一氧化氮在重复可逆性心肌缺血-再灌注所造成的心肌顿抑时对细胞超微结构的影响

The ultramicroscopic effects of NO on myocardial stunning cau sed by the recurrent, reversible myocardial ischemia-reperfusion injury

目的 :了解一氧化氮 (NO)在重复可逆性心肌缺血 再灌注所造成的心肌顿抑时 ,对心肌细胞超微结构的影响。方法 :健康新西兰兔 15只 ,随机分为 3组 (每组 5只 ) :第一组为对照组 ,第二组在静脉内注射NO合成底物L 精氨酸 (L Arg组 ) ,第三组在静脉内注射一氧化氮合酶抑制剂L 硝基 精氨酸 (L NNA组 )。兔用戊巴比妥钠静脉注射麻醉后 ,结扎前降支制成心肌缺血—再灌注模型 ,用ESR法测定血液中NO含量 ,记录左心室最大上升速率dp/dtmax。将实验动物缺血 10min ,共三次 ,第 1、2次缺血后再灌注 10min ,第 3次缺血后再灌注 12 0min。取心肌组织 ,电子透射显微镜观察心肌细胞超微结构。结果 :与对照组相比较 ,L Arg组NO含量明显增高 ,dp/dtmax下降明显 ,电镜检查心肌细胞损伤明显 ,表现在肿胀线粒体数目增多 ,线粒体肿胀明显 ,嵴凸模糊 ,个别肌丝模糊。而L NNA组NO含量明显减少 ,dp/dtmax下降较轻 ,电镜检查心肌细胞肿胀线粒体数目减少 ,线粒体肿胀减轻 ,肌丝清晰。结论

Objective:To investigate the effects of NO on cardiomyocyte injuries in myocardial stunning caused by the recurrent, reversibl e myocardial ischemia reperfusion injury Methods:New Zealand w hite rabbits were anesthetized with intravenous pentobarbital A suture ligatur e was passed around the left anterior descending coronary artery(LAD), so it cou ld be snare occluded and reperfused The LAD was occluded for 10min three times , the first and second occlusions were followed by 10min of reflow, after the th ird occlusion, the reperfusion was 120min Fifteen rabbits were randomly divide d into three groups: 1 control group n=5 2 L Arg group n=5 3 L NNA grou p n=5 The contents of NO in the blood were measured by ESR and the dp/dtmax we re recorded The myocardial tissues were obtained for the observation of cardiom yocyte injuries with electron microscopy Results:Compared with control group,in L Arg group, the contents of NO increased markedly and dp/dt m ax decreased markedly,the cardiomyocyte seemed to have more severe magnification s of cardiomyocyte injury: some of sarcomeres became blurred, the number of swel led mitochondria increased But in L NNA group: the contents of NO decreased m arkedly, the decreased dp/dt max and the number of the swelled mitochondri a were less than that in control group, there were no blurred sarcomeres Conclusion: NO might have a harmful effect on cardiomyocyte injury in myocardial stunning