Glucose utilization and glycogen turnover are accelerated in hypertrophiedrat hearts during severe low-flow ischemia

We undertook this study to determine if the metabolism of exogenous glucose and glycogen in hypertrophied hi arts differed from that in normal hearts during severe ischemia. Thus, rates of glycolysis ((H2O)-H-3 production) an d oxidation ((CO2)-C-14 production) from exogenous glucose and glycogen wer e measured in isolated a working control (n=13) and hypertrophied (n=12) he arts from sham-operated and aortic-banded rats during 40 min of severe low- flow ischemia, Hearts, in which glycogen was prelabelled with [5-H-3]- or [ C-14]-glucose, were paced and perfused with Krebs-Henseleit solution contai ning 1.2 mM palmitate. 5.5 mM [5-H-3]- or [C-14]-glucose (different from th e isotope used to label glycogen), 0.5 mM lactate and 100 mu U/ml insulin d uring ischemia. Rates of glycolysis from exogenous glucose (3301 +/- 122 v 2467 +/- 167 nmol/min/g dry wt. mean +/- S.E.M., P<0.05) and glucose from g lycogen (808 +/- 27 v 725 +/- 21 nmol/min/g dry wt. P<0.05) were accelerate d in hypertrophied hearts compared to control hearts. However, rates of oxi dation of exogenous glucose and glucose from glycogen were not significantl y different between the two groups. As observed in normoxic non-ischemic he arts, glucose from glycogen was preferentially oxidized compared to exogeno us glucose. Additionally, rates of glycogen synthesis (167 +/- 7 v 140 +/- 9 nmol/min/g dry wt, P<0.05) were increased in hypertrophied hearts compare d to control hearts during severe low-flow ischemia indicating that glycoge n turnover (i.e, simultaneous synthesis and degradation) Mras accelerated i n the hypertrophied heart. Thus, we demonstrate that glucose utilization an d glycogen turnover are accelerated in the hypertrophied heart during sever e low-flow ischemia as compared to the normal heart. (C) 1999 Academic Pres s.