Enhancement of glucose uptake in stunned myocardium: Role of glucose transporter

This study quantifies the myocardial glucose uptake and clarifies the pathway of augmented glucose uptake in myocardium reperfused after a brief period of ischemia (stunned myocardium). The glucose uptake rate was determined from the time course of the sugar phosphate (SP) resonance in rat myocardium (d[SP]/dt) with ³¹P nuclear magnetic resonance after the substitution of glucose with its analog 2-deoxyglucose. The d[SP]/dt in stunned myocardium 11.03 ± 0.05 (SE) μmol·g wet wt^-1·min^-1; n = 8] increased significantly compared with nonischemic control myocardium (0.18 ± 0.03 μmol.g wet wt^-1·min^-1; n = 8; P < 0.0001), reaching the maximal stimulatory uptake rate during exposure to insulin(1.05 ± 0.04μmol·g wet wt^-1·min^-1;n = 8). Twenty minutes after reperfusion, the d[SP]/dt was still augmented (0.41 ± 0.05 μmol.g wet wt^-1·min^-1; n - 5; P < 0.05 vs. control myocardium). To elucidate further the mechanism of augmented glucose uptake, N⁶-(L-2-phenylisopropyl)adenosine (PIA; 100 μmol/l) a potent blocker of the glucose transporter, was administered to stunned hearts and, as a control, to insulin-stimulated hearts. PIA significantly and comparably inhibited the increase in d[SP]/dt in stunned myocardium (0.36 ± 0.07 μmol·g wet wt^-1·min^-1;n = 4;P < 0.0001 vs. without PIA) and in insulin-stimulated myocardium (0.38 ± 0.02 μmol·g wet wt^-1·min^-1; n = 4; P < 0.0001 vs. without PIA). These results indicate that the augmented glucose uptake in stunned myocardium is maintained by the glucose transporter, the amount of which is almost equal to that which can be maximally recruited by insulin.