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Updated: Aug 7, 2026
Semi-Minimal Invasive Method to Induce Myocardial Infarction in Rats and the Assessment of Cardiac Function by an Isolated Working Heart System
Published on: June 11, 2020
ACE inhibition decreases postoperative mortality in rats with left ventricular hypertrophy and myocardial infarction
W Linz1, G Wiemer, H L Schmidts
1Hoechst-Marion-Roussel, TD Cardiovascular Agents, Frankfurt/Main, Germany.
Insights
Ramipril, an ACE inhibitor, improved survival in hypertensive rats with left ventricular hypertrophy (LVH) and myocardial infarction (MI). It also reduced infarct size in normotensive rats, indicating improved cardiac metabolism and function.
Area of Science:
- Cardiovascular Research
- Pharmacology
- Experimental Medicine
Background:
- Hypertension and left ventricular hypertrophy (LVH) significantly increase mortality following myocardial infarction (MI).
- Understanding the impact of interventions on cardiac function and metabolism in these conditions is crucial for improving patient outcomes.
Purpose of the Study:
- To investigate the effects of ACE inhibition with ramipril on survival, cardiac function, and metabolism in rats with induced LVH, hypertension, and MI.
- To compare the efficacy of ramipril in hypertensive versus normotensive models of MI.
Main Methods:
- Male Sprague Dawley rats underwent aortic constriction (AC) to induce hypertension and LVH, followed by myocardial infarction (MI).
- Ramipril (1 mg/kg/day) was administered for 6 weeks to assess its effects on mortality, infarct size, cardiac contractility, and myocardial metabolism.
- Control groups included sham AC, AC alone, AC with sham MI, normotensive with sham MI, MI, and MI with ramipril.
Main Results:
- Hypertensive rats with LVH and MI exhibited a 68% postoperative mortality rate, reduced to 42% with ramipril treatment (a 26% decrease).
- Ramipril reduced infarct size by 50% in normotensive rats but showed minimal effect in hypertensive rats due to already smaller infarcts.
- Ramipril treatment improved cardiac contractility, normalized biochemical markers in coronary effluent (LDH, CK, lactate), increased prostacyclin output, and enhanced myocardial energy phosphates.
Conclusions:
- ACE inhibition with ramipril significantly increases survival in hypertensive rats with LVH and MI, likely by improving tolerance to ischemia and reducing arrhythmias.
- Ramipril enhances myocardial metabolism in both hypertensive and normotensive rats undergoing MI, evidenced by improved cardiac function and energy status.
Unlabelled:
In male Sprague Dawley rats with left ventricular hypertrophy (LVH) and hypertension induced by aortic constriction (AC) and subsequent myocardial infarction (MI) by occlusion of the left coronary artery the effects of ACE inhibition with ramipril (RA 1 mg/kg/day via the drinking water during 6 weeks) on survival as well as cardiac function and metabolism were investigated. Respective groups (sham AC; AC; AC + sham MI; normotensive animals with sham MI; MI; MI + RA) served as comparisons. Following MI hypertensive rats with AC and LVH revealed an increased postoperative mortality (68%) when compared to normotensives without AC (28%). ACE inhibition with ramipril significantly reduced mortality in hypertensive rats by 26%. Untreated hypertensive animals with LVH clearly showed reduced MI size (6.2 +/- 2.3%) in comparison with untreated normotensive animals and MI (31.0 +/- 3.3%). In hypertensive rats with MI which died during the study a significant increase in infarct size was found compared to those which survived MI. In normotensive animals ramipril reduced infarct size by 50%. Due to the quite small infarct size observed in hypertensive rats, ACE inhibition did not further reduce MI in these animals. LVH as well as hydroxyproline/proline ratio was diminished by ACE inhibitor treatment. In the isolated hearts of ramipril treated rats contractility was improved when compared to the respective untreated groups with MI. In the coronary effluent of isolated hearts from rats with AC and MI lactate dehydrogenase and creatine kinase activities as well as lactate levels were increased. Ramipril treatment starting one week before MI normalized these parameters and in addition increased prostacyclin output. Hearts with MI from treated normotensive animals contained increased energy rich phosphates when compared to hearts from untreated rats with MI.
Conclusions:
Hypertensive rats with LVH undergoing MI experience increased postoperative mortality probably due to a reduced tolerance to myocardial ischemia and occurrence of arrhythmias. In these animals ACE inhibition with ramipril increased survival. Both, increased survival in hypertensive and reduction in infarct size in normotensive rats by ACE inhibition with ramipril was accompanied by an improved myocardial metabolism.
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