Background. It was shown earlier that high-density lipoproteins of rat blood plasma increased the frequency and strength of contraction of an isolated rat heart. The main protein component of high-density lipoproteins, apolipoprotein A-I, isolated from human blood plasma, increased the force of cardiac contractions, with little effect on the frequency. A method for obtaining recombinant apolipoprotein A-I developed at the Institute of Biochemistry allows for facilitating the research into cardiotropic properties of this protein.Aim. The purpose of this experiment was to study the effect of recombinant apolipoprotein A-I on the performance of an isolated rat heart and to compare it with the action of native apolipoprotein A-I.Methods. The experiment was performed on Wistar male rats weighing 230–250 g. Isolated hearts of the rats were routinely perfused retrograde, and isovolume pressure in the left ventricle was measured. Recombinant apolipoprotein A-I was obtained in E. coli cells in the form of a chimeric polypeptide followed by the conversion of protein into a mature form of recombinant apolipoprotein A-I.Results. It was shown that recombinant apolipoprotein A-I with a concentration of 20 μg/ml caused a stable increase in pressure in the left ventricle, while the magnitude of the coronary flow and heart rate changed insignificantly. The maximum inotropic effect was registered for 20 min from the beginning of perfusion and amounted to 147.5% relative to the reference values. It was found out that in the presence of recombinant apolipoprotein A-I, the maximum rate of contraction of the left ventricle increased. At the same time, the diastole had a tendency to increase and was larger in comparison with the initial data at 10 and 20 minutes of perfusion.Conclusion. The recombinant apolipoprotein A-I under study has cardiotonic properties similar to its native form. However, the mechanism for implementing the inotropic effect requires further study.Received 3 September 2018. Revised 8 October 2018. Accepted 11 October 2018.Funding: The study did not have sponsorship.Conflict of interest: Authors declare no conflict of interest.Author contributionsConception and study design: A.R. Kolpakov, R.A. KnyazevData collection and analysis: N.V. Trifonova, A.V. Ryabchenko, M.V. KotovaCritical revision of the article: R.A. KnyazevDrafting the article R.A. KnyazevCritical revision of the article: A.R. Kolpakov, L.M. Polyakov Final approval of the version to be published: R.A. Knyazev, N.V. Trifonova, A.V. Ryabchenko, M.V. Kotova, A.R. Kolpakov, L.M. Polyakov