Assessment of energy metabolism in the developing brain following aglycemic hypoxia by1H and31P NMR |
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Authors: | Keith J Brooks John B Clark Timothy E Bates |
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Institution: | (1) Department of Neurochemistry, Institute of Neurology, University of London, Queen Square, WC1N 3BG London, England |
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Abstract: | 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 by1H and31P NMR. 30 minutes of aglycaemic hypoxia significantly decreased the levels of phosphocreatine (PCr), ATP, lactate and intracellular
pH (pHi). After a 30 minute recovery period there was incomplete recovery of PCr and ATP with lactate increasing by 50% with pHi normal. When the aglycemic hypoxia was carried out in media which had no added calcium (≈10 μM) 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 voltagegated 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.
Dedication This article is dedicated to our friend and colleague Herman Bachelard. We wish to thank him for his comradeship,
advice and support over many years. Our hope for him is a long and fruiful retirement and that he will remain active in the
neurosciences for many years, even though the establishment has blown for “full time”. |
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Keywords: | Brain ischemia neonatal calcium 31P NMR 1H NMR |
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