title: Does nitric oxide contribute to progressive cardiac tissue damage and dysfunction after infarction?
abstract: Myocardial infarction induces contractile dysfunction and remodeling that can lead to heart failure. Nitric oxide has been proposed as one of the major actors of this pathophysiologic process. We note that N (G)-nitro-L-arginine methyl ester (L-NAME) administration from day 2 to day 7 after myocardial infarction in rats improves stroke volume, preserves cardiac compliance, and reduces infarct expansion. Our observations lead to the hypothesis that the mechanisms by which cytokines contribute to myocardial remodeling and dysfunction in the days after infarction might involve *NO signalling pathways.
authors.affiliation: Laboratoire TIMC-PRETA, UMR5525, IFRT 130, Université Joseph Fourier, Grenoble, France.
authors.forename: Corinne
authors.initials: C
authors.lastname: Berthonneche
authors.forename: Marie-Claire
authors.initials: MC
authors.lastname: Toufektsian
authors.forename: Stéphane
authors.initials: S
authors.lastname: Tanguy
authors.forename: Catherine
authors.initials: C
authors.lastname: Ghezzi
authors.forename: Joël
authors.initials: J
authors.lastname: de Leiris
authors.forename: François
authors.initials: F
authors.lastname: Boucher
mesh_terms: D000818:Animals; D018450:Disease Progression; D006331:Heart Diseases / Q000378:metabolism* / Q000473:pathology*; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism*; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar
chemical_list: D009569:Nitric Oxide; D052247:Nitric Oxide Synthase Type II