咪达普利对陈旧性心肌梗死非梗死区心肌跨室壁复极离散度及短暂外向钾电流的影响

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目的 探讨咪达普利对陈旧性心肌梗死非梗死区心肌跨室壁复极离散度(TDR)以及短暂外向钾电流(Ito)的影响。方法24只兔随机分为3组,两组结扎左冠状动脉回旋支制成心肌梗死模型,手术后1周1组给予咪达普利 0.625mg·kg-1·d-1口服(咪达普利组),另1组则给予安慰剂口服(陈旧性心肌梗死组);第3组开胸但不结扎冠状动脉也给予安慰剂口服(假手术组)。3个月后酶解分离得到左心室壁远离梗死中心区的3层心肌单细胞(心外膜下心肌细胞、中层心肌细胞和心内膜下心肌细胞),用膜片钳技术研究跨室壁复极离散度(TDR)以及3层心肌细胞的短暂外向钾电流(Ito)的改变。结果 心肌梗死后3个月,非梗死区的心肌细胞发生了肥厚和重构,3层心肌细胞的动作电位时限(APD)明显延长,其中心内膜下心肌细胞的APD明显短于心外膜下心肌细胞和中层心肌细胞(P<0.01),与假手术组对比呈相反的跨室壁离散。陈旧性心肌梗死TDR也明显增加,但TDR在咪达普利组和假手术组间差异不明显。陈旧性心肌梗死3层心肌细胞的Ito密度均降低,以心外膜下心肌细胞和中层心肌细胞较明显(P<0.05),咪达普利组和假手术组相比,Ito密度无明显改变(P>0.05)。结论陈旧性心肌梗死远离梗死中心区的左心室心肌细胞发生代偿性肥厚,APD延长,TDR增加,3层心肌细 Objective To investigate the effect of imidapril on transmural wall repolarization dispersion (TDR) and transient outward potassium current (Ito) in non-infarcted area of ​​elderly patients with myocardial infarction. Methods Twenty-four rabbits were randomly divided into three groups. The left coronary artery ligation was ligated into the myocardial infarction model in two groups. One week after the operation, 1 group was given imidapril 0.625 mg · kg-1 · d-1 orally And the other group were given placebo orally (old myocardial infarction group); group 3 thoracotomy but without ligation of the coronary artery was also given placebo orally (sham operation group). Three months later, three layers of single myocardium (epicardial, midmyocardial, and subendocardial cells) were isolated by enzymolysis and left ventricular wall was removed from the infarct center. Repolarization dispersion (TDR), and transient outward potassium current (Ito) in three layers of cardiomyocytes. Results Myocardial cell hypertrophy and remodeling occurred in non-infarcted area 3 months after myocardial infarction. The APD of 3-layer myocardial cells was significantly prolonged. APD in subendocardial cells was significantly shorter than that in epicardium Inferior myocardial cells and middle myocardial cells (P <0.01), compared with the sham-operated group, the opposite transversal dispersion. TDR was also significantly increased in patients with old myocardial infarction, but there was no significant difference in TDR between the Imidapril group and the sham operation group. The Ito density of three layers of cardiomyocytes in old myocardial infarction group were decreased to the more obvious in epicardial cardiomyocytes and middle cardiomyocytes (P <0.05), while there was no significant difference in Ito density between Imidapril group and sham operation group (P> 0.05). Conclusion The compensated hypertrophy, prolonged APD and TDR increase in left ventricular myocytes far away from infarct center in patients with old myocardial infarction
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