犬低血流心肌缺血诱导GLUT1基因表达增加

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(GLUT1)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GLUT1数量，采用Northern印迹法分析缺血心肌GLU T1 mRNA表达，采用免疫印迹法分析心肌GLUT1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GLUT1 mRNA和GLUT1多肽表达明显增加，分别为 正常心肌的3.6倍和1.6倍(P<0.01)。无论在正常或缺血心脏，GLUT1表达均无部位差异 。结论：心肌缺血能诱导缺血心肌局部GLUT1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。GLUT1表达增强可能是一种重要的心肌缺 血后代偿性保护机制。

Low-flow myocardial ischemia increasing the expression of GLUT1 gene in canine

Objective:To investigate the mechanism of increased glucose uptake, the expression of myocardial glucose transporter1 (GLUT1) was determined after low flow myocardial ischemia. Methods: An in vivo open chest canine model of low flow myocardial ischemia was used to correlate myocardial glucose uptake with the number of GLUT1. The expression of myocardial GLUT1 glucose transporter was determined by semiquantitative Northern blotting and immunoblotting. Results: GLUT1 mRNA and GLUT1 polypeptide expression was substantially increased in ischemic region from the experimental hearts when compared to normal hearts. There was no significant regional difference in GLUT1 expression in either normal or ischemic hearts.Conclusion:Myocardial ischemia induces a factor or factors which stimulate GLUT1 expression in ischemic myocardial regions. Enhanced GLUT1 expression may be an important protective mechanism by which myocardial cells enhance glucose uptake and metabolism during low flow myocardial ischemia. [