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目的:探讨经静脉注射骨髓间充质干细胞(MSCs)对心肌梗塞大鼠模型心功能的影响及其在体内的分布情况。方法:在心肌梗塞后1周将标记的MSCs注射到大鼠舌下静脉内,在细胞移植后不同时间点取心、肝、脾、肺、肾脏器,进行组织学检查,观察移植细胞的分布。选取心肌梗塞模型大鼠通过心脏超声评价移植后3周、6周心功能改变情况。结果:静脉注射MSCs后其组织结构未发现明显异常改变,早期主要分布在正常心肌组织内,1周后主要分布在梗塞及交界区内,正常心肌组织内很少见细胞存留。超声检查发现在细胞移植后实验组(12只)左心室没有进一步扩大,左心功能明显好于对照组(12只):[左心室收缩末期内径(0.92±0.16)∶(1.078±0.15)cm;左心室舒张末期内径(0.66±0.13)∶(0.79±0.11)cm;左心室短轴缩短率(28.4±4.2)∶(24.3±3.1)%;左室射血分数(52.7±4)∶(42.89±4.2)%,P均<0.05]。结论:静脉注射移植MSCs后细胞可以分布到重要组织器官内,移植细胞有向梗塞心肌组织内迁移的趋势,能明显延缓左心室重构及其所导致的心功能恶化。
Objective: To investigate the effects of intravenous injection of bone marrow mesenchymal stem cells (MSCs) on cardiac function in myocardial infarction rat model and its distribution in vivo. METHODS: The labeled MSCs were injected into the sublingual vein of rats at 1 week after myocardial infarction. Heart, liver, spleen, lung and kidney were taken at different time points after transplantation. Histological examination was performed to observe the distribution of transplanted cells . The changes of cardiac function in 3-week and 6-week after transplantation were evaluated by cardiac ultrasound in rats with myocardial infarction. Results: After MSCs were injected intravenously, no obvious abnormal changes were observed in their tissue structure. The cells were mainly distributed in normal myocardium in the early stage, mainly in the infarction and junctional zone after 1 week, and rare in the normal myocardium. Ultrasonography showed that the left ventricle of the experimental group (12 rats) did not expand further after transplantation, and the left ventricular function was significantly better than that of the control group (12 rats): [0.92 ± 0.16] (1.078 ± 0.15) cm ; Left ventricular end-diastolic diameter (0.66 ± 0.13) :( 0.79 ± 0.11) cm; shortening of left ventricular short axis (28.4 ± 4.2) :( 24.3 ± 3.1)%; left ventricular ejection fraction (52.7 ± 4) 42.89 ± 4.2)%, P <0.05]. CONCLUSION: After transplanted MSCs into the vein, the cells can be distributed to important tissues and organs. The transplanted cells tend to migrate toward the infarcted myocardium, which can significantly delay the left ventricular remodeling and the worsening of cardiac function.