Aim To investigate the effects of nitric oxide (NO) in different concentration, nitric oxide synthase (NOS) activity and total antioxidative capability (T-AOC) in cardiac tissue, and the influence of isosorbide dinitrate (ISDN) in different dose after myocardial infarction (MI). Methods 32 New Zealand rabbits were randomly divided into four groups: sham-operated group, MI group, low dose of ISDN group (LISDN, 1.5 mg/kg·d), high dose of ISDN group (HISDN, 4.0 mg/kg·d), with the drugs gastric gavage three times everyday for six weeks. The NO concentration, all isoforms of NOS activity and T-AOC of cardiac tissue homogenate, adjacent to the infarcted area, were detected. The pathological changes were observed by microscope and electron microscope. Results The NO concentrations of MI group and HISDN group were higher than those of sham-operated group and LISDN group (0.980±0.180 μmol/g, 1.112±0.210 μmol/g, 0.497±0.129 μmol/g, 0.637±0.126 μmol/g, p<0.05 or 0.01). The inducible NOS (iNOS )activity in myocardial tissue of MI group and HISDN group was higher than that of sham-operated group and LISDN group (1 519±175 u/g, 1 659±175 u/g, 565±112 u/g, 852±106 u/g, p<0.01), while T-AOC was lower (856±183 u/g, 901±174 u/g, 1 654±207 u/g, 1 467±302 u/g,p<0.05). And constitutive NOS (cNOS) activity in myocardial tissue of MI group and HISDN group was lower than that of sham-operated group and LISDN group (1 034±301 u/g, 903±274 u/g, 1 615±227 u/g, 1 436±210 u/g, p<0.05). The injured pathological changes were light in sham-operated group and LISDN group. Conclusion High concentration of NO decreased the antioxidative capability of cardiomyocyte and led to injury after MI while low concentration of NO showed beneficial effects.