Cerebral energy metabolism in fetal guinea pigs during moderate maternal hypoxemia at 0.75 of gestation.

There is evidence from fetal sheep near term that cerebral oxygen delivery decreases during a moderate maternal hypoxemia, whereas cerebral oxygen consumption is maintained. However, since in immature fetuses circulatory centralization may be in part ineffective, cerebral concentrations of high-energy phosphates may fall during a moderate maternal hypoxemia due to an insufficient cerebral oxygen supply. On the other hand anaerobic glycolysis may accelerate to prevent the depletion of high-energy phosphates. To determine, whether or not there is an energy failure in the immature fetal brain in this situation, we studied the effects of 60 min moderate maternal hypoxemia on cerebral concentrations of high-energy phosphates and glycolytic intermediates in fetal guinea pigs at 0.75 gestation. Maternal hypoxemia resulted in no change in fetal mixed arterio-venous pH (7.41 +/- 0.05 vs. 7.38 +/- 0.05; n.s.) or PCO2 (39.0 +/- 4.2 vs. 36.4 +/- 5.6 mmHg; n.s.), but in a fall in fetal PO2 (17.3 +/- 2.2 vs. 11.2 +/- 1.9 mmHg; P < 0.01). There was an increase in fetal cerebral concentrations of lactate (1.50 +/- 0.24 vs. 2.82 +/- 0.91 mumol/g; P < 0.01), whereas those of high-energy phosphates remained unchanged. From these results we conclude that during moderate isocapnic hypoxemia cerebral energy metabolism of immature fetal guinea pigs is maintained by an acceleration of the anaerobic glycolytic rate.