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Interleukin‐10 improves left ventricular function in rats with heart failure subsequent to myocardial infarction
Author(s) -
Stumpf Christian,
Seybold Katrin,
Petzi Sebastian,
Wasmeier Gerald,
Raaz Dorette,
Yilmaz Atilla,
Anger Thomas,
Daniel Werner G.,
Garlichs Christoph D.
Publication year - 2008
Publication title -
european journal of heart failure
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.149
H-Index - 133
eISSN - 1879-0844
pISSN - 1388-9842
DOI - 10.1016/j.ejheart.2008.06.007
Subject(s) - medicine , myocardial infarction , preload , heart failure , cardiology , cytokine , cardiac function curve , ventricular remodeling , inflammation , tumor necrosis factor alpha , chemokine , hemodynamics
Evidence has shown that pro‐inflammatory cytokines, especially TNF‐α, are involved in the inflammatory response in the remodelling process after myocardial infarction (MI). Although IL‐10, an anti‐inflammatory cytokine, has been shown to antagonize some of the deleterious effects of TNF‐α, little is known about its role in post‐MI left ventricular (LV) dysfunction. The aim of the present study was to investigate whether a therapy with rhIL‐10 could be beneficial in an animal model of post‐MI heart failure (HF). Rats with experimental MI were treated with rhIL‐10 (75 mn;g/kg/d sc) starting directly after MI induction, and continuing for 4 weeks. Controls were untreated MI and sham‐operated rats. Cardiac function was assessed by echocardiography and cardiac catheterization 4 weeks after MI induction. Membrane‐bound and soluble fractions of TNF‐α, IL‐6 and IL‐10, the ratio of TNF‐α to IL‐10, serum levels of MCP‐1 as well as myocardial macrophage infiltration, were analyzed. Treatment with rhIL‐10 significantly improved post‐MI LV function (FS +127%;, d P /d t max +131%; LVEDP–36%). This effect was associated with a significant decrease in pro‐inflammatory cytokine and chemokine levels (TNF‐α, IL‐6, MCP‐1) and furthermore resulted in a reduced myocardial infiltration of macrophages.