诱导型一氧化氮合酶在GK糖尿病大鼠心肌梗死后的表达

目的本研究通过制作GK糖尿病大鼠及非糖尿病大鼠心肌梗死模型,观察诱导型一氧化氮合酶(iNOS)的表达在糖尿病大鼠合并心肌梗死时与非糖尿病大鼠心肌梗死时的变化,为冠心病合并糖尿病的心脏病理改变提供理论基础与科学依据。方法应用体质量在200～250g的雄性GK糖尿病大鼠及其对照雄性Wistar大鼠通过开胸手术结扎麻醉大鼠冠状动脉左前降支制作大鼠在体心肌梗死模型。心肌梗死模型制作前测量血糖。手术成功后分组饲养大鼠3周。3周后,测量血糖,活体剪取心脏,进行iNOS的免疫组织化学染色及实时聚合酶链反应(RT-PCR)检测。结果①GK糖尿病大鼠血糖明显高于Wistar大鼠血糖(P<0.05);②Wistar心肌梗死组与GK心肌梗死组在缺血区可见到心肌细胞iNOS大量阳性染色,但GK心肌梗死组与Wistar心肌梗死组相比,iNOS阳性染色减少,二者吸光度测定值差异有统计学意义(P<0.05);③Wistar心肌梗死组与GK心肌梗死组iNOSmRNA表达在缺血区明显增加,但GK心肌梗死组iNOSmRNA表达减少,二者之间差异有统计学意义(P<0.05)。结论iNOS在糖尿病大鼠合并心肌梗死时其在缺血区的表达是降低的,表明高血糖可能抑制iNOS的表达,使体内一氧化氮(NO)生成减少,不利于梗死后血供的恢复。

Expression of inducible nitric oxide synthase in diabetic rats with myocardial infarction

Objective To investigate the expression of inducible nitric oxide synthase(iNOS)in GK diabetic rats with myocardial infarction by using myocardial infarction models of diabetic rats and non-diabetic rats.Methods Experiments were carried out in male GK diabetes rats and male Wistar rats(both weighed 200～250 g).Left anterior descending coronary artery(LADCA)was ligated with silk ligature in anesthetized rats.Rats were divided into four groups and raised for 3 weeks.Before operation,blood glucose of each rat was measured.3 weeks after operation,blood glucose of each rat was also measured before hearts of all survived rats were excised,then the expression of iNOS was detected in all groups.Results ①Blood glucose of GK rats was significantly higher than that of Wistar rats(P<0.05);② Positive staining of iNOS increased in ischemic zone of Wistar operated group and GK operated group,but the expression of iNOS in GK operated group decreased compared with Wistar operated group(P<0.05);③The expression of iNOS mRNA increased in ischemic zone of Wistar operated group and GK operated group,but The expression of iNOS mRNA in GK operated group decreased compared with Wistar operated group(P<0.05).Conclusion The expression of iNOS in GK diabetic rats with myocardial infarction decreased compared with Wistar rats with myocardial infarct,which indicated that high glucose may decrease the expression of iNOS and the production of nitric oxide in ischemic zone,and do harm to the restore of blood supply after myocardial infarction.