alexa Reversal of Cardiac Remodeling and Subcellular Defects by Prazosin in Heart Failure Due to Myocardial Infarction | OMICS International
ISSN: 2155-9880

Journal of Clinical & Experimental Cardiology
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Research Article

Reversal of Cardiac Remodeling and Subcellular Defects by Prazosin in Heart Failure Due to Myocardial Infarction

Andrea Babick, Vijayan Elimban and Naranjan S. Dhalla*
Institute of Cardiovascular Sciences, St Boniface Hospital Research, Department of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada
Corresponding Author : Naranjan S. Dhalla
Institute of Cardiovascular Sciences
St. Boniface Hospital Research, 351 Tache Avenue Winnipeg
MB Canada R2H 2A6
Tel: (204) 235-3417
Fax: (204) 237-0347
E-mail: [email protected]
Received June 27, 2012; Accepted July 25, 2012; Published July 27, 2012
Citation: Babick A, Elimban V, Dhalla NS (2012) Reversal of Cardiac Remodeling and Subcellular Defects by Prazosin in Heart Failure Due to Myocardial Infarction. J Clin Exp Cardiolog S5:009.doi:10.4172/2155-9880.S5-009
Copyright: © 2012 Babick A, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Abstract

Background: This study was undertaken to test if α-Adrenoceptor (AR) blockade with prazosin reverses cardiac remodeling and ameliorates subcellular defects in heart failure due to Myocardial Infarction (MI). Methods: Heart failure in rats was induced by MI for 12 wks and then treated with or without prazosin (10 mg/kg/ day) for 8 wks. Both control and experimental animals were assessed hemodynamically and echocardiographically for evaluating changes in heart function and cardiac remodeling, respectively. Left Ventricle (LV) was used for determining biomedical and molecular activities. Results: Cardiac dysfunction, as evident from depressed LV systolic pressure, rates of changes in pressure development and decay, cardiac output, ejection fraction and fractional shortening as well as increased LV end diastolic pressure, in 20 wks infarcted animals, was corrected partially by prazosin treatment. Different parameters of cardiac remodeling including increased LV posterior wall thickness and LV systolic diameter in failing hearts were fully or partially reversed whereas increased LV diastolic diameter was unaltered by prazosin therapy. Reversal of lung congestion and cardiac hypertrophy in MI animals by prazosin was associated with depression in the elevated levels of plasma norepinephrine, unlike epinephrine or dopamine. Depressions in Sarcoplasmic Reticular (SR) Ca2+-uptake activity as well as protein content for Ca2+-pump ATPase and phospholamban in failing hearts were reversed partially whereas depressed SR Ca2+-release activity and myofibrillar Ca2+-stimulated ATPase activity were not affected by prazosin. Alterations in mRNA levels for SR Ca2+-pump ATPase, SR Ca2+-release channels, and α-myosin heavy chain and β-myosin heavy chain in MI-induced heart failure were not influenced by prazosin treatment. Conclusions: It is suggested that the activation of α-AR system may be associated with cardiac remodeling and heart failure and the reverse cardiac remodeling by α-AR blockade may improve cardiac performance by attenuating defects in SR Ca2+-pump.

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