Abstract
Abstract: :
Purpose: The present study was undertaken to determine the effect of modulating intraretinal nitric oxide (NO) levels on retinal oxygen tension (PO2) and the electroretinogram (ERG). Methods: Intraretinal oxygen profiles and ERG measurements were obtained from the dark–adapted retina of anesthetized cats using a double–barreled oxygen microelectrode. Vitreal ERG responses to bright flashes were also obtained. The NO levels were modulated by two–50 µl intravitreal injections of either nitric oxide synthase (NOS) inhibitors or a NO donor: NG–nitro–L– arginine methyl ester (L–NAME, 2.5 mM vit. conc, eNOS inhibitor), 1–(2–trifluoromethylphenyl) imidazole (TRIM, 200 µM vit. conc, nNOS inhibitor) and S–nitroso–N–acetylpenicilliamin (SNAP, 200 µM vit. conc, NO donor). Pre– and post–treatment PO2 profiles and ERG responses were obtained. Results: After L–NAME treatment, the inner retinal PO2 increased by ∼100% compared to pre–treatment PO2. The treatment with TRIM followed 6.5 hrs after L–NAME injections decreased the inner retinal PO2 to near zero. Injections of SNAP restored the inner retinal PO2 to near pre–treatment value. The outer retinal oxygenation was relatively unchanged by the either NOS inhibitors or NO donor. Vitreal a– and b–wave amplitudes in response to bright flashes were reduced by 35% and 40%, respectively, by the L–NAME treatment. TRIM treatment alone increased the a– and b–wave amplitudes by 14% and 30%, respectively. The treatment with SNAP after L–NAME and TRIM increased the a– and b–wave amplitudes by ∼10%. Conclusions: These findings suggest that intravitreal administration of L–NAME, TRIM, and SNAP had selective local effects on the retina without systemic physiological effects. The inner retinal oxygenation was affected by the NOS inhibitors and NO donor treatments whereas the outer retina was unaffected. The vasodilatory/vasoconstriction mechanisms of NO modulation probably were involved in the changes in the intraretinal oxygen tension. ERG components were also affected, suggesting a modulation in the retinal activity due to the NOS inhibitors and NO donor treatments.
Keywords: electroretinography: non–clinical • metabolism • nitric oxide