1263 LACTIC ACID TOLERANCE IN THE NON-HYPOXIC FETAL LAMB

Abstract

Lactic acid is considered in contradictory ways: as a normal fetal nutrient or as an indicator of fetal distress. Fetal lactic acidemia has been induced experimentally by hypoxia, combining effects of hypoxia and lactic acidemia. We chose to separate these effects by infusing lactic acid into 14 late gestation fetal lambs via a continuous infusion technique, and into 5 lambs using a lactate clamp technique. Animals (Fetal Weight=3.5±0.2 kg) had catheters in the umbilical vein, fetal pedal artery, pedal vein and brachial vein, and, in 6 animals, the fetal hepatic vein. Animals were well oxygenated and well nourished after recovery for at least 7 days. Lactic acid infusion into the fetal brachial vein at an average of 20 mg/min for 90-180 min rapidly established a new metabolic steady state, increasing arterial lactate by 2.8±0.36 mM*, and decreasing arterial pH from 7.36±0.006 to 7.29±0.02*. Umbilical lactate uptake determined by the Pick Principle fell from 7.3±1.2 to 3.1±1.7 mg/min* during infusion, and fetal arterial glucose increased from 1.02±0.06 mM to 1.13±0.05 mM*, decreasing both umbilical glucose uptake from 18.2±1.4 to 14.9±2.7 mg/min* and umbilical glucose/oxygen quotient (GOQ) from .51±.05 to .39±.02*. During infusion, hepatic lactate/oxygen quotient rose from 0.31±0.08 to .77±.12*, and hepatic GOQ reversed from +0.33±.05 (consumption) to -0.56±0.27* (production). [*=p <0.05, paired].Rapid continuous fetal lactic acid infusion is well tolerated by the non-hypoxic fetal lamb, and alters fetal metabolism of glucose and lactic acid.