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Progression of heart failure after myocardial infarction in the rat
Journal article   Open access   Peer reviewed

Progression of heart failure after myocardial infarction in the rat

J Francis, R. M Weiss, S. G Wei, A. K Johnson and R. B Felder
American journal of physiology. Regulatory, integrative and comparative physiology, Vol.281(5), pp.R1734-R1745
11/01/2001
DOI: 10.1152/ajpregu.2001.281.5.R1734
PMID: 11641147
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https://doi.org/10.1152/ajpregu.2001.281.5.R1734View
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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.

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