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糖尿病对缺血预适应大鼠心肌缺血再灌注的影响及其机制研究
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糖尿病对缺血预适应大鼠心肌缺血再灌注的影响及其机制研究
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糖尿病对缺血预适应大鼠心肌缺血再灌注的影响及其机制研究
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Journal Article
糖尿病对缺血预适应大鼠心肌缺血再灌注的影响及其机制研究
2011
Overview
目的探讨糖尿病对缺血预适应（IPC）大鼠心肌缺血再灌注（I/R）的影响及其可能机制。方法取糖尿病SD大鼠及非糖尿病SD大鼠各30只,建立冠状动脉阻断的在体心肌I/R模型,各分为3组（n=10）：假手术（Sham）组开胸后穿线做套环,但不收紧结扎线,持续155min,全程旷置作为基础水平对照;I/R组手术穿线平衡35min后,持续收紧结扎冠状动脉主干造成缺血30min,放松后行再灌注90min;IPC组手术穿线平衡35min后,缺血5min,再灌注5min,反复3次,而后重复I/R组操作。测定各组缺血前及实验结束后的血清肌酸激酶（CK）、乳酸脱氢酶（LDH）水平,心肌组织丙二醛（MDA）含量和超氧化物歧化酶（SOD）活性,心肌梗死范围以及心肌葡萄糖摄取率。结果非糖尿病大鼠中,I/R组和IPC组CK、LDH活性及MDA含量显著高于Sham组（P〈0.01或P〈0.05）,且I/R组显著高于IPC组（P〈0.05或P〈0.01）;I/R组及IPC组SOD活性显著低于Sham组（P〈0.01）,且I/R组显著低于IPC组（P〈0.05）;IPC组心肌梗死面积显著低于I/R组（P〈0.05）,而心肌葡萄糖摄取率显著高于I/R组（P〈0.05）。在糖尿病大鼠中,IPC组与I/R组的上述指标比较均无统计学差异（P〉0.05）。结论糖尿病可抑制IPC对在体大鼠缺血再灌注心肌的保护作用,其机制可能与心肌胰岛素抵抗有关。
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