模拟缺血再灌注后心肌细胞的胰岛素抵抗现象  

The phenomenon of insulin resistance in cardiomyocytes during post-simulated ischemic reperfusion

作　　者：李勇刚[1] 陈焕文[1] 张尔永[1] 隋东虎[1] 石应康[1] 

机构地区：[1]四川大学华西医院心胸外科

出　　处：《中华胸心血管外科杂志》2007年第5期335-337,共3页Chinese Journal of Thoracic and Cardiovascular Surgery

基　　金：国家自然科学基金资助(30270567)

摘　　要：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 myocardial insulin sensitivity and the time course during post-isehemic reperfusion. Methods An experimental model of simulated ischemia reperfusion （SUR） was developed using isolated adult rat cardiomyocytes. The glucose uptake of cardiomyoctyes stimulated by insulin （0 IU/L, 0.01 IU/L, 20 IU/L） was detected with isotopic tracer technique. Results After 60 mins of simulated ischemia, cardiomyocyte viability at 15 min and 60 min of reperfusion did not decrease significantly （ P 〉 0.05, vs control）. Insulin stimulated glucose transport into cardiomyocytes in a dose-dependent fashion. Glucose uptake stimulated by insulin into cardiomyocytes was both decreased significantly in 15 mins reperfusien group and in 60 mins reperfusien group （ P 〈 0.05, vs control）, and glucose uptake in 60min reperfusion group was much more than that in 15rain reperfusien group. Cardiomyocytes during reperfusien are responsiveness to insulin, but at the same time, cardiomyocytes exhibit notable acute insulin resistance. The magnitude of insulin resistance in cardiomyocytes is most severe during the initial reperfusion stage. Acute insulin resistance is probably a new mechanisan of myocardial isehemia-reperfusien injmy.

关 键 词：心肌再灌注损伤 胰岛素 葡萄糖 代谢 

分 类 号：R654.1[医药卫生—外科学] R587.1[医药卫生—临床医学]