Abstract
This study was performed to examine the roles of body temperature, NMDA receptors and nitric oxide (NO) synthase in post-ischemic retinal injury in rats. Cell loss in the ganglion cell layer and thinning of the inner plexiform layer were observed 7 days after ischemia. Cell loss in the ganglion cell layer but not thinning of the inner plexiform layer was reduced by hypothermia during ischemia. Intravenous injection of dizocilpine (MK-801) or Nomega-nitro-L-arginine methyl ester (L-NAME) prior to ischemia ameliorated retinal injury. These results suggest that activation of NO synthase following NMDA receptor stimulation is involved in ischemia-induced retinal injury.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Body Temperature / drug effects
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Dizocilpine Maleate / pharmacology
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Enzyme Inhibitors / pharmacology
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Ischemia*
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Male
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NG-Nitroarginine Methyl Ester / pharmacology*
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Neuroprotective Agents / pharmacology
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Nitric Oxide Synthase / antagonists & inhibitors
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Nitric Oxide Synthase / physiology*
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Rats
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Rats, Sprague-Dawley
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Receptors, N-Methyl-D-Aspartate / antagonists & inhibitors
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Receptors, N-Methyl-D-Aspartate / physiology*
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Retina / metabolism
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Retinal Diseases / etiology*
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Retinal Diseases / metabolism
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Retinal Diseases / prevention & control
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Retinal Vessels*
Substances
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Enzyme Inhibitors
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Neuroprotective Agents
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Receptors, N-Methyl-D-Aspartate
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Dizocilpine Maleate
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Nitric Oxide Synthase
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NG-Nitroarginine Methyl Ester