GIK对缺血/再灌注犬心肌超微结构的影响

Effects of high-dose glucose-insulin-potassium(GIK) on ultramicrostructure in a canine model of myocardial ischemia and reperfusion

目的:观察葡萄糖-胰岛素-钾液(GIK)、葡萄糖-钾液(GK)对急性心肌缺血/再灌注(MI/R)犬心肌缺血区内心肌细胞改变的影响,分析GIK中的胰岛素对MI/R心肌细胞的保护作用。方法:将犬心肌定量缺血(左前降支血流量降低80%)50 min,再灌注4 h,建立犬MI/R模型。24只杂种犬随机分为GIK组、GK组和盐水对照组(n=8),于再灌注前5 min,分别输注GIK、GK和生理盐水。再灌注4 h后,计算梗死区占缺血区重量的百分比,并制作电镜切片于透射电镜下观察。结果:GIK可显著减少心肌梗死(MI)的范围[GIK组(5.2±0.8)%vs.盐水对照组(9.4±0.8)%,P<0.05];而GK组MI的范围(8.5±0.9)%则与盐水对照组无明显差异。与盐水对照组相比,GIK组对非缺血心肌的超微结构无影响,对缺血心肌有一定的保护作用。GK对缺血心肌无保护作用。结论:再灌注时,静脉输注GIK可减轻心肌超微结构的损伤,其中的胰岛素是GIK上述作用的关键成分。

AIM： To study the effect of glucose-insulin-potassium（GIK） on changes of dog myocardial cells after ischemia-reperfusion injury following acute myocardial ischemia/reperfusion（MI/R） and to explore the role of insulin in the protective effects of GIK on myocardium.METHODS： In anesthetized open-chest dogs,the left anterior descending coronary artery（LAD） was partially occluded（80% reduction in its blood flow） for 50 min and reperfused for 4 h.Dogs were randomly divided into three groups： GIK,GK and saline.All treatments began at 5 min before reperfusion [infused at 2 ml/（kg·h）,i.v.] and continued during the 4-h reperfusion.The ratio of necrosis area was determined.Myocardial infarction was determined by the ultrastructure of ischemic myocardium at the end of the reperfusion.RESULTS： The ratio of myocardial necrosis showed attenuation in GIK group [（5.2±0.8）% vs.saline（9.4±0.8）%,P0.05],but no reduction was observed in myocardial infarct size in the GK group [（8.5±0.9）% vs.saline（9.4±0.8）%].Compared with saline,GK had no significant effects on the ultrastructure of ischemic myocardium,whereas GIK had significant effects on the ultrastructure of ischemic myocardium.CONCLUSION： GIK exerts some protective effects on myocardium by alleviating ultrastructural injury of myocardium.Insulin may play a leading role in the actions of GIK.