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目的:了解自体骨骼肌卫星细胞心肌移植对心肌梗死大鼠心室重构的影响及可能机制。方法:实验于2004-03/06在第三军医大学大坪医院野战外科研究所三室完成。45只Wistar大鼠随机分为3组,假手术组、对照组及移植组,每组各15只。①对照组及移植组大鼠经结扎冠状动脉前降支建立心肌梗死模型;假手术组除不结扎左前降支外,其余操作同对照组和移植组。②将体外培养2周的大鼠自体卫星细胞以注射的方式移植到移植组大鼠梗死区周围。③4周后测定各组大鼠心室质量及质量指数、血管内皮生长因子mRNA及血管内皮生长因子蛋白质的表达、缺血心肌毛细血管密度的变化,同时观察移植细胞在梗死区的生长、增殖情况并探讨它们相互的关系。结果:45只大鼠,实验中假手术组及移植组死亡3只,对照组死亡4只,进入结果分析35只。①卫星细胞在梗死区中可增殖分化为横纹肌纤维。②卫星细胞移植4周后,移植组及对照组左室质量、右室质量、左室质量指数(左室质量/体质量)及右室质量指数(右室质量/体质量)比假手术组均明显增加[左室质量:(621.25±25.34),(699.82±47.38),(550.33±21.47)mg,P<0.001,0.001;右室质量:(192.92±26.83),(219.82±38.23),(160.08±19.63)mg,P<0.01,0.001;左室质量指数:(2.36±0.20),(2.69±0.07),(2.12±0.05)mg/g,P<0.001,0.001;右室质量指数:(0.73±0.09),(0.84±0.11),(0.61±0.02),P<0.001,0.001];移植组左室质量、左室质量指数及右室质量指数比对照组明显减低(P<0.001,0.001,0.01)。③移植组大鼠缺血心肌中毛细血管密度及血管内皮生长因子mRNA、血管内皮生长因子蛋白质的表达较之假手术组、对照组亦明显升高[(523.42±82.14),(378.23±43.16),(430.73±65.04)n/mm2,P<0.001,0.01;1.601±0.251,0.582±0.066,0.590±0.072,P<0.001,0.001;0.148±0.030,0.110±0.012,0.117±0.014,P<0.001,0.01]。结论:卫星细胞在心肌梗死区中可增殖分化为具有弹性和收缩功能的横纹肌样细胞,并通过自分泌和旁分泌的形式增加血管内皮生长因子的表达,促使缺血心肌毛细血管增生,从而抑制心室重构过程。
Objective: To investigate the effect and possible mechanism of autologous skeletal muscle satellite cell transplantation on ventricular remodeling in myocardial infarction rats. Methods: The experiment was performed at Room 3, Institute of Field Surgery, Daping Hospital, Third Military Medical University from March to June 2004. Forty-five Wistar rats were randomly divided into 3 groups: sham operation group, control group and transplantation group, 15 rats in each group. ① The control group and the transplantation group were established myocardial infarction model by ligation of the anterior descending coronary artery; the sham-operated group except the control group and the transplantation group without ligating the left anterior descending artery. ② The autologous satellite cells cultured in vitro for 2 weeks were transplanted into the infarct area of the transplantation group by injection. After 4 weeks, the ventricular mass and quality index, the expression of vascular endothelial growth factor mRNA and vascular endothelial growth factor (VEGF) protein and the changes of capillary density in ischemic myocardium were measured. The growth and proliferation of transplanted cells in infarct area were also observed Explore their mutual relations. Results: Forty five rats were killed in the sham-operation and transplantation groups, and four in the control group, and 35 in the control group. ① satellite cells in the infarct area can proliferate and differentiate into striated muscle fibers. After 4 weeks of satellite cell transplantation, left ventricular mass, right ventricular mass, left ventricular mass index (left ventricular mass / body mass) and right ventricular mass index (right ventricular mass / body mass) in the transplantation group and the control group were significantly lower than those in the sham operation group (621.25 ± 25.34), (699.82 ± 47.38), (550.33 ± 21.47) mg, P <0.001, 0.001 respectively; right ventricular mass: (192.92 ± 26.83), (219.82 ± 38.23), 160.08 ± 19.63) mg, P <0.01, 0.001 respectively; Left ventricular mass index: (2.36 ± 0.20), (2.69 ± 0.07), (2.12 ± 0.05) mg / 0.73 ± 0.09), (0.84 ± 0.11), (0.61 ± 0.02), P <0.001,0.001]. The left ventricular mass, left ventricular mass index and right ventricular mass index in the transplantation group were significantly lower than those in the control group (P <0.001, 0.001 , 0.01). (3) Compared with sham operation group and control group, capillary density, expression of vascular endothelial growth factor (VEGF) and vascular endothelial growth factor (VEGF) protein in ischemic myocardium were significantly increased in transplantation group [(523.42 ± 82.14), (378.23 ± 43.16) (430.73 ± 65.04) n / mm2, P <0.001,0.01; 1.601 ± 0.251,0.582 ± 0.066,0.590 ± 0.072, P <0.001,0.001; 0.148 ± 0.030,0.110 ± 0.012,0.117 ± 0.014, P <0.001, 0.01]. CONCLUSIONS: Satellite cells proliferate and differentiate into striated muscle-like cells with elastic and contractile function in myocardial infarction area and increase the expression of vascular endothelial growth factor by autocrine and paracrine forms to promote the proliferation of ischemic myocardium capillaries, thus inhibiting Ventricular remodeling process.