Abstract
A glucose load was administered to the fetus in utero by maternal infusion prior to hypoxia in 12 sheep experiments. The placental transport mechanism for glucose appeared saturated at high maternal concentrations of glucose and dependent on oxygen as a source of energy. The changes observed in the fetal EEG, cardiovascular, acid-base, and metabolic parameters during and in recovery from hypoxia were similar to a group of 17 experiments in which glucose had not been given prior to hypoxia. A glucose load was administered to the fetus in utero by maternal infusion prior to hypoxia in 12 sheep experiments. The placental transport mechanism for glucose appeared saturated at high maternal concentrations of glucose and dependent on oxygen as a source of energy. The changes observed in the fetal EEG, cardiovascular, acid-base, and metabolic parameters during and in recovery from hypoxia were similar to a group of 17 experiments in which glucose had not been given prior to hypoxia.
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