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作 者:袁志柳[1] 王艺明[2] 沈正[1] 陈保林[3] 黄达枚[1] 刘兴德[1]
机构地区:[1]贵阳医学院附院心内科 [2]贵阳医学院附院心理科,贵州贵阳550004 [3]贵州省人民医院,心内科550002
出 处:《贵阳医学院学报》2006年第3期238-240,共3页Journal of Guiyang Medical College
摘 要:目的:探讨在体条件下,非创伤性双下肢缺血后处理(N-W IPTC)对缺血-再灌注(I/R)心肌梗死面积(IS)和心肌组织中蛋白激酶Cα(PKCα)表达的影响。方法:采用SD大鼠心肌I/R模型,应用Evan’s蓝、TTC染色,观察N-W IPTC对IS的影响;运用免疫组化技术观察N-W IPTC对心肌组织PKCα表达的影响。结果:与I/R组比较,N-W IPTC组的IS显著降低(P<0.01或P<0.05);与I/R组比较,N-W IPTC组心肌细胞膜PKCα表达明显多于I/R组(P<0.01)。结论:N-W IPTC能有效降低I/R心肌的IS,其机制可能与促进心肌细胞膜PKCα的表达有关。Objective: To observe the protective effects of non-wounded leg ischemic postconditioning (N-WIPTC) on ischemia/reperfusion (I/R) myocardial injury in rats. Methods: 24 Sprague-Dawley rats weredivided randomly into four groups and the models of ischemia/reperfusion myocardial injury were produced. The infarction sizes (IS) were measured with Evan' s and Trc staining, and the expression of protein kinase C (PKCα) in myocardial tissue was investigated by immunohistochemistry. Results: Compared with those of I/R group, the ISs of N-WIPTC were lower (P 〈0. 01 or P 〈0. 05), and the expression of PKCα was significantly higher in N-WIPTC groups (P 〈 0. 01 ). Conclusions: N-WIPTC could significantly decrease the IS during I/R. The mechanism might be the promoted expression of PKCα in myocardial tissue after N-WIPTC.
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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