摘要
目的测定链脲佐菌素(STZ)诱导的不同周期精尿病大鼠对心肌缺血／再灌注(I／ R)损伤的影响及其与心肌脂质过氧化反应程度及血浆一氧化氮(NO)变化的关系。方法阻断和开放左冠状动脉前降支建立大鼠急性心肌I／R模型。用TTC染色测定大鼠心肌 I／R后梗死面积;用T／BARS法测定脂质过氧化反应程度;用硝酸还原酶法测定NO含量结果 STZ处理后2周,糠尿病组(2WD)心肌梗死面积比对照组(2WC)明显缩小,STZ处理后16周(16WD),梗死面积比对照组(16WC)增加;心脏组织的脂质过氧化物反应产物 2WD组较2WC组低,但是在16WD组中较16WC组显著增加;血浆NO水平2WD组较 2WC组增高,但是16WD组较16WC组显著减少。结论 STZ诱导的大鼠急、慢性期糖尿病对心肌I／R损伤呈现相反的作用。这可能是由于大鼠急、慢性期糖尿病相反的心肌脂质过氧化反应程度及NO改变而引起。
Objective To determine the effects of different-term STZ-induced diabetes of rats on ischemia/reperfusion （I/R） injury of myocardium and to determine if I/R injury is related to diabetes-inudced alterations in lipid peroxidation and No levels. Methods The models of I/R injury, were induced by occlusion and reperfusion of the left descending coronary artery （LDCA） of rats. I/R-indueed infarct size was determined using triphenyhetrazolium chloride（TYC） staining; Lipid peroxidation was measured bv thiobarbituric acid-reactive substances （T-BARS） methods. NO production was quantitied by nitrite/nitrate colormetrie method. Results Two weeks after STZ treatment, infarct size deceased in the diabetic rats （2WD） compared with the control group （2WC）. Whereas 16 weeks after STZ treatment, the infarct size increased in the diabetic rats compared with the 16WC group. Lipid peroxidation in the heart tissue decreased in 2WD and increased in 16WD group compared with the time-matched control groups. Plasma NO levels increased in 2WD rats whereas NO levels decreased markedly in 16WD group e,mpared with time-matched controls. Conclusion Short- and long-term STZ induced diabetes exert opposite influences on myocardial I/R injury, and these contradictory influences may depend on different alterations in Lipid peroxidation and NO levels.
出处
《国外医学（内科学分册）》
2006年第3期131-135,共5页
Foreign Medical Sciences(Section of Internal Medicine)
