Ren Yong, Zhang Cun-tai, Wu Jie, Ruan Yan-fei, Pu Jun, He Li, Wu Wei, Chen Bai-di, Wang Wen-guang, Wang Lin
Department of Cardiology, Tongji Hospital, Affiliated of Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
Zhonghua Xin Xue Guan Bing Za Zhi. 2006 Sep;34(9):825-8.
To evaluate the effects of antiarrhythmic peptide (AAP10) on ventricular arrhythmias in rabbits with healed myocardial infarction (OMI).
Thirty rabbits were randomly divided into three groups (n = 10 each): Sham group, left thoracotomy was performed without coronary ligation; OMI group and OMI + AAP10 group, the circumflex coronaries were ligated. Three months post operation, the electrophysiological and antiarrhythmic effects of AAP10 were assessed in the arterially perfused rabbit left ventricular wedge preparation. Sham and OMI group were perfused with Tyrode's solution and OMI + AAP10 group was perfused with Tyrode's solution + AAP10 (80 nmol/L). Transmembrane action potentials were recorded simultaneously from endocardium and epicardium together with a transmural ECG by use of 2 separate intracellular floating microelectrodes. The stimulus-response-interval (SRI) of the epicardium and the incidence of ventricular tachycardia (VT) were observed. Whole heart and left ventricular weights, the left ventricular thickness at infarct border zone were measured.
Whole heart and left ventricular weights as well as the left ventricular thickness at the infarct border zone significantly increased post infarction. VT was induced in 8 out of 10 rabbits in OMI group and in 2 out of 10 rabbits in OMI + AAP10 group (P < 0.05). SRI was also significantly shortened in OMI + AAP10 group compared to OMI group [SRI-1: (20.59 +/- 0.79) ms vs. (28.71 +/- 0.55) ms; SRI-2: (30.42 +/- 0.74) ms vs. (38.67 +/- 0.49) ms, all P < 0.01]. However, the action potential morphology and duration were similar between OMI and OMI + AAP10 groups.
The antiarrhythmic peptide (AAP10) can increase gap junctional intercellular conductance without affecting the action potential morphology and duration and decrease the incidence of inducible ventricular tachycardia.
评估抗心律失常肽(AAP10)对陈旧性心肌梗死(OMI)家兔室性心律失常的影响。
30只家兔随机分为三组(每组n = 10):假手术组,仅行左胸切开术,不结扎冠状动脉;OMI组和OMI + AAP10组,结扎左旋冠状动脉。术后3个月,在动脉灌注的家兔左心室楔形标本上评估AAP10的电生理和抗心律失常作用。假手术组和OMI组用台氏液灌注,OMI + AAP10组用台氏液+ AAP10(80 nmol/L)灌注。使用2根单独的细胞内漂浮微电极同时记录心内膜和心外膜的跨膜动作电位以及透壁心电图。观察心外膜的刺激-反应间期(SRI)和室性心动过速(VT)的发生率。测量全心和左心室重量以及梗死边缘区的左心室厚度。
梗死后全心和左心室重量以及梗死边缘区的左心室厚度显著增加。OMI组10只家兔中有8只诱发出VT,OMI + AAP10组10只家兔中有2只诱发出VT(P < 0.05)。与OMI组相比,OMI + AAP10组的SRI也显著缩短[SRI-1:(20.59 ± 0.79) ms对(28.71 ± 0.55) ms;SRI-2:(30.42 ± 0.74) ms对(38.67 ± 0.49) ms,均P < 0.01]。然而,OMI组和OMI + AAP10组之间的动作电位形态和时程相似。
抗心律失常肽(AAP10)可增加缝隙连接细胞间电导,而不影响动作电位形态和时程,并降低诱发性室性心动过速的发生率。