Does nitric oxide contribute to progressive cardiac tissue damage and dysfunction after infarction?
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.
Berthonneche
Corinne
C
Laboratoire TIMC-PRETA, UMR5525, IFRT 130, Université Joseph Fourier, Grenoble, France.
Toufektsian
Marie-Claire
MC
Tanguy
Stéphane
S
Ghezzi
Catherine
C
de Leiris
Joël
J
Boucher
François
F
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
D009569:Nitric Oxide; D052247:Nitric Oxide Synthase Type II