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Objective: To cultivate the high purity of the experimental requirements rat bone marrow mesenchymal stem cells (BM-MSCs) and the identification of multipotent differentiation capacity, for further research laid the foundation. Methods: whole bone marrow adherent cultured rat BM-MSCs culture, cell morphology and growth characteristics were observed, and the application of flow cytometry for phenotypic identification of cell surface antigens of CD34, CD44, CD45, CD90, induced BM -MSCs differentiation of osteogenic, adipogenic and into cardiomyocytes. Results: BM-MSCs whole bone marrow culture method for the fibroblast-like cells, showed a colony-style growth. The majority of cells expressed CD44 (98.81%), CD90 (99.18%), and a very small amount of cells expressing CD34 (1.49%), CD45 (9.84%). Cultured cells under certain conditions to the fat cells, bone cells and cardiomyocyte-like cells induced to differentiate. Conclusion: The whole bone marrow adherence screening method is simple to obtain with multiple differentiation potential and higher purity of rat BM-MSCs fast cell proliferation, which can meet the demand for further in vitro and in vivo experiments. Objective To investigate the BM-MSCs transplantation for myocardial infarction, left ventricular function. SD rats as experimental study, ligation of the left anterior descending branch of the myocardial infarction model (MI) were randomly divided into a control group (only thoracotomy without ligation), infarction (anterior descending branch of the left coronary artery ligation injection of normal saline) and myocardial infarction BM-MSCs group (intervention group) (ligation after injection of DiI labeled BM-MSCs). 4 weeks after ultrasound detection of left ventricular diastolic diameter (LVEDD), left ventricular systolic diameter (LVESD) and left ventricular ejection fraction (LVEF) and fractional shortening (FS) and other indicators. Results Compared with the control group, the infarction group and intervention group LVESD significantly expand (3.33 ± 0.38 vs 7.26 ± 1.05 vs 4.49 ± 0.53, p lt; 0.05), LVEF (82.18 ± 3.34 vs 43.32 ± 6.63 vs 69.46 ± 7.81, p lt ; 0.05) and FS (45.71 ± 3.46 vs 18.76 ± 3.39 vs 34.84 ± 5.94, p lt; 0.05) significantly reduced infarction group LVEDD (6.18 ± 0.36 vs 8.94 ± 1.21, p lt; 0.05) significantly expand. Compared with the MI group, the intervention group LVEDD (8.94 ± 1.21 vs 6.86 ± 0.34, p lt; 0.05) and LVESD (7.26 ± 1.05 vs 4.49 ± 0.53, p lt; 0.05) significantly reduced LVEF (43.32 ± 6.63 vs 69.46 ± 7.81, p lt; 0.05) and FS (18.76 ± 3.39 vs 34.84 ± 5.94, p lt; 0.05) was significantly higher. Conclusion BM-MSCs transplantation can partially improve heart function in rats after MI. Objective To investigate the impact of BM-MSCs transplantation of rat ventricular arrhythmias after myocardial infarction. SD rats as subjects, ligation of the left anterior descending branch of myocardial infarction model (MI) were randomly divided into a control group (only thoracotomy without ligation), infarction (descending artery ligation of the left coronary artery before injection of physiological saline) and myocardial infarction BM-MSCs group (intervention group) (ligation after injection of DiI labeled BM-MSCs). Programmed electrical stimulation after 4 weeks observation arrhythmia inducibility and events. The results compared with the control group, the infarction group and the intervention group sustained ventricular tachycardia induced array number (4 vs 26 vs 12, p lt; 0.05), and ventricular tachycardia degenerated into ventricular fibrillation (0 vs 5 vs 4, p lt ; 0.05) and ventricular fibrillation caused death (0 vs 4 vs 4, p lt; 0.05) were significantly higher occurrence of infarction, sustained ventricular tachycardia induced significantly higher than those in the control group (66.7% vs 16.7%, p lt; 0.05). Compared with the MI group, the intervention group induced non-sustained ventricular tachycardia (16 vs 8, p lt; 0.05) and sustained ventricular tachycardia array (12 vs 26, p lt; 0.05) significantly reduced, but non-persistent induced rate of ventricular tachycardia and sustained ventricular tachycardia, and ventricular tachycardia degenerated into ventricular fibrillation and ventricular fibrillation caused death no significant difference in the incidence of. Conclusion BM-MSCs transplantation can reduce the rat ventricular arrhythmias induced events after myocardial infarction.
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