Objective：To restore cardiac autonomic pace function by autologous trans- plantation and committed differentiation of hone marrow mesenchymal stern cells, and explore the technique for the treatment of sick sinus syn...Objective：To restore cardiac autonomic pace function by autologous trans- plantation and committed differentiation of hone marrow mesenchymal stern cells, and explore the technique for the treatment of sick sinus syndrome. Methods ： Mesenchymal stern cells isolated from canine bone marrow were culture-expanded and differentiated in vitro by 5-azacytidine. The models of sick sinus syndrome in canines were established by ablating sinus node with radio-frequency technique. Differentiated mesenchymal stem cells labeled by BrdU were autologously transplanted into sinus node area through direct injection. The effects of autologous transplantation of mesenchymal stern cells on cardiac autonomic pace function in sick sinus syndrome models were evaluated by electrocardiography, pathologic and immunohistochemical staining technique. Results：There was distinct improvement on pace function of sick sinus syndrome animal models while differentiated mesenchymal stem cells were auto-transplanted into sinus node area. Mesenchymal stern cells transplanted in sinus node area were differentiated into similar sinus node cells and endothelial cells in vivo, and established gap junction with native cardiomyocytes. Conclusion ： The committed- induced mesenchymal stern cells transplanted into sinus node area can differentiate into a- nalogous sinus node cells and improve pace function in canine sick sinus syndrome models.展开更多
目的:探讨体外反搏保护缺血心肌的机制。方法:采用冠状动脉结扎法复制犬急性心肌缺血模型,检测缺血及外加反搏时缺血心肌肾素活性、血管紧张素Ⅱ(ANGⅡ)水平和血管紧张素转换酶(ACE)活性以及心肌细胞总、胞浆、胞膜蛋白激酶(PKC)活性,分...目的:探讨体外反搏保护缺血心肌的机制。方法:采用冠状动脉结扎法复制犬急性心肌缺血模型,检测缺血及外加反搏时缺血心肌肾素活性、血管紧张素Ⅱ(ANGⅡ)水平和血管紧张素转换酶(ACE)活性以及心肌细胞总、胞浆、胞膜蛋白激酶(PKC)活性,分析ANG Ⅱ与PKC之间的关系。结果:缺血能激活缺血区心肌肾素(0.97±0.19 vs 3.21±0.67)、ACE(13.7±5.2 vs 33.9±7.9)和ANGⅡ(20±3 vs 154±19),ECP能抑制三者(2.36±0.59,23.3±7.4,107±19)。缺血组细胞总、胞膜PKC活性明显高于假手术组(5.80±0.85 vs 7.76±0.92.3.43±0.76 vs6.59±1.06),胞浆PKC活性则明显低于假手术组(2.37±0.39 vs 1.16±0.29)。体外反搏对细胞总PKC无明显影响(7.15±0.64),使胞浆PKC恢复正常(2.67±0.52),对胞膜PKC(4.47±0.31)有一定抑制作用。ANGⅡ水平与胞膜PKC活性密切相关(r=0.873)。结论:体外反搏对缺血心肌局部肾素-血管紧张素系统有抑制作用,使PKC从胞浆移至胞膜,且ANGⅡ水平与胞膜PKC活性密切相关。提示体外反搏治疗心肌缺血时局部ANGⅡ可能通过PKC这一信号转导途径起作用。展开更多
文摘目的:比较不同结构心尖轴流泵的流体力学及溶血特性差异。方法 :在体外模拟循环台上测试外形尺寸相似的4种不同结构的轴流泵(包括单滑动面球支点、双滑动面球支点心尖轴流泵及保留后导叶和无后导叶的全悬浮心尖轴流泵)的流体力学和溶血特性。结果:单滑动面球支点心尖轴流泵和双滑动面球支点心尖轴流泵的流体力学特性及溶血特性相似,均可在11 000 r/min条件下产生100 mm Hg(1 mm Hg=133.32 Pa)的压力输出和5 L/min的流量输出,标准溶血指数(normalized index of hemolysis,NIH)分别为0.023和0.025 g/100 L。在产生相同压力和流量输出条件下,两型全悬浮心尖轴流泵转速明显增加,保留后导叶的全悬浮心尖轴流泵和无后导叶的全悬浮心尖轴流泵转速分别为17 000和23 000 r/min,NIH分别为0.072和0.13 g/100 L。结论:单滑动面球支点心尖轴流泵结构简单、效率高、溶血强度低,可作为心尖轴流泵的结构选择;双滑动面球支点心尖轴流泵结构优势尚需在长时间体内植入实验中证实。悬浮心尖轴流泵体积较小,但效率较低,溶血作用强,保留后导叶可明显提高悬浮心尖轴流泵效率,降低溶血强度。
文摘Objective：To restore cardiac autonomic pace function by autologous trans- plantation and committed differentiation of hone marrow mesenchymal stern cells, and explore the technique for the treatment of sick sinus syndrome. Methods ： Mesenchymal stern cells isolated from canine bone marrow were culture-expanded and differentiated in vitro by 5-azacytidine. The models of sick sinus syndrome in canines were established by ablating sinus node with radio-frequency technique. Differentiated mesenchymal stem cells labeled by BrdU were autologously transplanted into sinus node area through direct injection. The effects of autologous transplantation of mesenchymal stern cells on cardiac autonomic pace function in sick sinus syndrome models were evaluated by electrocardiography, pathologic and immunohistochemical staining technique. Results：There was distinct improvement on pace function of sick sinus syndrome animal models while differentiated mesenchymal stem cells were auto-transplanted into sinus node area. Mesenchymal stern cells transplanted in sinus node area were differentiated into similar sinus node cells and endothelial cells in vivo, and established gap junction with native cardiomyocytes. Conclusion ： The committed- induced mesenchymal stern cells transplanted into sinus node area can differentiate into a- nalogous sinus node cells and improve pace function in canine sick sinus syndrome models.
文摘目的:探讨体外反搏保护缺血心肌的机制。方法:采用冠状动脉结扎法复制犬急性心肌缺血模型,检测缺血及外加反搏时缺血心肌肾素活性、血管紧张素Ⅱ(ANGⅡ)水平和血管紧张素转换酶(ACE)活性以及心肌细胞总、胞浆、胞膜蛋白激酶(PKC)活性,分析ANG Ⅱ与PKC之间的关系。结果:缺血能激活缺血区心肌肾素(0.97±0.19 vs 3.21±0.67)、ACE(13.7±5.2 vs 33.9±7.9)和ANGⅡ(20±3 vs 154±19),ECP能抑制三者(2.36±0.59,23.3±7.4,107±19)。缺血组细胞总、胞膜PKC活性明显高于假手术组(5.80±0.85 vs 7.76±0.92.3.43±0.76 vs6.59±1.06),胞浆PKC活性则明显低于假手术组(2.37±0.39 vs 1.16±0.29)。体外反搏对细胞总PKC无明显影响(7.15±0.64),使胞浆PKC恢复正常(2.67±0.52),对胞膜PKC(4.47±0.31)有一定抑制作用。ANGⅡ水平与胞膜PKC活性密切相关(r=0.873)。结论:体外反搏对缺血心肌局部肾素-血管紧张素系统有抑制作用,使PKC从胞浆移至胞膜,且ANGⅡ水平与胞膜PKC活性密切相关。提示体外反搏治疗心肌缺血时局部ANGⅡ可能通过PKC这一信号转导途径起作用。
