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作 者:袁志柳[1] 刘兴德[2] 陈保林[3] 黄达梅[2] 高秀蓉[1] 焦桂萍[1]
机构地区:[1]贵州省人民医院干医科,邮政编码贵阳550002 [2]贵阳医学院附属医院心内科 [3]贵州省人民医院心内科
出 处:《微循环学杂志》2006年第2期27-28,31,共3页Chinese Journal of Microcirculation
摘 要:目的:探讨在体条件下,心肌缺血后处理(IPTC)是否具有减轻心肌缺血再灌注(I/R)损伤的作用及其可能机制。方法:采用SD大鼠心肌I/R模型,观察IPTC和缺血预处理(IPC)对心肌梗死面积(IS)的影响,检测磷酸肌酸激酶(CK)、丙二醛(MDA)及超氧化物歧化酶(SOD)含量,研究IPTC对I/R心肌MDA、SOD的影响。结果:IPTC和IPC大鼠IS明显降低(P<0.01),血清中CK、MDA含量显著降低(P<0.01),SOD含量明显升高(P<0.01),两组间IS、CK、MDA、SOD比较均无显著性差异(P>0.05)。结论:与IPC一样,IPTC能有效降低I/R大鼠心肌梗死面积,其机制可能与减少自由基损伤和抗氧化作用有关。Objective: To observe the effects of ischemic postconditioning (IPTC) on ischemiareperfusion (IR) myocardial injury in rats,and in- vestigate the possibly protective mechanism. Method: The IR myocardial injury model had been reproduced in Sprague-Dawley rats. The infarction sizes(IS) were measured. Malondialehyde(MDA), creatine kinase(CK) and superoxide dismutase(SOD) were investigated.Results: In IPTC and IPC rats, the infarction sizes and the concentration of CK and MDA in plasma were reduced significantly, the concentration of SOD in plasma were higher significantly (P<0.01). There was no significant difference between IPTC and IPC rats( P>0.05).Conclusion: These data suggest that myocardial ischemic postconditioning is as effective as ischemic preconditioning in reducing infarct size. Reducing oxygen free radical injury and strengthening the action of antioxidization may be one of the potential mechanisms of reducing the infarction size.
关 键 词:心肌梗死面积 缺血再灌注 缺血后处理 大鼠心肌 心肌缺血事件 SOD MDA 心肌保护作用 I/R损伤 再灌注心律失常
分 类 号:R542.22[医药卫生—心血管疾病] R542.2[医药卫生—内科学]
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