No abstract

Abstra ct. Hyperglycemia has been shown to induce arterial hypoxemia in the chronically catheterized fetal sheep. To investigate the mechanism behind this glucose-induced hypoxemia, eight pregnant ewes and their fetuses were studied. Fetal glucose infusion (1 1.9±0.6 mg glucose/kg per min) was associated with a doubling of the fetal plasma glucose concentration with concomitant elevation of the umbilical vein-distal arterial 02 content difference by 24 h of infusion (P < 0.01). Calculated fetal 02 consumption increased from 8.1±0.4 ml/kg per min in the control period to a maximum value of 10.6±0.3 ml/kg per min by third infusion day (P < 0.01), which is an increase of -30%. The degree of stimulation of fetal 02 consumption was related to the degree of fetal hyperglycemia but not to the degree of fetal hyperinsulinemia. The increase in fetal 02 consumption was accompanied by a significant increase in fetal 02 extraction with no change in either fetal 02 delivery or fetal blood 02 affinity. In addition, fetal hypercapnea with a mild fetal respiratory acidosis was induced by fetal hyperglycemia. The increase in fetal arterial Pco2 was linearly related (P < 0.001) to the magnitude of increase in fetal 02 consumption. These studies suggest that chronic fetal hyperglycemia induces a state ofaccelerated fetal oxidative metabolism and may be important in explaining the etiology behind certain unusual findings in human infants of diabetic mothers.

No abstract

No abstract

No abstract