Elevated fetal plasma lactate produces polyhydramnios in the sheep.

In human fetuses with hemolytic diseases such as erythroblastosis fetalis, hydrops fetalis or polyhydramnios often develops. The mechanism(s) that produces these fluid imbalances is unknown, although lactate concentrations have been reported to be elevated in hydropic human fetuses with erythroblastosis. In this study we explored the role of lactate in producing fetal fluid imbalances. In seven near-term fetal sheep, we infused 5 mol/L sodium lactate at a rate of 10 mmol/hr for 3 days. Fetal plasma lactate rose by 6.0 +/- 1.0 (mean +/- SE) mmol/L above control. Fetal plasma osmolality and Na+ increased slightly, Cl- decreased, and bicarbonate rose in proportion to the Cl- decrease. Fetal renal lactate excretion was 1.1 +/- 0.3 mmol/hr while Na+ excretion was 10.6 +/- 1.9 mEq/hr. Fetal urine flow increased by 1.9 +/- 0.4 L/day and the urine remained hypotonic relative to fetal plasma throughout the infusion. Amniotic fluid lactate and Na+ rose during the infusion period and remained elevated during a 24-hour recovery period. Amniotic plus allantoic fluid volume at autopsy was 5.3 +/- 0.8 L compared with a normal of 0.5 to 1.0 L. There was little evidence of fetal edema. In summary, a moderate sustained elevation in fetal plasma lactate concentration appears to be a powerful osmotic agent for fetal accumulation of fluid from the maternal compartment over a period of days. This may be the primary mechanism whereby hydrops fetalis or polyhydramnios develops in severely anemic human fetuses.