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Effects of dextromethorphan on ischemia induced electroretinogram changes in rabbit
W Cao1, M Zaharia, A Drumheller
1Department of Ophthalmology, Faculty of Medicine, Sherbrooke University, Quebec, Canada.
Abstract:
The present study was undertaken to determine whether dextromethorphan (DM), a potent N-methyl-D-aspartate antagonist, could attenuate the effects of ischemia on rabbit ERG. Retinal ischemia was induced by increasing intraocular pressure to 120 mm Hg for 30, 60, or 90 min. DM was intravenously administered before ischemia and maintained throughout the entire experimental period. ERGs were recorded prior to, during, and after ischemia. The results indicate that the b-wave hyperresponses and the delays in implicit times induced by 30 min. ischemia were suppressed by the administration of DM. Similar findings were obtained when ischemia lasted for 60 min, except that DM did not improve delayed implicit times, suggesting that cellular injury is still present. ERG changes resulting from 90 min ischemia were not reversed by DM treatment. Effects of DM treatment on a-wave were less prominent. Together, our results further support that DM can to some extent alleviate ischemic injury in the rabbit retina.
Insights
Dextromethorphan (DM) partially protected rabbit retinas from ischemic injury by suppressing ERG abnormalities. However, protection was limited, especially with prolonged ischemia, indicating residual cellular damage.
Area of Science:
- Ophthalmology
- Neuroscience
- Pharmacology
Background:
- Retinal ischemia can lead to significant visual impairment.
- N-methyl-D-aspartate (NMDA) receptor antagonists are explored for neuroprotective effects.
- Dextromethorphan (DM) is a known NMDA receptor antagonist.
Purpose of the Study:
- To investigate the neuroprotective potential of dextromethorphan (DM) against retinal ischemia in a rabbit model.
- To evaluate the effect of DM on electroretinogram (ERG) parameters during and after induced retinal ischemia.
Main Methods:
- Retinal ischemia was induced in rabbits by elevating intraocular pressure to 120 mm Hg for 30, 60, or 90 minutes.
- Dextromethorphan (DM) was administered intravenously prior to and during the ischemic period.
- Electroretinograms (ERGs) were recorded before, during, and after ischemia to assess retinal function.
Main Results:
- DM administration suppressed b-wave hyperresponses and delayed implicit times caused by 30-minute ischemia.
- DM showed partial efficacy for 60-minute ischemia, but did not reverse delayed implicit times, suggesting ongoing cellular injury.
- DM treatment did not reverse ERG changes associated with 90-minute ischemia.
- The effects of DM on the a-wave were less pronounced.
Conclusions:
- Dextromethorphan (DM) demonstrates a degree of neuroprotection against ischemic injury in the rabbit retina.
- The protective effects of DM are dependent on the duration of ischemia.
- DM may alleviate, but not fully prevent, cellular damage from moderate retinal ischemia.