Delayed expression of cytokines after reperfused myocardial infarction: Possible trigger for cardiac dysfunction and ventricular remodeling

Cécile Moro, Marie Gabrielle Jouan, Andry Rakotovao, Marie Claire Toufektsian, Olivier Ormezzano, Norbert Nagy, A. Tósaki, Joël De Leiris, François Boucher

Research output: Contribution to journalArticle

33 Citations (Scopus)

Abstract

Previous studies have shown that 1 wk after permanent coronary artery ligation in rats, some cellular mechanisms involving TNF-α occur and contribute to the development of cardiac dysfunction and subsequent heart failure. The aim of the present study was to determine whether similar phenomena also occur after ischemia-reperfusion and whether cytokines other than TNF-α can also be involved. Anesthetized male Wistar rats were subjected to 1 h coronary occlusion followed by reperfusion. Cardiac geometry and function were assessed by echocardiography at days 5, 7, 8, and 10 postligation. Before death, heart function was assessed in vivo under basal conditions, as well as after volume overload. Finally, hearts were frozen for histoenzymologic assessment of infarct size and remodeling. The profile of cardiac cytokines was determined by ELISA and ChemiArray on heart tissue extracts. As expected, ischemia-reperfusion induced a progressive remodeling of the heart, characterized by left ventricular free-wall thinning and cavity dilation. Heart function was also decreased in ischemic rats during the first week after surgery. Interestingly, a transient and marked increase in TNF-α, IL-1β, IL-6, cytokine-induced neutrophil chemoattractant (CINC) 2, CINC3, and macrophage inflammatory protein-3α was also observed in the myocardium of myocardial ischemia (MI) animals at day 8, whereas the expression of anti-inflammatory interleukins IL-4 and IL-10 remained unchanged. These results suggest that overexpression of proinflammatory cytokines occurring during the first week after ischemia-reperfusion may play a role in the adaptative process in the myocardium and contribute to early dysfunction and remodeling.

Original languageEnglish
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume293
Issue number5
DOIs
Publication statusPublished - Nov 2007

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Ventricular Remodeling
Myocardial Infarction
Reperfusion
Cytokines
Ischemia
Interleukin-4
Myocardium
Chemokine CXCL2
Tissue Extracts
Coronary Occlusion
Chemotactic Factors
Interleukin-1
Interleukin-10
Myocardial Ischemia
Ligation
Echocardiography
Wistar Rats
Dilatation
Interleukin-6
Coronary Vessels

Keywords

  • Myocardial ischemia
  • Tumor necrosis factor-α

ASJC Scopus subject areas

  • Physiology

Cite this

Delayed expression of cytokines after reperfused myocardial infarction : Possible trigger for cardiac dysfunction and ventricular remodeling. / Moro, Cécile; Jouan, Marie Gabrielle; Rakotovao, Andry; Toufektsian, Marie Claire; Ormezzano, Olivier; Nagy, Norbert; Tósaki, A.; De Leiris, Joël; Boucher, François.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 293, No. 5, 11.2007.

Research output: Contribution to journalArticle

Moro, Cécile ; Jouan, Marie Gabrielle ; Rakotovao, Andry ; Toufektsian, Marie Claire ; Ormezzano, Olivier ; Nagy, Norbert ; Tósaki, A. ; De Leiris, Joël ; Boucher, François. / Delayed expression of cytokines after reperfused myocardial infarction : Possible trigger for cardiac dysfunction and ventricular remodeling. In: American Journal of Physiology - Heart and Circulatory Physiology. 2007 ; Vol. 293, No. 5.
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AU - Ormezzano, Olivier

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