Oxidative Metabolism in Fetal Rat Brain during Maternal Anesthesia

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Abstract
Effects of maternally administered anesthetics on fetal cerebral metabolism as determined by direct tissue analysis were studied. Term pregnant rats that were paralyzed and had their lungs artificially ventilated were given N2O halothane or pentobarbital. Dams receiving N2O 70% halothane, 0.4% or pentobarbital, 50 mg/kg, remained normotensive, whereas halothane, 2%, or pentobarbital, 200 mg/kg, led to a 65% decrease in maternal blood pressure and a 3-fold increase in blood lactate. Halothane, 1 and 2%, was associated with maternal hyperglycemia, while pentobarbital, 200 mg/kg, decreased blood glucose. Fetal blood lactate and glucose tended to parallel maternal lactacidemia and glycemia. Fetuses of dams anesthetized with N20 showed decreases of 45 and 8% in cerebral phosphocreatine and ATP, respectively; cerebral lactate was comparable to that of control unanesthetized animals. These alterations presumably resulted from cerebral hypoxia and acidosis secondary to N20 anesthesia combined with paralysis. Fetuses of dams anesthetized with halothane, 0.4% and pentobarbital, 50 mg/kg, showed concentrations of cerebral metabolites comparable to those of control animals. Halothane, 2%, was associated with metabolic disturbances in fetal brain indicative of cerebral hypoxia. Pentobarbital, 200 mg/kg, although producing maternal hypotension and lactacidemia similar to corresponding changes produced by halothane, 2%, preserved a more optimal fetal cerebral energy state, as reflected in a lower lactate/pyruvate ratio and normal ATP. The metabolic influence of pentobarbital may serve to protect the hypoxic fetus from neurologic damage.