论文部分内容阅读
目的 :探讨纳洛酮在心肌缺血 再灌损伤时对血浆及心肌匀浆 β 内啡肽 (β EP)的影响。 方法 :新西兰兔 45只 ,随机分成 5组 :正常组 5只 ,心肌缺血组、缺血再灌注组、纳洛酮保护组和纳洛酮治疗组 ,每组 1 0只。制作心肌缺血模型和缺血再灌注损伤模型 ,并抽取不同时间点的静脉血 ,在心肌缺血、缺血再灌注、纳洛酮保护和纳洛酮治疗后 6h制作缺血心肌匀浆 ,采用放射免疫法分别测定 β EP的含量。结果 :心肌缺血 2h后血浆 β EP含量逐渐下降 ,较缺血前显著降低 (P <0 .0 5) ;而心肌匀浆上清液 β EP含量也降低。缺血再灌注后各时段 β EP含量明显高于缺血前 (P <0 .0 5或P <0 .0 1 ) ;纳洛酮保护组在 4h后血浆 β EP含量逐渐下降 ,与缺血前比较无显著性差异 (P >0 .0 5) ;纳洛酮治疗组 β EP在缺血后各时间点与缺血前比较均无显著性差异(P >0 .0 5)。 3组心肌匀浆上清液 β EP含量与缺血前的含量比较无明显变化。结论 :纳洛酮可有效降低心肌缺血及缺血再灌注损伤时血浆 β EP水平 ;从而减轻 β EP对血管和心肌组织的损伤作用
Objective: To investigate the effect of naloxone on β-endorphin (β EP) in plasma and myocardial homogenate during myocardial ischemia-reperfusion injury. Methods: Forty five New Zealand white rabbits were randomly divided into five groups: normal group (n = 5), ischemia group, ischemia reperfusion group, naloxone protection group and naloxone treatment group. The models of myocardial ischemia and ischemia-reperfusion injury were made and venous blood was collected at different time points. Ischemic myocardial homogenate was prepared 6h after myocardial ischemia, ischemia-reperfusion, naloxone protection and naloxone treatment, The contents of β EP were determined by radioimmunoassay. Results: Plasma β-EP level decreased gradually after 2 h of myocardial ischemia, which was significantly lower than that before ischemia (P <0.05); while β EP content of myocardial homogenate supernatant also decreased. The levels of β-EP at different time points after ischemia-reperfusion were significantly higher than those before ischemia (P <0.05 or P <0.01), while those in naloxone-treated groups decreased gradually after 4 hours, There was no significant difference between before and after ischemia (P> 0.05). There was no significant difference of β EP between naloxone treated group and before ischemia (P> 0.05). There was no significant difference in β EP content in myocardial homogenate supernatant between three groups before ischemia. Conclusion: Naloxone can effectively decrease the level of plasma β-EP in myocardial ischemia and ischemia-reperfusion injury, thereby reducing the damage of β-EP to vascular and myocardial tissue