Purpose. Nitric oxide (NO) or "endothelial cell relaxing factor" is a potent endogenous vasodilator that regulates cerebral, choroidal, and retinal blood flow. This study utilized N-nitro L-arginine (LNA) inhibition of nitric oxide synthase (NOS) to investigate the effects of NO on oxygen-induced retinopathy in a rat model of ROP. Methods. Timed gravid Sprague-Dawley rats produced litters that were divided at birth and placed in either 70% O2 or room air. Within both environments rat pups were again divided and injected with either saline or 100mg/kg of LNA. After 10 days, pups were sacrificed, brains harvested and globes enucleated. Whole mount retina preparations with ADPase-specific staining of retinal vasculature were photographed and areas of non-perfusion digitized. Brain NOS activity was measured with a radioimmunoassay utilizing the conversion of 14C-L-arginine to 14C-L-citrulline. Results. NOS activity in the brains of LNA treated pups was undetectable. Substantial NOS activity was detected in the brains of all saline injected pups. Rat pups raised in 70% O2 with NOS inhibition exhibited significantly greater areas of vascular non-perfusion when compared with pups raised in 70% O2 without NOS inhibition, 38.7% vs. 23.6% non-perfused retinal area (p=.0089, non-paired Student T-test). No significant differences in the areas of retinal non-perfusion were observed in the control or LNA treated room air rat pups. Conclusion. Inhibiting NOS potentiates oxygen-induced retinal non-perfusion. Nitric oxide may protect developing retinal vasculature from the effects of hyperoxic vasoconstriction.
|Original language||English (US)|
|Journal||Investigative Ophthalmology and Visual Science|
|State||Published - Feb 15 1996|
ASJC Scopus subject areas
- Sensory Systems
- Cellular and Molecular Neuroscience