day. The ventricular fibrillation threshold (VFT), transmural dispersion of repolarization (TDR) and action potential duration at 90% repolarization (APD90) were evaluated in three myocardial layers after eight weeks. Results] Compared DCM group, higher VFT and shorter TDR and APD90 in three myocardial layers were found in benazepril DCM group, but the APD90 in midmyocardium was shortened greater. Conclusion] Benazepril could indirectly decrease transmural heterogeneity of ventricular repolarization in rabbits of DCM, and this was an important mechanism why benazepril could suppress the occurance of ventricular arrhythmias.