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1. 中国医科大学第二临床学院核医学科
2. 中国医科大学第二临床学院核医学科,沈阳,110003
纸质出版日期:2002-11-01
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[1]王淑侠,刁尧,裴著果.线粒体Mn-SOD参与预适应大鼠心肌抗梗死保护作用的实验研究[J].核技术,2002(11):913-917.
WANG Shuxia DIAO Yao PEI Zhuguo. Contribution of mitochondrial Mn-SOD to Antiinfarct cardioprotection in preconditioned myocardium in rat[J]. Nuclear techniques, 2002, (11): 913-917.
为定量去甲肾上腺素 (NE)诱导的延迟相预适应抗心肌梗死保护强度
研究了预适应机体抗氧化剂酶活性变化与预适应保护的关系。将 5 0只大鼠分为NE组、I/R组和正常组。 3.1μmol/kgNE腹腔内注射诱发预适应
2 4h后开胸结扎左冠状动脉主干 (LCA)
造成LCA支配区缺血30min
再灌注 12 0min复制预适应模型
用伊文斯蓝、TTC染色分别显示左室未缺血区、梗死区、危险区。数码相机与实体显微镜结合拍摄左室切面
MetamorphImagingSystem软件定量各组左室梗死区 /危险区面积
放免法和黄嘌呤氧化酶法分别测定血清Cu2 + 、胞浆Cu2 +
Zn2 + -SOD含量、活性及线粒体Mn -SOD活性。结果显示
1)预适应保护可使心肌梗死面积减少 33.4 %;2 )预适应心肌线粒体Mn -SOD活性增高 ;3)血清及心肌细胞胞浆Cu2 +
Zn2 + -SOD含量、活性预适应组与非预适应组差别不显著。实验研究启示
NE可诱导大鼠产生延迟相心肌预适应保护
其机制可能是通过使心肌线粒体Mn -SOD活性增高
减少自由基损伤
产生预适应保护。
To quantify protected effect of norepinephrine (NE) induced delayed phase of ischemic preconditioning
the relationship between cardioprotection and superoxide dismutase(SOD) was studied. A total of 50 rats were randomly divided into three groups:NE group
I/R group and normal group
3.1 μmol/kg NE was injected into abdomen 24 hours before surgery as a trigger
both NE and I/R group underwent main left coronary artery occlusion for 30 minutes then reperfusion for 120 minutes. Ischemic risk area
infarct area and nonischemic area were identified by TTC
Evan’ s blue staining methods and calculated by Metamorph Imaging System software. Serum Cu 2+
Cytosol Cu 2+
Zn 2+-SOD content and activity
and activity of mitochondrial Mn-SOD activity were detected by radioimmunoassay and method xanthosine oxidase separately. Results showed that: 1) infarct size was reduced by 33.4% in preconditioned heart; 2) mitochondrial Mn-SOD activity was higher in preconditioned myocardium; 3) no significant difference about the activity and content of Cu 2+
Zn 2+-SOD either in serum or in myocardium was found. The above phenomena imply that preconditioned cardioprotection might be only related to mitochondrial Mn-SOD
mitochondrial Mn-SOD might be the final effector of NE induced preconditioning .
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