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Dextromethorphan reduces neocortical ischemic neuronal damage in vivo
C P George1, M P Goldberg, D W Choi
1Division of Neurosurgery, Stanford University Medical Center, CA 94305-5327.
Brain Research
|February 9, 1988
Summary
Dextromethorphan (DM), an N-methyl-D-aspartate (NMDA) receptor antagonist, significantly reduced brain damage in a rabbit model of acute ischemic stroke. DM treatment decreased severe neocortical neuronal damage by over 79% compared to controls.
Area of Science:
- Neuroscience
- Pharmacology
- Ischemic Stroke Research
Background:
- Acute transient focal cerebral ischemia is a leading cause of neurological damage.
- N-methyl-D-aspartate (NMDA) receptor overactivation contributes to excitotoxicity during ischemia.
- Dextromethorphan (DM) is a clinically tested NMDA receptor antagonist.
Purpose of the Study:
- To evaluate the neuroprotective efficacy of dextromethorphan (DM) in an in vivo model of acute transient focal cerebral ischemia.
- To determine the effect of DM on severe neocortical ischemic neuronal damage.
Main Methods:
- Rabbits underwent 1-hour occlusion of the left internal carotid and anterior cerebral arteries, followed by 4-hour reperfusion.
- Animals were pretreated with intravenous dextromethorphan (DM) or normal saline (NS) alone.
- Quantification of severe neocortical ischemic neuronal damage was performed.
Main Results:
- DM-treated animals exhibited a significant reduction in severe neocortical ischemic neuronal damage.
- The percentage of severe neocortical damage in DM-treated animals was 10.5%, compared to 49.6% in NS-treated animals.
- This represents a substantial neuroprotective effect of DM.
Conclusions:
- Dextromethorphan (DM) demonstrates significant neuroprotective properties against acute ischemic brain injury.
- DM's antagonism of the NMDA receptor may mediate its protective effects in cerebral ischemia.
- These findings support further investigation of DM as a potential therapeutic agent for stroke.