RECOVERY OF GLYCOLYSIS AND OXIDATIVE-METABOLISM DURING POSTISCHEMIC REPERFUSION OF HYPERTROPHIED RAT HEARTS

We investigated the source and extent of recovery of ATP production du ring postischemic reperfusion of isolated working hearts from abdomina l aortic-banded rats. Rates of glycolysis, glucose oxidation, lactate oxidation, and palmitate oxidation were measured in hypertrophied and control hearts [perfused with (in mM) 11 glucose, 0.5 lactate, and 1.2 palmitate] during and after 30 min of no-flow ischemia. In the initia l aerobic period glycolytic rates were 1.87-fold higher in hypertrophi ed hearts compared with control hearts (P < 0.05), with rates of carbo hydrate and palmitate oxidation being similar. During reperfusion, hyp ertrophied hearts recovered 40% of preischemic function compared with 71% in control hearts. Rates of glycolysis during reperfusion of hyper trophied hearts remained accelerated compared with control hearts (2.0 1-fold higher, P < 0.05), whereas oxidative metabolism returned to pre ischemic values in both groups. The efficiency of converting ATP produ ction into mechanical work decreased to 29% of preischemic values in h ypertrophied hearts during the postischemic reperfusion compared with a decrease to only 59% of preischemic values in control hearts. This s uggests that the recovery of glycolysis and oxidative metabolism in th e hypertrophied heart during postischemic reperfusion is not impaired, but rather the efficiency of converting ATP produced into mechanical function decreases.