The effects of hypoxia on glucose turnover in the fetal sheep.

The origin of the hypoxia-induced rise in fetal blood glucose concentration in fetal sheep of 124-135 days was investigated. Hypoxia was induced in pregnant sheep and fetuses with chronically implanted vascular catheters by causing the ewes to breathe 9% O2 and 3% CO2 in N2 for 60 min. The rise in fetal plasma glucose caused by a 60% reduction in maternal PaO2 was associated with a 50% fall in plasma insulin concentration. The fall in insulin and rise in glucose was prevented by the alpha-adrenergic blocking agent phentolamine but not by the beta-antagonist propranolol. Turnover of glucose in the fetus under these conditions was measured with [6-3H] and [U-14C] glucose. Hypoxia reduced fetal glucose consumption despite the hyperglycaemia. After 30 min of hypoxia there was no evidence of fetal production of glucose but by 60 min substantial production was evident. The reduced fetal consumption and increased production of glucose was inhibited by phentolamine but not by propranolol. It is concluded that in the fetal sheep hypoxia induced hyperglycaemia is first caused by reduced consumption of glucose and thus fetal glycogen stores are not depleted. If the hypoxia persists fetal blood glucose is elevated further by fetal production of glucose.