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Progression of heart failure after myocardial infarction in the rat

Progression of heart failure after myocardial infarction in the rat Abstract This study examined the early neurohumoral events in the progression of congestive heart failure (CHF) after myocardial infarction (MI) in rats. Immediately after MI was induced by coronary artery ligation, rats had severely depressed left ventricular systolic function and increased left ventricular end-diastolic volume (LVEDV). Both left ventricular function and the neurohumoral indicators of CHF underwent dynamic changes over the next 6 wk. LVEDV increased continuously over the study interval, whereas left ventricular stroke volume increased but reached a plateau at 4 wk. Plasma renin activity (PRA), arginine vasopressin, and atrial natriuretic factor all increased, but with differing time courses. PRA declined to a lower steady-state level by 4 wk. Six to 8 wk after MI, CHF rats had enhanced renal sympathetic nerve activity and blunted baroreflex regulation. These findings demonstrate that the early course of heart failure is characterized not by a simple “switching on” of neurohumoral drive, but rather by dynamic fluctuations in neurohumoral regulation that are linked to the process of left ventricular remodeling. left ventricular function echocardiography neurohumoral regulation sympathetic nerve activity paraventricular nucleus of hypothalamus Footnotes Support for this project was provided by a U.S. Department of Veterans Affairs Merit Review (R. B. Felder), American Heart Association Grant-in-Aid 96–010430 (R. M. Weiss), and National Heart, Lung, and Blood Institute Cardiovascular Interdisciplinary Research Fellowship HL-07121 (to J. Francis). Address for reprint requests and other correspondence: R. B. Felder, Dept. of Internal Medicine, E-318 GH, Univ. of Iowa College of Medicine, 200 Hawkins Dr., Iowa City, IA 52242 (E-mail: robert-felder@uiowa.edu ). The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked “ advertisement ” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. Copyright © 2001 the American Physiological Society http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Regulatory, Integrative and Comparative Physiology The American Physiological Society

Progression of heart failure after myocardial infarction in the rat

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Publisher
The American Physiological Society
Copyright
Copyright © 2011 the American Physiological Society
ISSN
0363-6119
eISSN
1522-1490
Publisher site
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Abstract

Abstract This study examined the early neurohumoral events in the progression of congestive heart failure (CHF) after myocardial infarction (MI) in rats. Immediately after MI was induced by coronary artery ligation, rats had severely depressed left ventricular systolic function and increased left ventricular end-diastolic volume (LVEDV). Both left ventricular function and the neurohumoral indicators of CHF underwent dynamic changes over the next 6 wk. LVEDV increased continuously over the study interval, whereas left ventricular stroke volume increased but reached a plateau at 4 wk. Plasma renin activity (PRA), arginine vasopressin, and atrial natriuretic factor all increased, but with differing time courses. PRA declined to a lower steady-state level by 4 wk. Six to 8 wk after MI, CHF rats had enhanced renal sympathetic nerve activity and blunted baroreflex regulation. These findings demonstrate that the early course of heart failure is characterized not by a simple “switching on” of neurohumoral drive, but rather by dynamic fluctuations in neurohumoral regulation that are linked to the process of left ventricular remodeling. left ventricular function echocardiography neurohumoral regulation sympathetic nerve activity paraventricular nucleus of hypothalamus Footnotes Support for this project was provided by a U.S. Department of Veterans Affairs Merit Review (R. B. Felder), American Heart Association Grant-in-Aid 96–010430 (R. M. Weiss), and National Heart, Lung, and Blood Institute Cardiovascular Interdisciplinary Research Fellowship HL-07121 (to J. Francis). Address for reprint requests and other correspondence: R. B. Felder, Dept. of Internal Medicine, E-318 GH, Univ. of Iowa College of Medicine, 200 Hawkins Dr., Iowa City, IA 52242 (E-mail: robert-felder@uiowa.edu ). The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked “ advertisement ” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. Copyright © 2001 the American Physiological Society

Journal

AJP - Regulatory, Integrative and Comparative PhysiologyThe American Physiological Society

Published: Nov 1, 2001

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