Introduction: Sepsis is a life-threatening condition characterized by organ dysfunction evoked by an abnormal host response to an infectious process. Statins, a class of lipid-lowering agents, possess immunomodulatory effects. Having in mind the potential benefit of treatment with statins in sepsis, we aimed to investigate the effects of statins on cardiac function and cardiac oxidative stress (OS) in the experimental sepsis rat model. Methodology: Thirty Wistar Albino rats (males, 8-weeks old, BW were randomly divided into 2 groups: Control group (C,) and animals with induced sepsis (SEPSIS,). After induced sepsis, all animals from the SEPSIS group were randomly divided into 4 subgroups: animals with induced sepsis without treatment (S), animals with induced sepsis treated with a single dose of Atorvastatin, Simvastatin, and Rosuvastatin. After 72h from sepsis induction, all animals were sacrificed and hearts were isolated and perfused according to the Langendorff technique gradually increasing coronary perfusion pressures 40–120 cmH20. In coronary venous effluent were determined the biomarkers of cardiac OS. All data were analyzed by one-way Anova and Kruskal-Wallis tests $(p < 0.05)$. Results: There were no changes in cardiodynamic parameters in septic rats without treatment, as well in those treated with statins, except for coronary flow, where its values were statistically increased in the sepsis group compared to all other groups. Also, sepsis was associated with disturbed cardiac OS and most of the applied therapeutic protocols of statins have mitigated the release of hydrogen peroxide and lipid peroxidation index, while in the case of superoxide anion radical, only atorvastatin at CPP 120 cmH2O had such a positive effect. Conclusion: Given the conditions of the current experiment, we can generally conclude that the rat's hearts in septic conditions were exposed to elevated OS which was not related to its functional changes. Additionally, statin therapy has achieved positive effects in terms of reduced release of molecules that could cause oxidative damage to the rat heart.