论文部分内容阅读
目的探讨促红细胞生成素(EPO)对大鼠缺血再灌注损伤心肌的影响和可能机制。方法将成年健康雄性SD大鼠随机分为假手术组、缺血再灌注组、EPO预处理组,各组再灌注2h后血清检测一氧化氮(NO)含量和内皮型NO合酶(eNOS)活性、血清心肌型肌酸激酶同工酶(CK-MB)和心肌肌钙蛋白(cTnI)水平和心肌肌浆网钙泵(SERCA)活性。结果与缺血再灌注组比较,EPO预处理组血清NO含量升高(P<0.05),eNOS活性明显增加(P<0.05);血清CK-MB和cTnI水平降低(P<0.05);SERCA活性升高(P<0.05)。结论 EPO能增加NO水平、eNOS和SERCA活性,有效减轻缺血再灌注心肌损伤,其机制可能与保护内皮细胞、减轻细胞内钙超载有关。
Objective To investigate the effect and possible mechanism of erythropoietin (EPO) on myocardial ischemia-reperfusion injury in rats. Methods Adult healthy male Sprague-Dawley rats were randomly divided into sham operation group, ischemia reperfusion group and EPO pretreatment group. Serum levels of nitric oxide (NO) and endothelial nitric oxide synthase (eNOS) (CK-MB) and cardiac troponin (cTnI) levels and cardiac muscle sarcoplasmic reticulum calcium pump (SERCA) activity were measured. Results Compared with the ischemia-reperfusion group, serum NO level increased (P <0.05), eNOS activity increased (P <0.05), serum CK-MB and cTnI levels decreased in EPO pretreatment group (P < Increased (P <0.05). Conclusions EPO can increase NO level, eNOS and SERCA activity, effectively reduce myocardial ischemia-reperfusion injury, and its mechanism may be related to protecting endothelial cells and reducing intracellular calcium overload.