Nitric oxide (NO), produced in cardio myocytes by nitric oxide synthase, is a key regulator of myocardial function. It regulates vascular tone and structure, inhibits platelet aggregation and thrombus formation, leukocyte adhesion and vascular proliferation, resulting in vasodilator, anti-inflammatory and anti-aggregation effects. NO regulates cardiovascular function through two distinct pathways - indirect pathway via the soluble guanylate cyclase activation and direct pathway by the proteins S-nitrosylation. We suggest that reduced NO bioavailability underlies the development of acute coronary syndrome, and its severe form acute myocardial infarction. The aim of our research was the assessment of tissue content of nitric oxide derivatives (NOD) in isoproterenol-induced myocardial infarction in rats. The study was performed on 40 adult male rats (Ratta albicans) divided into 5 groups: sham (L1=11), control 0.9% NaCl (L2=11), and with experimental myocardial infarction (L3=6, L4=6; L5=6), induced by the subcutaneous injection o Isoproterenol Hydrochloride solution 100 mg/kg. Rats were sacrificed over 6 hours, 24 hours and 7 days respectively. Tissue content of nitric oxide derivatives (NOD) was evaluate using the method described by Метельская В. А. and Гуманова Н. Г. (2005), and modified by Gudumac V. et al. (2010). The results were presented as median and interquartile range. Groups were compared using Kruskal-Wallis and Dunn nonparametric tests (SPSS 23.0). The investigated groups have shown statistically insignificant difference for tissue NOD content (p < 0.05). There was registered initially a slight increase in L3 (+ 9%), followed by return to initial concentrations in L4, with a repeated increase in L5 (+ 7%). Our study results confirm that acute myocardial infarction is associated with reduced NO bioavailability due to increased oxidative stress and peroxynytrite formation. Exogenous supply of NO is beneficial and protects the myocardium from ischemia–reperfusion injury during cardiac ischemia.