Assessment of energy metabolism in the developing brain following aglycemic hypoxia by H-1 and P-31 NMR

The role played by external calcium and calcium channels in the recovery from aglycaemic hypoxia in cortical brain slices from 10-day old rats was investigated by H-1 and P-31 NMR. 30 minutes of aglycaemic hypoxia significantly decreased the levels of phosphocreatine (PCr), ATP, lactate and intracellular pH (pH(i)). After a 30 minute recovery period there was incomplete recovery of PCr and ATP with lactate increasing by 50% with pH(i) normal. When the aglycemic hypoxia was carried out in media which had no added calcium (similar to 10 mu M) the PCr and ATP recovery was significantly greater. Application of diltiazem or verapamil but not nifedipine significantly improved the recovery from the aglycemic hypoxia. These data suggest that calcium influx through L-type voltage-gated calcium channels is involved in the ischemic damage in neonatal brain which manifests itself as a decrease in the energy state and an increase in lactate.