Oxygen free radicals adversely affect the regulation of vascular tone by nitric oxide in the rabbit retina under high intraocular pressure.
Flash electroretinograms (ERG) were recorded in the rabbit eye submitted to high intraocular pressure (HIOP) induced by the suction-cup method. When intraocular pressure rose to 100 mmHg, ERG was suppressed but rapidly recovered even under HIOP when animals were pre-treated either intravitreously with a nitric oxide donor, sodium nitroprusside, or intravenously with free radical scavengers, superoxide dismutase (SOD)+catalase. In contrast, injection of a nitric oxide synthesis inhibitor, nitro-L-arginine, into the vitreous cavity inhibited the protective effect of SOD+catalase during HIOP-induced ERG extinction. These results suggest that nitric oxide could play a role in the regulation of ocular vessel tone and that severe ischemia can impede this effect through oxygen-derived free radical generation.
Veriac
S
S
Laboratory of Cellular Physiology, University of Montpellier, France.
Tissie
G
G
Bonne
C
C
D000818:Animals; D004596:Electroretinography / Q000187:drug effects; D005609:Free Radicals; D009569:Nitric Oxide / Q000494:pharmacology; D009599:Nitroprusside / Q000494:pharmacology; D009798:Ocular Hypertension / Q000503:physiopathology*; D011817:Rabbits; D012171:Retinal Vessels / Q000503:physiopathology*; D013482:Superoxide Dismutase / Q000494:pharmacology; D014655:Vascular Resistance / Q000502:physiology*
D005609:Free Radicals; D009599:Nitroprusside; D009569:Nitric Oxide; D013482:Superoxide Dismutase