Enalapril and Losartan Are More Effective Than Carvedilol in Preventing Dilated Cardiomyopathy in the Syrian Cardiomyopathic Hamster

To assess the role of the renin—angiotensin (RAS) and adrenergic systems in the development and progression of dilated cardiomyopathy in the Syrian cardiomyopathic hamster (SCH), echocardiographic parameters were evaluated in 6-month-old animals after 5 months of treatment with enalapril (25 mg/kg/d...

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Published in:Journal of cardiovascular pharmacology and therapeutics 2008-09, Vol.13 (3), p.199-206
Main Authors: Crespo, Maria J., Cruz, Nildris, Altieri, Pablo I., Escobales, Nelson
Format: Article
Language:English
Subjects:
Adrenergic beta-Antagonists - pharmacology
Angiotensin II Type 1 Receptor Blockers - pharmacology
Angiotensin-Converting Enzyme Inhibitors - pharmacology
Animals
Blood Pressure - drug effects
Carbazoles - pharmacology
Cardiac Output - drug effects
Cardiomyopathy, Dilated - diagnostic imaging
Cardiomyopathy, Dilated - physiopathology
Cardiomyopathy, Dilated - prevention & control
Cricetinae
Disease Models, Animal
Disease Progression
Enalapril - pharmacology
Losartan - pharmacology
Male
Mesocricetus
Propanolamines - pharmacology
Renin-Angiotensin System - drug effects
Stroke Volume - drug effects
Time Factors
Ultrasonography
Ventricular Function, Left - drug effects
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Summary:To assess the role of the renin—angiotensin (RAS) and adrenergic systems in the development and progression of dilated cardiomyopathy in the Syrian cardiomyopathic hamster (SCH), echocardiographic parameters were evaluated in 6-month-old animals after 5 months of treatment with enalapril (25 mg/kg/day) plus losartan (10 mg/kg/day), or with carvedilol (1 mg/kg/day). Cardiac output indexes (COI) increased by 53% after RAS blockade and by 20% after β-blockade in SCH. Moreover, LVEDV and LVESV decreased 30% and 62%, respectively (P < .05) during RAS blockade, whereas ejection fraction (EF) increased by 48%. By contrast, carvedilol reduced LVESV by only 28% (P < .05) and increased EF by only 15% (P < .05). These results suggest that RAS activation plays a critical role in the development of cardiac dysfunction in SCH and that suppression of RAS may be more effective than β-blockade in retarding the development of cardiomyopathy in SCH. Owing to timing (pre—heart failure stage) and to the single dose protocol, the implications of this study for human subjects remain to be clarified.
ISSN:1074-2484
1940-4034
DOI:10.1177/1074248408320006