摘要目的 利用大鼠自体颈部静脉移植模型观察动脉化的静脉移植血管氧化应激对线粒体的损伤,探讨冠脉搭桥术后静脉桥再狭窄的发病机制.方法 将动物分成对照组和实验组,对照组将静脉血管桥吻合于颈静脉,实验组吻合于颈动脉,术后4周取材行病理检查,检测移植血管组织活性氧(ROS)、丙二醛(MDA)、超氧化物岐化酶(SOD)水平及线粒体膜电位,线粒体膜流动性.结果 对照组和实验组比较:血管内膜增厚[(1.92±0.87)μm比(32.66±5.32)μm],血管组织ROS升高(23.57±9.21比69.33±15.76),MDA水平升高[(5.32±0.49)nmol/mg pro比(16.83±3.53)nmol/mg pro],SOD活性下降[(14.74±3.58)U/mg pro比(4.77±2.07)U/mg pro],上述各组数据差异均有统计学意义(P＜0.01);对照组和实验组移植血管组织的线粒体膜电位降低[(162.74±10.66)mV比(97.53±12.82)mV],线粒体膜黏滞系数η升高(0.226±0.025比0.417±0.069),上述各组数据差异均有统计学意义(P＜0.01).结论 静脉移植物处于氧化应激状态,ROS通过损伤线粒体诱导内膜增生,其机制可能和静脉承受了高氧的动脉血流有关.

abstractsObjective To explore the underlying mechanisms of bypass vein restenosis after arterialization, and study the oxidative stress and mitochondrial function on arterialized vein autograft. Methods A segment of jugular vein-to-carotid artery interposition grafting was performed on SD rats (n = 10). Four weeks postoperatively, vein autografts were harvested, and the levels of reactive oxygen species ( ROS), malondialdehyde (MDA), superoxidase dismutase (SOD) of the graft were measured and mitochondrial membrane potential (△Ψ) and fluidity were determined. Results In contrast to vein-to-vein anastomosis controls, the average neointimal thickness, ROS, MDA and SOD levels, the mitochondrial membrane potential (△ψ) and the viscous coefficient (η) of mitochondrial membrane in the arterialized vein autografts were (32.66 ±5.32) μm vs ( 1.92 ±0.87) μm (P＜0.001 ), 69.33 ± 15.76 vs 23.57 ±9. 21 (P＜0.01 ), ( 16. 83 ±3.53) nmol/mg pro vs (5.32 ±0.49) nmol/mg pro (P＜0.01 ), (4.77 ±2.07) U/mg pro vs (14.74 ±3.58) U/mg pro (P＜0.01), (97.53±12.82) mV vs (162.74±10.66) mV (P＜0.01 ), 0.417 ±0.069 vs 0.226 ±0.025 ( P＜0.01 ). As compared with control group, average neointimal thickness, ROS and MDA levels and the viscous coefficient (η) of mitochondrial membrane in the arterialized vein autografts were significantly increased, SOD level and the mitochondrial membrane potential (△Ψ) were significantly decreased. Conclusion The hyperoxia and hypertension may increase arterialized vein autograft oxidative stress. The oxidative stress causes mitochondrial dysfunction and may contribute to graft neointimal hyperplasia.