腺苷A1受体激动剂延迟预处理对兔心肌缺血再灌注损伤的保护作用  被引量:3

Protection of adenosine A1 receptor agonist delayed preconditioning for myocardial ischemia reperfusion injury in rabbits

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作  者:冉珂[1] 卢向航[1] 李晋[1] 徐军美 常业恬[1] 

机构地区:[1]中南大学湘雅二医院麻醉科,长沙410011

出  处:《重庆医科大学学报》2010年第4期535-537,共3页Journal of Chongqing Medical University

摘  要:目的:探讨腺苷A1受体激动剂2-氯环戊腺苷(2-chloro-N6-cyclopentyla denosine,CCPA)延迟预处理对兔心肌缺血再灌注损伤的保护机制。方法:30只健康新西兰雄性大白兔随机分成3组:假手术组(C组)、缺血再灌注组(I/R组)、CCPA组(组),每组10只。C组仅行左冠脉套线而不阻断160min,I/R组行左冠脉阻断40min,再灌注120min,P组在静注CCPA0.mg/kg24h后处理同I/R组。各组分别于左冠前降支阻断前20min(T1)、左冠前降支阻断20min(T2)、左冠前降支阻断40mi(T3)、心肌再灌注1h(T4)心肌再灌注2h(T5)5个时点抽取颈内动脉血测定血清中IL-10含量。再灌注120min后,测心肌热休克蛋白70(Heat shock protein70,HSP70)蛋白表达和心梗面积,电镜下观察细胞超微结构变化。结果:与I/R组比,P组IL-10含量和HSP70表达增高(P<0.05),心肌梗死面积减少(P<0.05),细胞结构损伤减轻。结论:CCPA延迟预处理通过增高心肌HSP7表达和IL-10水平来减轻缺血再灌注损伤发挥心肌保护作用。Objective:To investigate the protection mechanism of adenosine A1 receptor agonist(2-chloro-N^6-cyclopentyladenosine, CCPA)delayed preconditioning for rabbit myocardium during ischemia reperfusion.Methods:Thirty New Zealand male white rabbits were randomly assigned to Sham group,I/R group and CCPA group,with ten in each.Group CCPA was given CCPA 0.1 mg/kg before myocardial ischemia.Twenty-four hours later the I/R and CCPA underwent 40 min of coronary occlusion followed by 2 h of reperfusion.Blood samples were taken from arterial line at 20 min before occlusion(T)1,20 min after occlusion(T2),40 min after occlusion(T)3,1 h after reperfusion(T)4and 2 h after reperfusion(T)5for determination of the plasma levels of IL-10.At the end of the reperfusion,infarct size(IS)and area at risk(AAR)were defined by Evans blue and TTC staining.The heart was harvested and levels of the HSP70 were determined by Western blot analysis,and ultrastructures were observed under the electron microscopy.Results:The IL-10 and HSP70 levels of group CCPA was higher than those of group I/R.The CCPA(P〈0.05)reduced infarct size(22.1%±3.8%)of the left ventricular area at risk compared with the I/R(41.8%±4.3%)(P〈0.05).The injury of group I/R was severer than that of group CCPA under the light microscope.Conclusion:CCPA can increase the levels of HSP70 and IL-10 during ischemia-reperfusion,which maybe the molecular mechanism of CCPA delayed preconditioning on cardioprotection.

关 键 词:腺苷A1受体激动剂 延迟相预处理 心肌 缺血再灌注 

分 类 号:R365[医药卫生—病理学] R364[医药卫生—基础医学]

 

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