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Abstract #15839 Published in IGR 2-3
Nitric oxide is involved in sustained and delayed cell death of rat retina following transient ischemia
Ju W; Kim K; Park S; Park D; Park C; Oh S; Chung J; Chun MMolecular Brain Research 2000; 881: 231-236
The authors have investigated the role of nitric oxide (NO) in the rat retina following ischemic injury induced by transient increase of intraocular pressure. The thickness of both the inner plexiform layer and inner nuclear layer decreased during early postischemic stages (up to one week). In late postischemic stages (two to four weeks), the thickness of the outer nuclear layer (ONL) decreased markedly. Thus, mechanisms other than excitotoxic ones may contribute to postischemic retinal cell death. Treatment of rats with N(G)-nitro-L-arginine methyl ester, a nitric oxide synthase (NOS) inhibitor, significantly reduced ischemic damage. The findings suggest that NO is involved in the mechanism of ischemic injury, and plays a key role in the delayed and sustained cell death in the ONL following transient retinal ischemia.
Dr. W. Ju, Department of Anatomy, College of Medicine, The Catholic University of Korea, 505 Banpo-dong, Socho-gu, 137-701, Seoul, South Korea
Classification:
1.3 Pathogenesis (Part of: 1 General aspects)
