The Effect of the Nonspecific Nitric Oxide Synthase Inhibitor N G ‐Nitro‐l‐Arginine Methyl Ester on the Choroidal Compensatory Response to Myopic Defocus in Chickens

Purpose. Chick eyes show rapid compensation to retinal defocus. One component of this mechanism involves changes in the thickness of the choroid: when the retina is exposed to myopic defocus, the choroid thickens, pushing the retina forward; conversely, when the eye is exposed to hyperopic defocus, the choroid thins. The underlying mechanism(s) for these changes are unknown. We tested the hypothesis that nitric oxide might play a role. Methods. We examined the effect of the nonspecific nitric oxide synthase inhibitor N G ‐nitro‐l‐arginine methyl ester (l‐NAME) on the compensatory choroidal thickening in response to myopic defocus using two visual paradigms: first, in previously form‐deprived “recovering” eyes and, second, in eyes wearing +15 D spectacle lenses. l‐NAME was injected intravitreally after removal of the diffuser or immediately before putting on the lenses. In addition, we looked at the effect of l‐NAME on experimentally thickened choroids (induced by 1 week of recovery from deprivation myopia or 1 week of +15 D lens wear) and on choroids of normal eyes. Eyes were measured using A‐scan ultrasonography before the injections and at subsequent intervals for several days. As a control for the injection procedure, eyes with the same visual conditions were injected with saline. Fellow eyes were untreated and uninjected. Results. l‐NAME inhibited choroidal thickening in both previously form‐deprived eyes (2 vs. 117 μm; p < 0.001) and eyes wearing +15 D lenses (3 vs. 137 μm; p < 0.02). The effect was rapid, transient, and dose dependent (ED 50 , 0.26 μmoles). l‐NAME produced thinning in experimentally thickened choroids (recovering: −116 μm; lenses: −219 μm) and in normal choroids (−47 μm) within 7 hours. Conclusions. Nitric oxide may play a role in modulating choroidal thickness. The mechanism is as yet unknown.