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目的 :通过检测低血流心肌缺血后心肌细胞葡萄糖转运子 1(GL UT1)基因的表达 ,探讨心肌细胞对葡萄糖摄取增加的代谢机制。方法 :建立犬低血流心肌缺血模型 ,放射性核素标记方法检测心肌葡萄糖摄取量和 GL U T1数量 ,采用 North-ern印迹法分析缺血心肌 GL U T1m RNA表达 ,采用免疫印迹法分析心肌 GL U T1多肽表达。结果 :与正常心脏比较 ,低血流心肌缺血后 ,缺血心肌 GL UT1m RNA和 GL UT1多肽表达明显增加 ,分别为正常心肌的 3.6倍和 1.6倍 (P<0 .0 1)。无论在正常或缺血心脏 ,GL UT1表达均无部位差异。 结论 :心肌缺血能诱导缺血心肌局部 GL UT1表达增加 ,致使心肌细胞在低血流心肌缺血过程中葡萄糖摄取和代谢增强。 GL U T1表达增强可能是一种重要的心肌缺血后代偿性保护机制
OBJECTIVE: To investigate the expression of glucose transporter 1 (GLUT1) gene in cardiomyocytes after hypoperfusion myocardial ischemia and to explore the metabolic mechanism of cardiomyocytes increasing glucose uptake. Methods: The myocardial ischemia model of canine hypoglycemia was established. The myocardial glucose uptake and the number of GL U T1 were detected by radionuclide labeling. The expression of GL U T1m RNA in ischemic myocardium was detected by North-ern blotting. GL U T1 polypeptide expression. RESULTS: Compared with normal heart, the GL UT1m RNA and GLUT1 polypeptide expressions in ischemic myocardium were significantly increased after hypoxia-ischemia, which were 3.6 times and 1.6 times that of normal myocardium (P <0.01). There was no site difference in GL UT1 expression in normal or ischemic heart. CONCLUSION: Myocardial ischemia can induce the increase of GL UT1 expression in ischemic myocardium, resulting in enhanced glucose uptake and metabolism in myocardial cells during myocardial ischemia. GL U T1 expression may be an important compensatory mechanism after myocardial ischemia