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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Animals, Cell Differentiation, Cell Survival, Echocardiography, Fetal Tissue Transplantation, Immunohistochemistry, Male, Myocardial Infarction, Myocytes, Cardiac, Rats, Rats, Wistar, Regeneration.
user
Does [ Transplantation of fetal cardiomyocyte regenerate infarcted myocardium in rats ]? Context: To investigate the feasibility and efficiency of fetal cardiomyocyte transplantation into the rat model of myocardial infarction. Cardiomyocytes were isolated from aborted human embryos aged 12 - 16 weeks and cultured for 5 days to confirm their viability. Rat model of extensive myocardial infarction (MI) was established in 18 male Wistar rats by ligating the descending anterior branch of left coronary artery and the 18 rats were randomly divided into 2 groups: transplantation group (n = 7, 2 x 10(6) fetal cardiomyocytes were transplanted into the myocardial scar) and culture medium injection group (n = 6, culture medium was injected into the myocardial scar) 5 days after extensive MI was caused. Another 6 rats undergoing sham operation were used as controls. Echocardiography was performed before and 60 +/- 3 days after the implantation to assess the left ventricular (LV) remodeling and cardiac function. Then the rats were killed and their heart were harvested to undergo HE staining, immunohistochemical examination with antibody against human alpha-actin smooth muscle (SMA) isoform, and light microscopy. Light microscopy revealed the presence of engrafted human fetal cardiomyocytes in the infarcted myocardium and the presence of nascent intercalated disks connecting the engrafted fetal cardiomyocytes and the host myocardium. The engrafted fetal cardiomyocytes were SMA positive. Serial echocardiography revealed that cell transplantation prevented scar thinning, LV further dilatation and dysfunction while the control animals developed scar thinning, significant LV dilatation accompanied by progressive deterioration in LV contractility.
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Fetal cardiomyocytes can be implanted and survive in the infarcted myocardial cells, thus preventing the scar thinning, and LV further dilatation and dysfunction. Final Decision: yes