Abstract
An isolated perfused working heart preparation was used to investigate the role of lactate in the energy metabolism of the fetal heart. Hearts were perfused under working conditions with Krebs-Henseleit buffer containing either glucose 5mM or glucose 5mM and lactate 5mM combined. Insulin 100 μU/ml was present in all perfusions. Pressure development in both great vessels was maintained at 55 mmHg and mean atrial pressure was adjusted to 6 mmHg. Glucose uptake was measured by production of 3H2O from 23H glucose and lactate uptake by measuring changes in buffer concentration. With glucose as the sole exogenous substrate its utilization(3.48 ± .29 μmol/min/g dry), corrected for lactate production by the heart(3.06 ± μmol/min/g dry)could account for only 56 ± 9% of the total oxygen consumption of the heart(20.7 ± μmol/min/g dry). When both glucose and lactate were present in the buffer, glucose uptake was inhibited(0.71 μmol/min/g dry)and lactate- uptake(6.55 μmol/min/g dry)accounted for approximately 91 ± 12% of the total oxygen consumption(22.3 ± 1.8 μmol/min/g dry). These findings suggest that lactate oxidation is the primary source of metabolic energy for the fetal heart in late gestation, since glucose alone does not satisfy the oxidative needs of the fetal heart and since the presence of lactate profoundly suppresses glucose uptake. Lactate is the primary metabolic substrate for the fetal heart when present in concentrations similar to those observed in vivo, much as lipids are the primary metabolic substrate in more mature hearts.
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