Document Detail


Effects of long-term therapy with ACE inhibitors, captopril, enalapril and trandolapril, on myocardial energy metabolism in rats with heart failure following myocardial infarction.
MedLine Citation:
PMID:  8576937     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Although pharmacological therapy with angiotensin converting enzyme (ACE) inhibitors has proved to be effective in patients with heart failure (HF), the experimental basis of this effect has not yet been addressed. In the present study, animals with HF were treated with an oral administration of 10 mg/kg/day captopril, 10 mg/kg/day enalapril and 3 mg/kg/day trandolapril from the 2nd to 12th week after the operation. HF was induced by permanent occlusion of the left coronary artery of the rat at 2 mm from its origin. Treatment of the HF rats with the ACE inhibitors enhanced the decrease in mean arterial blood pressure, attenuated the rise in left ventricular end-diastolic pressure, an indirect marker of preload, and diminished the reduction in cardiac output and stroke volume indices of the HF animal. Treatment also reversed the reduction in ATP, creatine phosphate, creatine and the mitochondrial oxygen consumption rate of the viable left and right ventricles of the HF animal. The improvement of the cardiac output index and high-energy phosphate levels of the HF rat by the ACE inhibitors was associated with the recovery of the mitochondrial oxygen consumption rate. In sham-operated animals, treatment with the ACE inhibitors reduced mean arterial pressure and left ventricular systolic pressure, but not metabolic variables concerning myocardial energy metabolism. The present results provide evidence that ACE inhibitor therapy improves cardiac function and myocardial energy metabolism of experimental animals with chronic heart failure. The mechanism underlying the benefit of long-term treatment with ACE inhibitors is probably attributable to recovery or preservation of the mitochondrial function and reduction in preload.
Authors:
A Sanbe; K Tanonaka; R Kobayasi; S Takeo
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of molecular and cellular cardiology     Volume:  27     ISSN:  0022-2828     ISO Abbreviation:  J. Mol. Cell. Cardiol.     Publication Date:  1995 Oct 
Date Detail:
Created Date:  1996-03-13     Completed Date:  1996-03-13     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0262322     Medline TA:  J Mol Cell Cardiol     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  2209-22     Citation Subset:  IM    
Affiliation:
Department of Pharmacology, Tokyo University of Pharmacy and Life Science, Japan.
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MeSH Terms
Descriptor/Qualifier:
Adenine Nucleotides / metabolism
Angiotensin-Converting Enzyme Inhibitors / pharmacology,  therapeutic use*
Animals
Captopril / pharmacology,  therapeutic use
Enalapril / pharmacology,  therapeutic use
Energy Metabolism / drug effects
Heart Failure / drug therapy*,  etiology,  metabolism
Hemodynamics / drug effects
Indoles / pharmacology,  therapeutic use
Lactates / metabolism
Male
Mitochondria, Heart / drug effects,  metabolism
Myocardial Infarction / complications*,  pathology
Myocardium / pathology
Organ Size / drug effects
Oxygen Consumption / drug effects
Phosphocreatine / metabolism
Rats
Rats, Wistar
Chemical
Reg. No./Substance:
0/Adenine Nucleotides; 0/Angiotensin-Converting Enzyme Inhibitors; 0/Indoles; 0/Lactates; 62571-86-2/Captopril; 67-07-2/Phosphocreatine; 75847-73-3/Enalapril; 87679-37-6/trandolapril

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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