Effects of chronic fetal hyperglycemia upon oxygen consumption in the ovine uterus and conceptus

Anthony F Philipps, P. J. Porte, S. Stabinsky, T. S. Rosenkrantz, J. R. Raye

Research output: Contribution to journalArticle

73 Scopus citations

Abstract

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 (11.9±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 O2 content difference by 24 h of infusion (P < 0.01). Calculated fetal O2 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 O2 consumption was related to the degree of fetal hyperglycemia but not to the degree of fetal hyperinsulinemia. The increase in fetal O2 consumption was accompanied by a significant increase in fetal O2 extraction with no change in either fetal O2 delivery or fetal blood O2 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 O2 consumption. These studies suggest that chronic fetal hyperglycemia induces a state of accelerated fetal oxidative metabolism and may be important in explaining the etiology behind certain unusual findings in human infants of diabetic mothers.

Original languageEnglish (US)
Pages (from-to)279-286
Number of pages8
JournalJournal of Clinical Investigation
Volume74
Issue number1
StatePublished - 1984
Externally publishedYes

ASJC Scopus subject areas

  • Medicine(all)

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