EFFECT OF HYPOXIA ON GLUCOSE-MODULATED CEREBRAL LACTIC-ACIDOSIS, AGONAL GLYCOLYTIC RATES, AND ENERGY-UTILIZATION

Newborn and 1-mo-old swine were exposed to identical durations (18 min ) and degrees of hypoxia (O-2 content = 4 mL/dL), to examine the effec ts of hypoxia on cerebral energy metabolism and intracellular pH (pH(i )) in vivo, using P-31 and H-1 nuclear magnetic resonance spectroscopy . Hypoxia produced the same extent of reductions in phosphocreatine (P Cr) (63 +/- 28% and 65 +/- 10%, newborns and 1-mo-olds, respectively) and pH(i) (6.93 +/- 0.06 and 6.89 +/- 0.06, respectively) for either a ge group. The magnitude of changes in PCr, lactate, and pH(i) was larg er for subgroups of data collected when cardiovascular instability was present, suggesting that hypotension and possibly reduced cerebral pe rfusion contributed to cerebral energy failure and lactic-acidosis for either age group. There were no correlations between the blood plasma glucose concentration at 18 min of hypoxia and the extent of change i n PCr, lactate, or pH(i) for either age group. During a subsequent per iod of complete ischemia induced via cardiac arrest after 20 min hypox ia, the decline in PCr and nucleoside triphosphate (NTP), and increase in lactate followed similar rates compared with previously studied ag e-matched animals that were normoxic before ischemia. The rate constan ts for the change in PCr, NTP, and lactate during ischemia showed no c orrelation with the blood plasma glucose concentration measured immedi ately before cardiac arrest. These results suggest that cerebral glyco lytic rates and energy utilization during ischemia are unaffected by a preceding interval of hypoxia and that hyperglycemia does not delay c erebral energy failure during hypoxia or combined hypoxic-ischemia.