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

We have investigated the role of nitric oxide (NO) in the rat retina follow ing ischemic injury induced by transient increase of intraocular pressure. The thickness of both the inner plexiform layer and inner nuclear layer dec reased during early postischemic stages (up to 1 week). In late postischemi c stages (2-4 weeks), the thickness of the outer nuclear layer (ONL) decrea sed markedly. Thus, mechanisms other than excitotoxic ones may contribute t o postischemic retinal cell death. Treatment of rats with N-G-nitro-L-argin ine methyl ester, a nitric oxide synthase (NOS) inhibitor, significantly re duced ischemic damage. Our findings suggest that NO is involved in the mech anism of ischemic injury, and plays a key role in the delayed and sustained cell death in the ONL following transient retinal ischemia. (C) 2000 Elsev ier Science B.V. All rights reserved.