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目的准确评价缺血再灌注心肌的胰岛素敏感性及其时相规律,为临床干预提供依据。方法建立成年大鼠心肌细胞模拟缺血60 min 再灌注模型,应用同位素示踪技术观察不同浓度(0 IU/L、0.01 IU/L、20 IU/L)胰岛素刺激大鼠心肌细胞的葡萄糖摄取效应。结果缺血60 min 后再灌注15 min 和60min,心肌细胞活性比率无明显降低(P>0.05)。胰岛素能促进各组心肌细胞的葡萄糖摄取,并呈剂量依赖性。缺血再灌注15 min 组和再灌注60 min 组心肌细胞胰岛素刺激的葡萄糖摄取较对照组均明显降低(P<0.05)。再灌注60 min 组心肌细胞胰岛素刺激的葡萄糖摄取较再灌注15 min 组明显增加(P<0.05)。结论缺血60min 后,再灌注心肌细胞保留了对胰岛素的反应性,同时,再灌注心肌细胞发生明显的急性胰岛素抵抗,再灌注初期尤为严重。急性胰岛素抵抗很可能是缺血再灌注心肌损伤的又一重要机制。
Objective To evaluate the insulin sensitivity and time-history of myocardial ischemia-reperfusion accurately and provide the basis for clinical intervention. Methods The myocardial ischemia reperfusion model was established in 60 min ischemia reperfusion in adult rat cardiomyocytes. The effects of different concentrations of insulin (0 IU / L, 0.01 IU / L, 20 IU / L) on myocardial glucose uptake were observed by isotope labeling . Results After ischemia 60 min and reperfusion 15 min and 60 min, the activity of cardiomyocytes was not significantly reduced (P> 0.05). Insulin can promote glucose uptake in each group of cardiomyocytes in a dose-dependent manner. Insulin-stimulated glucose uptake in cardiomyocytes in 15 minute ischemia reperfusion group and 60 min reperfusion group was significantly lower than that in control group (P <0.05). Insulin stimulated glucose uptake in cardiomyocytes significantly increased at 60 min after reperfusion compared with that at 15 min after reperfusion (P <0.05). Conclusions After 60min of ischemia, reperfused cardiomyocytes retain insulin responsiveness, and at the same time, acute insulin resistance occurs in reperfused cardiomyocytes, especially in the early stage of reperfusion. Acute insulin resistance is likely to be another important mechanism of myocardial ischemia-reperfusion injury.