Berger R, Gjedde A, Hargarter L, Hargarter S, Krieglstein J, Jensen A
Department of Obstetrics and Gynecology, Ruhruniverstät Bochum, Germany.
Pediatr Res. 1997 Sep;42(3):311-6. doi: 10.1203/00006450-199709000-00011.
Recent studies in immature fetal animals demonstrated only a slight or variable increase in the cerebral glycolytic rate during moderate isocapnic hypoxemia. However, the methods used in those studies did not allow for detection of small differences or of regional redistributions of the cerebral glycolytic rate. Hence, a global increase or a regional redistribution of the cerebral glycolytic rate during hypoxemia accompanied by a severe increase in tissue lactate concentration in a few brain areas may have been overlooked in these studies. Because these pathophysiologic mechanisms seem to considerably exacerbate neuronal cell damage due to hypoxic/ischemic insults, we were keen to clarify this point. We, therefore, applied the 2-deoxyglucose method to fetal guinea pigs in utero and measured total and regional cerebral glucose utilization in fetuses of this species at 0.75 of gestation during maternal isocapnic hypoxemia. At 0.75 of gestation guinea pig dams were chronically catheterized. Control groups were exposed to room air, whereas study groups were exposed to a hypoxic atmosphere (10% oxygen, 2% carbon dioxide, and 88% nitrogen). To measure total and regional cerebral glucose utilization during normoxemia and isocapnic hypoxemia, we injected i.v. 100 microCi of 2-[3H]deoxyglucose into the dams. Total and regional cerebral glucose utilization were determined from the steady-state clearance of 2-deoxyglucose between the maternal arterial plasma and the fetal brain, the glucose concentration in the maternal arterial plasma, and the "lumped constant." During isocapnic hypoxemia, total fetal cerebral glucose utilization was not significantly higher than that previously measured during normoxemia (8 +/- 0.8 versus 8 +/- 1.0 micromol/100 g/min). Furthermore, no redistribution of cerebral glucose utilization could be detected. We conclude that moderate isocapnic hypoxemia in the immature fetal brain does not lead to any significant increase or redistribution of glucose utilization or to any major lactate accumulation. This may be related to the low cerebral metabolic demands of brain tissue at this stage of development. Whether this is the main reason for the known resistance of the immature fetal brain toward ischemic neuronal cell damage remains to be established.
