Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

PURPOSE: Angiotensin-converting enzyme (ACE) inhibitors show beneficial long-term hemodynamic effects in chronically infarcted hearts. The purpose of this study was to test whether prevention of the deterioration of mechanical function by ACE inhibitors is related to beneficial effects on high-energy phosphate metabolism that is deranged in heart failure. METHODS: Twelve-week old rats were randomly assigned to ligation of the left coronary artery [mycardial infarction (MI)] or sham operation (Sham) and to the ACE inhibitor quinapril (+Q) (6 mg/kg/day per gavage) or placebo treatment. Eight weeks later, cardiac function was measured in the isolated heart by a left ventricular balloon (pressure-volume curves), and energy metabolism of residual intact myocardium was analyzed in terms of total and isoenzyme creatine kinase activity (spectrophotometry), steady-state levels [adenosine triptosphate (ATP), phosphocreatine], and turnover rates (creatine kinase reaction velocity) of high-energy phosphates [31P nuclear magnetic resonance (NMR)] and total creatine content [high-performance liquid chromatography (HPLC)]. RESULTS: Quinapril prevented post-MI hypertrophy and partially prevented left ventricular contractile dysfunction [maximum left ventricular developed pressure 166+/-6, 83+/-16 (p < 0.05 MI vs. Sham), 139+/-13 mm Hg (p < 0.05 quinapril treated vs. untreated) in Sham, MI and MI+Q hearts]. Residual intact failing myocardium showed a 17% decrease of MM-CK and a 16% decrease of mito-CK activity. Total creatine was reduced by 23%, phosphocreatine by 26% and CK reaction velocity by 30%. Parallel to improved function, treatment with quinapril largely prevented the impairment of energy metabolism occuring post-MI. CONCLUSIONS: quinapril treatment results in an improvement of high-energy phosphate metabolism, of energy reserve via the creatine kinase reaction, and of contractile performance post-MI.


Journal article


J Cardiovasc Magn Reson

Publication Date





215 - 225


Adenosine Triphosphate, Angiotensin-Converting Enzyme Inhibitors, Animals, Creatine Kinase, Disease Models, Animal, Energy Metabolism, Heart Failure, Isoquinolines, Magnetic Resonance Spectroscopy, Myocardial Infarction, Quinapril, Rats, Rats, Wistar, Tetrahydroisoquinolines, Ventricular Remodeling