Introduction. Experimental modeling on small laboratory animals (mice, rats) allows the elucidation of the intracellular biochemical mechanisms underlying the cardiac ischemia. Isoproterenol, a non-selective synthetic beta-agonist, used in high doses induces severe oxidative stress accompanied by intracellular acidosis with increased membrane permeability. The research aim was to identify the metabolic changes induced by isoproterenol in cardiac tissue in order to prove the utility and reliability of chemical non-invasive methods for experimental studies. The study design was approved by Research Ethics Committee. Material and methods. The research was performed on 40 male adult rats randomly divided into 5 groups: sham, control (only solution of 0.9% NaCl), experimental (solution of Isoproterenol Hydrochloride 100 mg/ kg subcutaneously one dose) – AMI.6h, AMI.24h, AMI.7d. The amount of ischemia-modified albumin (IMA) and advanced oxidation protein products (AOPP) were assessed in serum. Statistical analysis was performed by applying KruskalWallis and Mann-Whitney nonparametric tests (SPSS 23.0 software). Results. The highest serum values of IMA (by 20%, p<0.05*), and AOPP (by approximately 24%, p>0.5) compared to sham and control groups were recorded in the experimental pre-infarction AMI.6h group. The subsequent dynamics is accompanied by the reduction of IMA levels by 11% in AMI.24h, the same values being maintained in AMI.7d (p<0.05*), while AOPP amount recorded a tendency to maintain elevated levels (by 21%) in the state of infarct (AMI.24h) and post-infarction (AMI.7d) (by 22%, p>0.5). The serum content of AOPP, compared to IMA, was insignificantly higher in all experimental groups (p>0.5). Conclusion. The elevated amount of IMA and AOPP in early diagnostics of acute myocardial infarction detects pre-infarction state with reversible ischemic alterations. Proper medication prevents necrosis and improves the clinical outcome. Further enlarged studies are required.