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This Article Full Text Full Text (PDF) All Versions of this Article: 293/5/H3014    most recent 00797.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Moro, C. Articles by Boucher, F. Search for Related Content PubMed PubMed Citation Articles by Moro, C. Articles by Boucher, F.

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

¹Coeur and Nutrition, Laboratoire Techniques de l'Imagerie, de la Modélisation et de la Cognition-Physiologie Cardio-Respiratoire, Expérimentale, Therapeutique et Appliquée, Domaine de la Merci, University of Grenoble, and ²Service de Cardiologie et Hypertension Arterielle, le Centre Hospitalier Universitaire, Grenoble, France; and ³Department of Pharmacology, Health and Science Center, University of Debrecen, Debrecen, Hungary

Submitted 10 July 2007 ; accepted in final form 10 September 2007

Previous studies have shown that 1 wk after permanent coronary artery ligation in rats, some cellular mechanisms involving TNF- 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- 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-, IL-1, IL-6, cytokine-induced neutrophil chemoattractant (CINC) 2, CINC3, and macrophage inflammatory protein-3 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.

myocardial ischemia; tumor necrosis factor-