Cardiovascular diseases cause 17.3 million deaths worldwide, about 10% are due to acute myocardial infarction - the most lethal form of IHD. Prolonged ischemia and hypoxia stimulates the generation of reactive oxygen species resulting i oxidative stress, metabolic disturbances and cardiomyocites injury. Small animal models are usually used to study the pathobiochemical mechanisms underlying the human pathologies. Forty adult male rats were randomly divided into 5 groups: sham (L1=11), control 0.9% NaCl (L2=11), and experimental myocardial infarction (L3=6, L4=6; L5=6), induced by the subcutaneous injection of Isoproterenol Hydrochloride solution 100 mg/kg, and sacrificed over 6 hours, 24 hours and 7 days respectively. Tissue malonil dialdehyde (MDA), ischemia modified albumin (IMA) and lactate values were evaluate. The results were presented by median and interquartile range. Groups were compared using Kruskal-Wallis and Dunn nonparametric tests (SPSS 23.0). The investigated groups have shown statistically significant difference for tissue levels of MDA and lactate (p < 0.05), but IMA content was statistically insignificant (p ˃ 0.05). Both MDA and IMA content in tissue have presented initially a slight increase in L3, followed by a significant decrease in L4, with a return in L5 to the baseline levels. The dynamics of lactate values was opposite: the decrease in L3, return to initial concentrations in L4, and decrease again in L5. Our study prove that high doses of isoproterenol exacerbate oxidative stress, alter cell membrane permeability, and induce metabolic disturbances and ireversible lesions in cardiac tissue. Isoproterenol induced model offers the opportunity to study biochemical mechanisms of acute myocardial infarction.