Suppr超能文献

梗死大鼠心脏中肥厚诱导的动作电位改变及培哚普利抑制血管紧张素转换酶的作用

Hypertrophy induced alteration of action potential and effects of the inhibition of angiotensin converting enzyme by perindopril in infarcted rat hearts.

作者信息

Thollon C, Kreher P, Charlon V, Rossi A

机构信息

Laboratoire de Physiologie cellulaire cardiaque, Université Joseph Fourier, Grenoble, France.

出版信息

Cardiovasc Res. 1989 Mar;23(3):224-30. doi: 10.1093/cvr/23.3.224.

Abstract

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.

摘要

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。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验