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一种新型血管紧张素转换酶抑制剂(依那普利)对心肌梗死后左心室功能不全大鼠的影响。

Effects of a new angiotensin-converting enzyme inhibitor (idrapril) in rats with left ventricular dysfunction after myocardial infarction.

作者信息

Jeremic G, Masson S, Luvara G, Porzio S, Lagrasta C, Riva E, Olivetti G, Latini R

机构信息

Department of Cardiovascular Research, Istituto "Mario Negri," Milan, University of Parma, Italy.

出版信息

J Cardiovasc Pharmacol. 1996 Mar;27(3):347-54. doi: 10.1097/00005344-199603000-00006.

Abstract

We evaluated the effects of a new angiotensin-converting enzyme (ACE) inhibitor (idrapril) in terms of hemodynamics and ventricular remodeling after myocardial infarction in rats. The animals were randomly assigned to four experimental groups. Myocardial infarction was induced by left coronary artery ligation in the first two groups treated with either idrapril (300 mg kg-1 day-1) or vehicle for 4 weeks after myocardial infarction. Two groups of sham-operated rats were treated accordingly. Hemodynamics were measured, and the diastole-arrested hearts were analyzed morphometrically to quantify left ventricular (LV) remodeling and infarct size. In infarcted rats, idrapril reduced the arterial systolic blood pressure (SBP) from 128 +/- 10 to 97 +/- 6 mm Hg (p < 0.05) and LV end-diastolic pressure (LVEDP) from 19 +/- 3 to 13 +/- 3 mm Hg (p < 0.01). The decrease in diastolic wall stress conferred by idrapril to infarcted rats (from 499 +/- 99 to 269 +/- 68 dynes mm-2, p < 0.05) was mainly due to a reduction in LVEDP and, to a lesser extent, in LV volume. Idrapril also reduced body and heart weights as compared with those of vehicle-treated animals. Four-week treatment with idrapril initiated immediately after myocardial infarction reduced LVEDP and limited LV wall stress, a major prognostic factor for the progression toward chronic ventricular failure.

摘要

我们评估了一种新型血管紧张素转换酶(ACE)抑制剂(依那普利)对大鼠心肌梗死后血流动力学和心室重构的影响。将动物随机分为四个实验组。在前两组中,通过左冠状动脉结扎诱导心肌梗死,心肌梗死后分别用依那普利(300mg/kg·天-1)或赋形剂治疗4周。相应地对两组假手术大鼠进行治疗。测量血流动力学指标,并对心脏舒张期停搏的心脏进行形态学分析,以量化左心室(LV)重构和梗死面积。在梗死大鼠中,依那普利使动脉收缩压(SBP)从128±10mmHg降至97±6mmHg(p<0.05),左心室舒张末期压力(LVEDP)从19±3mmHg降至13±3mmHg(p<0.01)。依那普利使梗死大鼠的舒张期壁应力降低(从499±99达因/平方毫米降至269±68达因/平方毫米,p<0.05),这主要是由于LVEDP降低,其次是左心室容积减小。与赋形剂处理的动物相比,依那普利还降低了体重和心脏重量。心肌梗死后立即开始的四周依那普利治疗降低了LVEDP并限制了左心室壁应力,左心室壁应力是向慢性心力衰竭进展的一个主要预后因素。

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