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 deli very decreases during a moderate maternal hypoxemia, whereas cerebral oxygen consumption is maintained. However, since in immature fetuses c irculatory centralization may be in part ineffective, cerebral concent rations 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 h igh-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 hyperemia on cerebral concentrati ons of high-energy phosphates and glycolytic intermediates in fetal gu inea 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 i n 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 mu mol/g; P < 0.01), whereas those of high-energy p hosphates remained unchanged. From these results we conclude that duri ng moderate isocapnic hypoxemia cerebral energy metabolism of immature fetal guinea pigs is maintained by an acceleration of the anaerobic g lycolytic rate.