Effects in Sheep of Hypoxia on Levels of Lactate, Pyruvate, and Glucose in Blood of Mothers and Fetus

Abstract

Extract: In nine experiments with sheep, effects of hypoxia on levels of lactate, pyruvate, and glucose in maternal and fetal blood were strudied. Bolld samples were obtained simlultaneously from the four uterine and umbilical vassels prior to, during, and following and episode of severe hypoxia.

The concentration of lactate, pyruvate, and hydrogen ions, and the CO₂ tension was greater in the umbilical circulation than in the uterine circulation during the period prior to hypoxia. Threre was no apparent exchange of lactate or pyruvate across the placenta in either direction at this time. The concentration of glucose in the umbilical vein, however, was directly related to that of the uterine vein.

When progressively mild-to-severe hypoxia occurred in the fetus and placenta, first pyruvate, then lactate, accumulated within the umbilical circulation. The venous-arterial (V-A) differnce of lactate in the uterine and umbilical vessels, as well as total uterine and fetal excess lactate production, increased significantly during the final 10% interval of the period of hypoxia. The concentration of lactate in the uterine vein blood was directly related to the concentration of lactate in the umbilical vein during this final period. The decrease in the concentration of glucose in the uterine vein blood was greater than the decrease in the umbilical vein blood.

The metablism of lactate proceeded slowly after relier from hypoxia. Though the concentration of lactate was still elevated approximately 30 min into recovery, the V-A and maternal-fetal concentration diffrences were similar to prehypoxic values.

Speculation: The placenta regulates the metabolic response of the fetus to hypoxia by providing a pathway wherby excess lactate produced by the fetus can be eliminated. The mechansim by which this is accomplished might involve a change in the electrochemical gradient across the membrane, anatomical changes within the membrane, or altertions of enzyme pathways at the placental site.

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