Shi Xiangmin, Shan Zhaoling, Yuan Hongtao, Guo Hongyang, Wang Yutang
Department of Cardiology, Chinese PLA General Hospital 28 Fuxing Road, Haidian District, Beijing 100853, P.R. China.
Int J Clin Exp Med. 2014 Dec 15;7(12):5310-6. eCollection 2014.
This study aims to investigate the effect of captopril and losartan on the electrophysiology of myocardial cells parameters in ventricular vulnerable period and effective refractory period of myocardial ischemia rats.
96 wistar rats were enrolled in the study and divided into six groups: Captopril myocardial ischemia group, losartan myocardial ischemia group, myocardial ischemia control group, captopril normal group, losartan normal group and normal control group (n=16). We observed morphological changes of myocardial tissue in each group. The cardiac electrophysiological parameters in effective refractory period of each group were measured. Creatine kinase (CK), alanine aminotransferase (GOT), lactate dehydrogenase (LDH), the expression of Cardiotrophin 1 (CT-1) and malonaldehyde (MDA) were detected.
Compared the losartan and captopril group with the control group, (P<0.05). Losartan and captopril can shorten the ventricular vulnerable period of the normal group and ischemic group. There was no interaction effect between losartan and captopril group and the acute myocardial ischemia group. The effect of losartan and captopril on time window in ventricular vulnerable period showed that compared with the control group (P<0.05). Losartan and captopril had a significant effect on prolonged effective refractory period of normal and ischemic rats. There was no interaction effect between losartan and captopril group and the acute myocardial ischemia group. Compared with the myocardial ischemia control group, CK, GOT, LDH and MDA decreased in captopril and losartan myocardial ischemia groups (P<0.05).
Losartan and captopril had a significant effect on prolonged effective refractory period and shorten ventricular vulnerable period, they can also effectively prevent arrhythmias.
本研究旨在探讨卡托普利和氯沙坦对心肌缺血大鼠心室易损期和有效不应期心肌细胞电生理参数的影响。
选取96只Wistar大鼠，分为六组：卡托普利心肌缺血组、氯沙坦心肌缺血组、心肌缺血对照组、卡托普利正常组、氯沙坦正常组和正常对照组（n = 16）。观察各组心肌组织形态学变化。测量各组有效不应期的心脏电生理参数。检测肌酸激酶（CK）、谷丙转氨酶（GOT）、乳酸脱氢酶（LDH）、心肌营养素1（CT - 1）的表达及丙二醛（MDA）含量。
氯沙坦组和卡托普利组与对照组比较，（P < 0.05）。氯沙坦和卡托普利可缩短正常组和缺血组的心室易损期。氯沙坦和卡托普利组与急性心肌缺血组之间无交互作用。氯沙坦和卡托普利对心室易损期时间窗的影响显示，与对照组比较（P < 0.05）。氯沙坦和卡托普利对正常和缺血大鼠的有效不应期延长有显著作用。氯沙坦和卡托普利组与急性心肌缺血组之间无交互作用。与心肌缺血对照组比较，卡托普利和氯沙坦心肌缺血组的CK、GOT、LDH及MDA降低（P < 0.05）。
氯沙坦和卡托普利对延长有效不应期和缩短心室易损期有显著作用，还可有效预防心律失常。
