重组人促红细胞生成素后处理缺血/再灌注前后骨骼肌诱导型一氧化氮合酶及一氧化氮的变化

背景：促红细胞生成素对包括心脑在内的多种组织器官的缺血/再灌注损伤有保护作用。 目的：观察重组人促红细胞生成素后处理对家兔后肢腓肠肌缺血/再灌注前后诱导型一氧化氮合酶、一氧化氮和超微结构的影响。 方法：将家兔随机分为空白对照组、模型组和重组人促红细胞生成素组，后2组建立兔左后肢腓肠肌缺血/再灌注实验模型，其中重组人促红细胞生成素组在兔左后肢缺血2 h后静脉注射重组人促红细胞生成素。 结果与结论：再灌注后4，12 h，重组人促红细胞生成素组诱导型一氧化氮合酶表达水平及一氧化氮浓度增高幅度较模型组低(P < 0.05)。电镜下腓肠肌细胞超微结构显示，模型组内皮细胞膜溶解，肿胀明显，肌纤维内线粒体水肿。重组人促红细胞生成素组肌纤维损伤较轻，肌节内Z线及肌节内各带结构基本正常，大部分线粒体结构正常，显示重组人促红细胞生成素组超微结构损伤程度明显轻于模型组。结果证实，重组人促红细胞生成素后处理可通过抑制诱导型一氧化氮合酶蛋白的表达，减少再灌注后过量一氧化氮生成，改善骨骼肌缺血/再灌注损伤。

Effects of recombinant human erythropoietin postconditioning on inducible nitric oxide synthase and nitric oxide in rabbit hindlimb gastrocnemius before and after ischemia/reperfusion injury

BACKGROUND:In recent years, many studies have shown that erythropoietin plays a protective role in many tissues and organs from ischemia/reperfusion injury including the heart and brain. OBJECTIVE:To observe the effects of recombinant human erythropoietin postconditioning on inducible nitric oxide synthase, nitric oxide and ultrastructure in rabbit hindlimb gastrocnemius before and after ischemia/reperfusion injury. METHODS:Adult rabbits were randomly divided into three groups: blank control, model, and recombinant human erythropoietin postconditioning. The rabbits in the latter two groups were created into experimental models of ischemia/reperfusion injury of left hind limb gastrocnemius. At 2 hours after ischemia, the rabbits in the recombinant human erythropoietin postconditioning group were intravenously injected with recombinant human erythropoietin. RESULTS AND CONCLUSION:At 4 and 12 hours after reperfusion, inducible nitric oxide synthase and nitric oxide levels were significantly lower in the recombinant human erythropoietin postconditioning group than in the model group (P < 0.05). The electronic microscope results of gastrocnemius cell ultrastructure showed that in the model group, endothelial cell membrane was lysed and obviously swollen, and mitochondrion in the muscle fiber was also swollen; compared with the model group, the muscle fiber injury was obviously mild in the recombinant human erythropoietin postconditioning group: Z line and the structure of each band within the sarcomere was basically normal, and the structure of most mitochondria was normal. These results showed that recombinant human erythropoietin postconditioning can downregulate the expression of inducible nitric oxide synthase protein expression and decrease nitric oxide levels after perfusion, and thereby improve ischemia/reperfusion injury of the skeletal muscle.