l-arginine ameliorates experimental autoimmune myocarditis by maintaining extracellular matrix and reducing cytotoxic activity of lymphocytes

摘要

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.