N‐Methyl‐D‐Aspartate antagonist reduces stroke size and regional glucose metabolism
- 1 June 1990
- journal article
- research article
- Published by Wiley in Annals of Neurology
- Vol. 27 (6) , 606-611
- https://doi.org/10.1002/ana.410270604
Abstract
Pharmacological inhibition of cell excitation during focal ischemia was studied in the rat middle cerebral artery occlusion model. The potent and selective N‐methyl‐D‐aspartate antagonist CGS 19755, administered 5 minutes prior to or 5 minutes following permanent middle cerebral artery occlusion, caused a substantial decrease in infarct size, which was associated with reduction of postischemic cerebral glucose hypermetabolism. These data support a role for excitation‐induced hypermetabolism in the pathogenesis of infarction following focal cerebrovascular occlusion.This publication has 24 references indexed in Scilit:
- Dynamics of Extracellular Metabolites in the Striatum after Middle Cerebral Artery Occlusion in the Rat Monitored by Intracerebral MicrodialysisJournal of Cerebral Blood Flow & Metabolism, 1989
- The specific NMDA receptor antagonist AP-7 attenuates focal ischemic brain injuryNeuroscience Letters, 1989
- Dextromethorphan reduces neocortical ischemic neuronal damage in vivoBrain Research, 1988
- Protective Effect of the Glutamate Antagonist, MK-801 in Focal Cerebral Ischemia in the CatJournal of Cerebral Blood Flow & Metabolism, 1988
- Kynurenate inhibition of cell excitation decreases stroke size and deficitsAnnals of Neurology, 1987
- Excitotoxity and the NMDA receptorTrends in Neurosciences, 1987
- Blockade of N -Methyl-D-Aspartate Receptors May Protect Against Ischemic Damage in the BrainScience, 1984
- Elevation of the Extracellular Concentrations of Glutamate and Aspartate in Rat Hippocampus During Transient Cerebral Ischemia Monitored by Intracerebral MicrodialysisJournal of Neurochemistry, 1984
- Cerebral circulation and metabolismJournal of Neurosurgery, 1984
- The pathophysiology of brain ischemiaAnnals of Neurology, 1983