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模拟缺血再灌注后心肌细胞胰岛素抵抗机制的初步研究
引用本文:李勇刚,陈焕文,张尔永,隋东虎,石应康. 模拟缺血再灌注后心肌细胞胰岛素抵抗机制的初步研究[J]. 中华胸心血管外科杂志, 2003, 25(1): 190-192. DOI: 10.3760/cma j.issn.1001-4497.2009.03.018
作者姓名:李勇刚  陈焕文  张尔永  隋东虎  石应康
作者单位:重庆医科大学儿童医院心胸外科,41111014;
摘    要:Objective Recent.studies have found a strong association of insulin resistance, which might occur during ischemia reperfusion in vitro in the experimental dogs, with disturbed function of cardiomyocytes. Obvious acute insulin resistance, along with glucose dysmetabolism in the reperfused cardiomyocytes, was furher observed in the study performed with ischemia-reperfused ventric- ular myocytes of rats. We tried to investigate preliminarily the molecular mechanisms of insulin resistance in the cardiomyocytes after ischemia reperfusion. Methods An experimental model of insulin-stimulated ischemia reperfusion (SI/R) was created by isolating cardiomyocytes from adult rats. Glucose uptake of the cardiomyoctyes was evaluated with isotope-labeling technique. Glucose trans- porter 4 (GLUT4) translocation induced by insulin was investigated with Western blot analysis, and the intracellular level of free Ca2+ ([Ca2+]I) was measured quantitatively with Ca2+ indicator Fura-2. Results Insulin can stimulated glucose uptake by cardiomyo- cytes, indicating that these cells were insulin-sensitive. Cardiomyocytes were demonstrated notable acute insulin resistmce during reperfusion. Insulin-stimulated GLUT4 translocation in the cardiomyocytes 15 minutes after reperfusion was 72.2% of that in the con- trol group(P<0.05), in which the GLUT4 content in plasma membrane remained unchanged. The finding suggested that a disturbed GLUT4 translocation might happen in the cardiomyocytes during insulin-stimulated ischemia-reperfusion. Calcium overload was identi- fied in the cardiomyocytes with ischemia reperfusion. At 15 minutes of reperfusion, [Ca2+]I was significantly higher in the reperfused cardiomyocytes than that in the control cardiomyocytes[(318.66±23.06)vs(130.70±0.82) nmol/L, P<0.05], and kept at a higher level [(177.79±17.46) nmol/L] at 60 minutes of reperfusion (P<0.05, vs control). Partial correlation analysis revealed a negative correlation of[Ca2+]I with insulin-induced ghcose uptake in the cardiomyoctyes (r = -0.557,P=0.006). Conclusion Disturbed GLUT4 translocation and decreased intrinsic activity may be important molecular mechanisms for the development of insulin resistance in the cardiomyocytes of rat during insulin-simulated ischemia reperfusion,. [Ca2+]I overload may account for the de- creased intrinsic activity d GLUT4.

关 键 词:心肌再灌注损伤   胰岛素   葡萄糖     

Mechanisms of insulin resistance during ischemia reperfusion in the cardiomyocytes of rat
LI Yong-gang,CHEN Huan-wen,ZHANG Er-yong,SUI Dong-hu,SHI Ying-kang. Mechanisms of insulin resistance during ischemia reperfusion in the cardiomyocytes of rat[J]. Chinese Journal of Thoracic and Cardiovascular Surgery, 2003, 25(1): 190-192. DOI: 10.3760/cma j.issn.1001-4497.2009.03.018
Authors:LI Yong-gang  CHEN Huan-wen  ZHANG Er-yong  SUI Dong-hu  SHI Ying-kang
Abstract:
Keywords:Myocardial reperfusion injury Insulin Glucose Calcium
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