[Protective effect of nitric oxide on ischemic retina]

Nitric oxide (NO) is a free radical and was regarded as noxious to life. But recent studies show that NO is an important substance for transcellular signal transduction. It also seems to act as a neurotransmitter in the nervous system. In ischemic nerve tissue a release of glutamate is one of the critical factors that increase neuronal death, and some experiments suggest that NO may be involved in this process. Here we provide evidence that NO provides neuroprotection in ischemic retinas in vivo. Albino rabbits' eyes were subjected to 60 minutes of ischemia by raising intraocular pressure. Before ischemia the eyes were treated intravitreously with the NO-precursor L-arginine, the NO synthase-inhibitor nitro-L-arginine methyl ester hydrochloride (L-NAME), the NO-donor sodium nitroprusside (SNP), or solvent only. The amplitude of the b-wave was measured and the recovery ratio of the b-wave was analyzed hourly after reperfusion. The recovery ratio of b-wave in the eyes with L-arginine and with SNP increased more rapidly than in the controls, while the recovery ratio in the eyes with L-NAME increased in a way similar to that of the controls. These results suggest that NO plays a neuroprotective role in ischemic retina. It may be involved with S-nitrosylation of some proteins, including one of the glutamate receptors, the N-methyl-D-aspertate (NMDA) receptor.