Thollon C, Kreher P, Charlon V, Rossi A
Laboratoire de Physiologie cellulaire cardiaque, Université Joseph Fourier, Grenoble, France.
Cardiovasc Res. 1989 Mar;23(3):224-30. doi: 10.1093/cvr/23.3.224.
Not much is known about alterations in electrical activity in the healthy part of a heart made hypertrophic as a result of local ischaemia, yet such an investigation might allow us to predict the stages leading to cardiac failure and so aid its prevention. We therefore studied the electrophysiological changes which occurred in rats in which ligation of the left coronary artery had produced hypertrophy of the non-infarcted myocardium. One month after the intervention the overall degree of hypertrophy of the ventricles reached 15.3%. This was accompanied in the healthy part of the left ventricle (septum) by altered electrical activity consisting of a lengthening of the action potentials at 25, 50, 75 and 90% of repolarisation. Myocardial hypertrophy was absent after chronic treatment of the animals with perindopril, an angiotensin converting enzyme inhibitor, given orally at 2 mg.kg-1 body weight, and the electrophysiological alterations induced by the infarct were partially eliminated: phase 2 of the myocardial action potential was shortened and phase 3 completely restored. We postulate that angiotensin may have a direct effect on the cardiac cell.
关于因局部缺血而肥厚的心脏健康部位的电活动改变,目前所知甚少,然而这样一项研究或许能让我们预测导致心力衰竭的各个阶段,从而有助于预防心力衰竭。因此,我们研究了左冠状动脉结扎导致非梗死心肌肥厚的大鼠所发生的电生理变化。干预一个月后,心室的总体肥厚程度达到了15.3%。在左心室(室间隔)的健康部位,这种肥厚伴随着电活动的改变,表现为复极化25%、50%、75%和90%时动作电位延长。给动物按2mg·kg-1体重口服血管紧张素转换酶抑制剂培哚普利进行慢性治疗后,未出现心肌肥厚,梗死引起的电生理改变也部分消除:心肌动作电位的2期缩短,3期完全恢复。我们推测血管紧张素可能对心肌细胞有直接作用。