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

    • 摘要: 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。

       

      Abstract: 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)%, P<0.05], 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.

       

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