Elevation of the ocular pressure in the anterior chamber of the rat ey
e caused major ischemic damage, manifested as changes in retinal morph
ology. The two most affected structures were the inner plexiform layer
, which decreased in thickness by 90%, and the number of ganglion cell
s, which decreased by 80%. Pretreatment of the animals with N-omega-ni
tro-L-arginine, a nitric oxide (NOS) inhibitor, almost completely abol
ished the ischemic damage. Administration of aminoguanidine, a NOS inh
ibitor se selective for the inducible enzyme, partially abolished the
ischemic damage. Moreover, administration of the NOS inhibitors 1 h af
ter ischemia, also protected the retina from damage, suggesting that s
imilarly acting drugs could be used clinically to limit ischemic injur
y in humans, We conclude that NOS, and therefore NO, may be involved i
n the mechanism of ischemic injury to the retina.