| Summary: | Scar smoothing out, angiogenesis stimulation and cardiomyogenesis in myocardial infarction still remain pressing issues despite the variety of existing methods. One of the ways to correct them is intramyocardial implantation of an alloplant biomaterial (ABM) suspension. ABM serves as an inhibitor of fibroneogenesis in various tissues with chronic inflammatory processes. No studies have been carried out with regards to acute myocardial infarction. Objective: to assess the dynamics of the number of bFGF-1 + cells and CD68 macrophages, the degree of angiogenesis amidst the use of ABM in the formation of postinfarction scar in the experiment. Materials and methods. Experimental studies were performed on 100 male Wistar rats weighing 0.18–0.25 kg. Coronary artery ligation was performed on all animals. In the experimental group, the ABM suspension (12 mg) was injected intramyocardially. We used histological, electron microscopic, immunohistochemical (CD68, bFGF-1), morphometric and statistical research methods. Hearts were procured at day 3, 7, 14, 30, and 45. Results. The use of an allogeneic biomaterial immediately after coronary artery stenosis could reduce the area of cicatricial myocardial degeneration by two fold by accelerating inflammatory response and the onset of early proliferative phase. In the reactive zone after ABM implantation, macrophage myocardial infiltration significantly decreased in comparison to the control group. The use of ABM ensures significant predominance of bFGF-1+ cells in the initial period of inflammation (3–14 days). Subsequently (14–45 days), inflammatory cytokine expression became several times less, which corresponded to biodegradation and resorption of the biomaterial. In the control group, during the acute phase of inflammation (3–14 days), bFGF-1+ cells were low in number. Subsequently (14–45 days), cytokine expression increased significantly, causing rapid accumulation of collagen fibers and scarring. In myocardial regeneration after a heart attack in the experiment, ABM stimulated angiogenesis, whose level was three times higher than in the control group. It was noted that ABM serves as a regulator of the neofibrillogenesis-fibroclasia balance in tissue. Conclusion. Macrophage migration inhibition and suppression of pro-inflammatory orientation of macrophages should be indicated as one of the directions of therapeutic correction strategy for ischemic myocardial injuries. Alloplant biomaterial used in the acute phase of myocardial inflammation can serve as such alternative.
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