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作 者:代友平[1] 唐国华[1] 习水平[1] 鲍翠玉[1]
机构地区:[1]咸宁医学院附属医院内科
出 处:《咸宁医学院学报》1996年第1期4-6,共3页Journal of Xianning Medical College
摘 要:本实验采用麻醉开胸兔急性心肌缺血再灌注损伤模型,心肌梗塞面积和危险区分别采用组织学和荧光粒子技术测定.实验分四组:对照组(n=9),预处理组(PC,n=8),高剂量超氧化物歧化酶(SOD)预处理组(HD-SOD-PC,n=8)和低剂量SOD预处理组(LD-SOD-PC,n=9).4次5分钟缺血和5分钟再灌注完成预处理.HD-SOD-PC组和LD-SOD-PC组预处理前20分钟分别静脉滴注SOD30000u/kg和15000u/kg,60分钟滴完.结果:梗死面积占危险区百分比对照组,预处理组,HD-SOD-PC组和LD-SOD-PC组分别为48.0±4.1%,14.1±2.8%,9.8±1.8%和11.6±2.4%(对照组与另三组之间P<0.05).预处理组,HD-SOD-PC组,LD-SOD-PC组差异无统计学意义.提示:预处理对兔心肌缺血再灌注损伤具有保护作用,氧自由基在兔预处理机制中不起重要作用.A model of acute ischemia-reperfusion injury was used in open chest anaesthetised rabbits. Myocardial infarct size and area at risk were determined by histology and fluorescent particles, respecfively. Four groups were studied: a control grop(n = 9),a preconditioned group(n = 8),a high-dose superoxide dismutase (SOD)-treat preconditioned group(HD-SOD-PC) (n=8)and a low-dose SOD-PC(LD-SOD-PC) (n = 9). Preconditioning was perfermed with episodes of 5 minutes of ischemia and 5 minutes of reperfusion. The free radical scavengers (30000 units/kg SOD for HD-SOD-PC group,15000 units/kg SOD for LD-SOD-PC group)were infused intravenously over 60 minutes staring 20 minutes before preconditioning. Infarct siza as the percentage of area at risk was 48. 0±4.1% in the control group,14. 1±2. 8% in the pc group,9.8±1. 8% in the HD-SOD-PC group(P<0. 05 vergus control for the last three values). The difference in infarct size as the parcent of area at risk among the PC,HD-SOD-PC,LD-SOD-PC groups were not significant. The results indicated that ischemic preconditioning delays ischemic myocardial necrosis;and free radical were unlikely to play a major role in the mechaism of the preconditioning in rabbit.
关 键 词:SOD 保护作用 心肌缺血再灌注损伤 HD 对照组 预处理 LD 组分 PC 粒子
分 类 号:R542[医药卫生—心血管疾病] R285.5[医药卫生—内科学]
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