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

• Published in: Brain research 2000-10, Vol.881 (2), p.231-236
• Main Authors: Ju, Won-Kyu, Kim, Keun-Young, Park, Sung-Jin, Park, Dae-Kyoon, Park, Cheol-Beom, Oh, Su-Ja, Chung, Jin-Woong, Chun, Myung-Hoon
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; Cell Death - drug effects; Cell Death - physiology; Enzyme Inhibitors - pharmacology; Enzyme Inhibitors - therapeutic use; Ischemia; Male; Medical sciences; NG-nitro- l-arginine methyl ester; NG-Nitroarginine Methyl Ester - pharmacology; NG-Nitroarginine Methyl Ester - therapeutic use; Nitric oxide; Nitric Oxide - metabolism; Ophthalmology; Rat; Rats; Rats, Sprague-Dawley; Reperfusion Injury - drug therapy; Reperfusion Injury - metabolism; Reperfusion Injury - pathology; Retina; Retina - drug effects; Retina - metabolism; Retina - pathology; Retinopathies
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/S0006-8993(00)02816-X

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.