Search

The effect of cerebral ischemia on cerebral metabolism and the electroencephalogram was studied with and without prior glucose infusion in near-term normoxic fetal sheep. At normal blood glucose levels, the electroencephalogram decreased in amplitude during ischemia. At elevated blood glucose levels the electroencephalographic amplitude was much less attenuated by ischemia although Fast Fourier Transforms revealed a shift toward slower frequencies. Under either normal or elevated blood gluocse conditions, ischemia caused cerebral oxygen consumption to decrease, glucose uptake to increase, and a net efflux of lactate to occur. Elevated blood glucose appears to help maintain electroencephalographic activity during ischemia, perhaps by fueling additional anaerobic energy production. The relationship between the electroencephalogram, brain metabolism, and brain damage remains to be defined.

We measured hemispherical cerebral blood flow and arteriovenous differences across the cerebral cortex for glucose, oxygen, and lactate during the two primary electroencephalographic patterns (high and low voltage) in unanesthetized, near-term fetal sheep. Oxygen consumption was 127 mumol/min/100 g brain in high voltage and was 14% higher in low voltage. Glucose uptake was 19 mumol/min/100 g and was 37% higher in low voltage. Cerebral blood flow was 112 ml/min/100 g and was 29% higher in low voltage. The glucose:oxygen quotient increased from 0.91 in high voltage to 1.08 in low voltage. There was a net lactate efflux of 3.2 mumol/min/100 g during low voltage compared to a net influx of 3.3 mumol/min/100 g in high voltage. During high voltage the fetal brain uses a small amount of lactate for oxidative metabolism. During low voltage, glucose uptake exceeds the oxygen uptake needed for completely aerobic consumption, and a portion of the energy utilized by the brain is produced anaerobically.

The effect of cephalic hypotension on brain metabolism was studied in 10 unanesthetized, normoxic (PaO2 >17 mm Hg), late-gestation fetal lambs. Perfusion pressure (cephalic arterial minus sagittal venous pressure) was 40 ±1 mm Hg (SEM) during control and was reduced to 10 ± 1 by occlusion of the Grachiocephalic artery. Cerebral blood flow was measured with microspheres, and arterial and sagittal vein blood samples were analyzed for oxygen content, glucose, and lactate. During the occlusion, oxygen consumption decreased from 125 ± 8 to 95 ± 4 (p < 0.05) (all values μmol 100 g−1 min−1), and glucose uptake increased from 20 ±3 to 25 ± 1 (p < 0.05). During the control period, there was no net lactate flux; during the occlusion, lactate excretion was 5.7 ± 1.4 (p < 0.005). The control glucose and oxygen uptakes demonstrated a normal 6:1 molar ratio; however, during the occlusion, 9.4 μmol 100 g−1 glucose min−1 were taken up in excess of expected aerobic glucose metabolism. If all of this glucose were anaerobically metabolized to lactate, three times the measured efflux would be produced. The transport properties of the fetal blood-brain barrier may be important factors in perinatal brain injury.