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 recove ry from aglycaemic hypoxia in cortical brain slices from 10-day old ra ts was investigated by H-1 and P-31 NMR. 30 minutes of aglycaemic hypo xia significantly decreased the levels of phosphocreatine (PCr), ATP, lactate and intracellular pH (pH(i)). After a 30 minute recovery perio d 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 A TP recovery was significantly greater. Application of diltiazem or ver apamil but not nifedipine significantly improved the recovery from the aglycemic hypoxia. These data suggest that calcium influx through L-t ype voltage-gated calcium channels is involved in the ischemic damage in neonatal brain which manifests itself as a decrease in the energy s tate and an increase in lactate.