Myocardial infarction is one of the common cardiovascular diseases. Sodium overload in the myocardium is another of the most important mechanisms underlying ischemia/reperfusion injury. Na⁺ entry into the cell through ion channels can be controlled using peptide toxins targeting ion channels. In our work, we analyze the use of mu-agatoxin-Aa1a, as a sodium channel modulator, as a cytoprotective agent in ischemia/reperfusion injury. For IRI modeling in vitro, the H9C2 culture was placed under oxygen-glucose deprivation conditions followed by reperfusion. Cell death and ion dynamics were recorded using a fluorescent plate reader. Reversible myocardial ischemia of rats in vivo was created by applying an occluder under the main branch of the left coronary artery. Histological and biochemical changes were recorded. The study demonstrated the ability of mu-agatoxin-Aa1a myocardial cells to adapt to rapidly changing extracellular conditions upon restoration of normal blood flow after a period of ischemia. Thus, the study allows us to consider mu-agatoxin-Aa1a as a biologically active molecule with a targeted effect to enhance the adaptation of cardiomyocytes to OGD/reperfusion conditions.