Аннотация:Myocardial infarction is the lead cause of death from cardiovascular diseases and is characterized by im-paired blood flow to the heart, massive death of cardiomyocytes (CMC) by necrosis and by apoptosis [1]. The death of CMC is accompanied by the development of inflammation. Reperfusion leads to the activa-tion of free-radical mechanisms of myocardial damage and the generalization of the inflammatory reac-tion [2]. During the first three days from the beginning of the ischemia-reperfusion (IR), cells of the mon-ocyte-macrophage type (MM) circulating in the bloodstream migrate to the affected area along the gradi-ent of chemokines and other regulatory factors. These cells differentiate into tissue macrophages that phagocytize damaged tissues and attract even more monocytes to the lesion area [3-5]. The main chemo-kine secreted by macrophages that recruits MM to the affected area is monocyte chemoattractant protein -1 (MCP-1). MCP-1 belongs to the family of CC-chemokines and is expressed by a wide range of cells: MM, endothelial cells, fibroblasts and others. It is a ligand of G-protein coupled receptor CCR2 [6–8]. Over the years, leading scientists from the Institute of Experimental Cardiology of the Ministry of Health of the Russian Federation developed an approach to regulation of the inflammatory reaction using frag-ments of the MCP-1 molecule [9–11]. In the present study we evaluated the effect of peptide IX, a 29–40 amino acid fragment of MCP-1, on the development of myocardial infarction in rats. Earlier, the team working on this topic demonstrated that in Boyden chamber peptide IX stimulated the monocyte migra-tion by itself (in a higher extent then MCP-1), in human blood in in vitro experiments and it increased the MCP-1-induced migration of THP-1 promonocyte cells and monocytes, and in in vivo models in rats pep-tide X attracted leukocytes and accelerated wound healing [11]. In previous joint studies, we showed an interesting result was that the introduction of the peptide resulted in a 6-fold decrease in mortality, along with a decrease in weight gain in rats. The size of myocardial damage remained unchanged [12–14].
The purpose of this study was to investigate the effect of peptide IX on the development of hemody-namic disorders in rats in the IR model at the peak of the inflammatory response and in the delayed post-infarction period.
