Arterial Hypoxemia and Hyperinsulinemia in the Chronically Hyperglycemic Fetal Lamb

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Abstract
Summary: Sustained fetal hyperglycemia was produced in eight chronically catheterized fetal lambs (seven twins, one singleton) by means of direct fetal glucose infusion. In twin preparations, only one twin was infused, the noninfused twin serving as a simultaneous in utero control. Glucose infusions lasted 7.6 ± 118 days and resulted in significant fetal hyperglycemia (from 20.3 ± 1.1 mg/dl to 58.2 ± 4.7 mg/dl, P < 0.001). The magnitude of the hyperglycemia was linearly related to the glucose infusion rate. Elevations of fetal plasma glucose and glucose infusion rate were associated with a significant fall in fetal arterial oxygen content (P < 0.001). In twin preparations studied, these relationships remained when the simultaneously sampled, noninfused twin was used as control. The fetal glucose-induced hypoxemia was not associated with fetal acidosis (tissue hypoxia) until the arterial oxygen content fell below 30% of baseline (mean base deficit in acidotic fetuses = 11.2 ± 2.2 meq/liter). Although Pao2 fell in hypoxemic fetuses (from 13.5 ±1.2 mmHg to 9.7 ±1.2 mmHg), the difference was not significant. Fetal plasma insulin rose during hyperglycemia from 10.2 ±3.1 μU/ml to a peak concentration of 26.2 ± 3.3 μU/ml, but this response was blunted in markedly hypoxemic fetuses. Neither fetal anemia nor hemoconcentration were evident in these preparations to account for the fall in fetal oxygen content. Speculation: Glucose-induced hypoxemia may be the result of accelerated fetal and/or uteroplacental oxygen consumption. In utero hypoxemia in the fetus of the pregnant diabetic may present a unifying hypothesis linking the known clinical findings of increased fetal red blood cell production, polycythemia, and late fetal demise in fetuses of diabetic mothers.