Nitric oxide is involved in sustained and delayed cell death of rat retina following transient ischemia

被引：44

作者：

Ju, WK ^{[1
]}

Kim, KY ^{[1
]}

Park, SJ ^{[1
]}

Park, DK ^{[1
]}

Park, CB ^{[1
]}

Oh, SJ ^{[1
]}

Chung, JW ^{[1
]}

Chun, MH ^{[1
]}

机构：

[1] Catholic Univ Korea, Coll Med, Dept Anat, Seoul 137701, South Korea

来源：

BRAIN RESEARCH | 2000年 / 881卷 / 02期

关键词：

nitric oxide; N-G-nitro-L-arginine methyl ester; ischemia; retina; rat;

D O I：

10.1016/S0006-8993(00)02816-X

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

We 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 1 week). In late postischemic stages (2-4 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. Our 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. (C) 2000 Elsevier Science B.V. All rights reserved.

引用

页码：231 / 236

页数：6

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