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L‐ arginine ameliorates experimental autoimmune myocarditis by maintaining extracellular matrix and reducing cytotoxic activity of lymphocytes
Author(s) -
Okabe Takaaki,
Hattori Miki,
Yuan Zuyi,
Kishimoto Chiharu
Publication year - 2008
Publication title -
international journal of experimental pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.671
H-Index - 72
eISSN - 1365-2613
pISSN - 0959-9673
DOI - 10.1111/j.1365-2613.2008.00609.x
Subject(s) - nitric oxide , arginine , myocarditis , cytotoxic t cell , nitric oxide synthase , extracellular , medicine , pharmacology , immunology , chemistry , endocrinology , biochemistry , amino acid , in vitro
Summary It was previously shown that administration of the nitric oxide synthase inhibitor N G ‐nitro‐ l‐ arginine methyl ester ( l‐ NAME) aggravated murine viral myocarditis by increasing myocardial virus titres. Experimental autoimmune myocarditis in mice and rats mimics human fulminant myocarditis. The effects of l‐ arginine, a precursor of nitric oxide, upon heart failure in experimental autoimmune myocarditis were evaluated. Dietary l‐ arginine ( l‐ arginine group) and l‐ arginine plus N G ‐nitro‐ l‐ arginine methyl ester ( l‐ arginine + l‐ NAME group) were administered to C57BL/6 mice immunized with porcine cardiac myosin over 3 weeks. An untreated myocarditis group was prepared. Cardiac damage was less in the l‐ arginine group compared with the other two groups, as was incidence of heart failure. In addition, extracellular matrix change was less prominent in the l‐ arginine group. Plasma concentrations of nitric oxide were elevated in the l‐ arginine group. Cytotoxic activities of lymphocytes were lower in l‐ arginine group than in other two groups. l‐ arginine treatment may be effective in preventing the development of heart failure in experimental myocarditis by maintaining extracellular matrix and reducing the cytotoxic activity of lymphocytes.