May 2003
Volume 44, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2003
The Examination of the Degeneration of Retinal Ganglion Cells Following Ischemia/Reperfusion in Rats, Cause of Reactive Oxygen Species, Using Radical Scavenger MCI-186
Author Affiliations & Notes
  • S. Kawai
    Biochemistry / Ophthalmology, Saitama Medical School / Saitama Medical Center, Saitama, Japan
  • T. Komoda
    Biochemistry, Saitama Medical School, Saitama, Japan
  • K. Kawai
    Ophthalmology, Saitama Medical Center, Saitama Medical School, Saitama, Japan
  • Footnotes
    Commercial Relationships  S. Kawai, None; T. Komoda, None; K. Kawai, None.
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 128. doi:
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      S. Kawai, T. Komoda, K. Kawai; The Examination of the Degeneration of Retinal Ganglion Cells Following Ischemia/Reperfusion in Rats, Cause of Reactive Oxygen Species, Using Radical Scavenger MCI-186 . Invest. Ophthalmol. Vis. Sci. 2003;44(13):128.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Abstract: : Purpose: Following retinal ischemia/reperfusion in the rat, retinal ganglion cell (RGC) degeneration occurs due to neurotoxicity of glutamate and nitric oxide (NO) generated by inducible nitric oxide synthese (NOS-2). We have previously presented that treatment with aminoguanidine significantly reduced the loss of RGCs following ischemia. However, several recent reports suggest that reactive oxygen species (ROS) play an important role of neurodegeneration as well. We have studied whether ROS caused the loss of RGCs following ischemia/reperfusion injury. Methods: Retinal ischemia was produced by transient elevation of intraocular pressure above systolic blood pressure for 75 minutes by intraocular cannulation. MCI-186, an radical scavenger, was injected intravenously two times of 3mg/kg, during ischemia and 30minutes after ischemia as group I for determining early phase of neurodegeneration, 4 and 5 days after ischemia as group II for determining late phase of neurodegeneretion and saline injected group as control. Loss of RGCs was determined quantitatively by retrograde labeling with Fluoro-Gold. Results: One week after ischemia, untreated animals lost 28.4±1.7% [mean±SD] RGCs centrally and 38.5±3.9% RGCs peripherally (n=4). Treatment with MCI-186 significantly reduced the loss of RGCs following ischemia 21.3±3.3% centrally (P=0.0339) and 31.4±2.7% peripherally (p=0.0339) in group I (n=3), however no significant difference in the both central (28.2±3.2%, p>0.9999) and peripheral (38.1±3.1%, p=0.5959) part of retina in the group II (n=3). Conclusions: Our results demonstrate that MCI-186 has neuroprotective effect in retinal ischemia/reperfusion in the rat. ROS play a part of role of early phase of RGCs degeneration following ischemia/reperfusion injury.

Keywords: neuroprotection • antioxidants • ischemia 
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