中文摘要：

目的研究抑制线粒体苯二氮卓类体 （mitochondrial benzodiazepine receptor, mBzR）对缺血大鼠乳头肌动作电位复极至90％的时间（90％ofduration of action potential，APDgo）和有效不应期（effective refractory period．ERP）的影响。方法建立体外大鼠乳头肌模拟心肌缺血模型，将50只大鼠随机分为正常对照组、单纯缺血组、4’-chlorodiazepam（16μmol／L）组、4’-chlorodiazepam（32μmol/L）组和4’-chlorodiazepam（64μmol／L）组，每组各10只。利用细胞内标准玻璃微电极技术，记录APD。和ERP的变化。结果与正常对照组相比，缺血组APD。和ERP显著减小（P〈0．05）。缺血加4’-chlorodiazepam的各组都可以显著减少缺血时APDg）和ERP的降低程度（P〈0．05）。结论缺血时，心肌细胞APD。和ERP逐渐缩短，这可能是缺血促进折返性心律失常的基础之一：而线粒体mBzR受体特异性的抑制剂4＇-chlorodiazepam可以显著地减少缺血所致的APD。和ERP的缩短，从而减少了折返形成的可能性，这可能是抑制线粒体mBzR受体阻止心室颤动发生的重要的电生理基础。

英文摘要：

Objective To investigate the effects inhibition on 90% of duration of action potential isolated ischemic papillary muscles of rat hearts. of mitochondrial benzodiazepine receptor （mBzR） （APDg0） and effective refractory period （ERP） of Methods The ischemia models were made and then the rats were divided randomly into five groups （n=10） ： the normal control group, the ischemia group, 4＇-chlorodiazepam （16 tzM） group, 4＇-chlorodiazepam （32 p~M） group and 4＇-chlorodiazepam （64 IxM） group. The intracellular standard glass microelectrode technique was used, and effects of mBzR inhibition on APD90 and ERP were observed in ischemic papillary muscles of rat hearts. Re- sults Ischemia resulted in progressive shortening of APDgo and ERP. 4＇-chlorodiazepam could blunt APDgo and ERP shortening during ischemia. Conclusion Progressive shortening of APDg0 and ERP in ischemia may be important bases for the genesis of ventricular arrhythmia. 4＇-chlorodiazepam could blunt the shortening of APD~0 and ERP during ischemia, indicating that mBzR inhibition may prevent ischemic ventricular arrhythmias by reducing the reentry.