【摘要】 目的 探讨纳洛酮在心肌缺血-再灌损伤时对血浆内皮素-1(ET-1)和一氧化氮(NO)的影响。方法 复制心肌缺血-再灌注模型,观察血浆内皮素-1和一氧化氮的动态变化及纳洛酮的影响。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。采用放射免疫法测定ET-1的含量,硝酸还原酶法测定NO的含量。结果 心肌缺血后ET-1水平呈上升趋势,4 h达高峰;而NO水平明显下降。缺血再灌注后0.5～1h ET-1含量高于缺血前(P<0.O5);纳洛酮保护组ET-1含量均低于缺血前(P<O.05);纳洛酮治疗组ET-1在缺血后0.5 h高于缺血前,其余各时间点与缺血前比较差异均无显著性(P>0.05)。而NO水平在缺血再灌注后均下降;保护组NO含量均高于缺血前(P<0.05);治疗组NO含量在缺血后0.5 h低于缺血前,其余各时间点与缺血前比较差异均无显著性(P>0.05)。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ET-1和提高NO水平;从而减轻ET-1对血管和心肌组织的损伤作用。更多还原

【Abstract】 AIM To study the effects of nalox-one on plasma endothelin-1 and nitric oxide during myocardiac ischemia-reperfusion ( I/R ) injury. METHODS Using myocardiac ischemia models and myocardiac ischemia -reperfusion injury models that was made by means of ligating sinistra corona-ria arteria,to investigate the change of plasma ET-1 and NO during I/R injury, and after the protection and treatment with naloxone,an antagonist of opoid receptor. 40 New Zealand rabbits were randomly assigned to 4 groupsCischemia group, nalox-one protection group, naloxone treatment group and ischemia-reperfusion group, 10 in each group). The blood was phlebotomized at different time in each group. The concentration of ET-1 was detected with radioimmunology method and NO with nitrate reductase method. RESULTS The levels of ET-1 had the trend of improvement after ischemia and were at its peak at the end of 4 h, but the levels of NO were significantly decreased. The ET-1 levels were significantly improved after 0. 5-1 h of injury compared with that before ischemia (P < 0. 05) 5 whereas its levels were significantly low in naloxone protection group ( P < 0. 05 ) , but the treatment group showed no significant change except after 0. 5 h of ischemia(P>0. 05). The levels of NO decreased after injury , whereas its levels in naloxone protection group increased significantly compared with that before ischemia ( P <C 0. 05 ). NO levels showed no significant change except 0. 5 h of ischemia in naloxone treatment group (P > 0.05). CONCLUSION Naloxone may effectively reduce the level of ET-1 and enhance the level of NO after myocardiac ischemia and during I/R injury; whereby it decreases the injury to vascular and myocardium.更多还原