重复心肌缺血/再灌注损伤时一氧化氮对细胞凋亡的影响  

Effect of nitric oxide on apoptosis caused by recurrent reversible myocardial ischemia/reperfusion injury

作　　者：英明中[1] 李小鹰[1] 陈孝[2] 赵保路[2] 张得良[2] 

机构地区：[1]中国人民解放军总医院南六科,北京100853 [2]中国科学院生物物理所,北京100101

出　　处：《第四军医大学学报》2005年第6期525-527,共3页Journal of the Fourth Military Medical University

摘　　要：目的: 采取促进或抑制一氧化氮 (NO)的方法,了解在重复可逆性心肌缺血 /再灌注损伤时,血液中NO的动态变化对细胞凋亡的影响.方法: 新西兰兔 15只,随机分为 3组(n=5): ①对照组;②在静脉内注射NO合成底物L 精氨酸为L Arg组;③iv一氧化氮合酶抑制剂L 硝基 精氨酸为L NNA组.将动物用戊巴比妥钠iv麻醉后,结扎前降支制成心肌缺血 /再灌注模型,用电子自旋共振法测定血液中NO含量,将兔心肌缺血 10min,共 3次,第 1, 2次缺血后再灌注10min,第 3次缺血后再灌注 120min.结果: 第 1次缺血 /再灌注 5min时NO升高的顺序依次为L Arg组最大 (28 0±2 0)、对照组次之(23 0±4 20),与对照组比较P<0 01,而L NNA组较缺血前降低(5 9±0 7),与对照组比较P<0 01. 细胞凋亡指数:L Arg组(0 33±2 60 )最大,对照组 ( 0 23±2 30 )次之、L NNA组(0 13±1 30)最小.结论: 再灌注早期NO的大量生成促进细胞凋亡,参与心肌缺血 /再灌注损伤的过程.AIM: To observe the relationship between the NO levels in the blood detected by electron spin resonance (ESR) and the myocardial apoptosis caused by the recurrent,reversible myocardial ischemia/reperfusion injury.METHODS: Fifteen New Zealand white rabbits were randomly divided into three groups (n=5): control group, L-Arg group,and L-NNA group.The rabbits were anesthetized with intravenous pentobarbital.A suture ligature was passed around the left anterior descending coronary artery (LAD) to have it snare occluded and reperfused.The LAD was occluded for 10 min three times.The first and second occlusions were followed by 10 min of reflow and after the third occlusion,the reperfusion was 120 min.RESULTS: Compared with those in control group at 5 min after the first reperfusion,NO and apoptosis levels (0.33±2.60) were elevated significantly in L-Arg group.In L-NNA group,NO and apoptosis level (0.13±1.30) decreased significantly.CONCLUSION: Elevated NO and apoptosis are involved in the process of myocardial ischemia/reperfusion injury.

关 键 词：电子自旋共振谱学 一氧化氮 细胞凋亡 

分 类 号：R541.4[医药卫生—心血管疾病]