EFFECT OF NITRIC-OXIDE SYNTHASE INHIBITION ON BLOOD-FLOW AFTER RETINAL ISCHEMIA IN CATS

Purpose. To determine the effect of nitric oxide synthase inhibition o n blood flow in the cat retina and on changes in the electroretinogram after 1 hour of ocular ischemia. Methods. After the induction of gene ral anesthesia, one eye in each of 18 cats was subjected to 60 minutes of ischemia by raising intraocular pressure above systolic arterial p ressure. One group (n = 9) was administered 30 mg/kg L-NG-nitro-argini ne-methylcester (L-NAME) intravenously 60 minutes before ischemia. The other group (n = 9) was administered an equivalent volume of saline i ntravenously. Five minutes after the end of ischemia, blood flow in th e retina, choroid, and iris-ciliary body was measured using injections of radioactively labeled microspheres. Electroretinographic studies w ere carried out before, during, and 1, 2, 3, and 4 hours after ischemi a ended. Arterial blood gas tension, systemic arterial pressure, hemat ocrit, and anesthetic levels were controlled in each experiment. Resul ts. Basal blood flow in iris-ciliary body was decreased by L-NAME, whe reas retinal and choroidal blood flow was unchanged. Postischemic hype remia was unaltered in the choroid and reduced in the retina. There wa s enhancement of postischemic hyperemia in the iris-ciliary body, but this effect may have resulted from a decrease in basal flow in the L-N AME group. Electroretinographic a- and b-wave recoveries were not alte red by L-NAME; L-NAME infusion significantly decreased b-wave amplitud e. Conclusions. Nitric oxide appears to be a significant factor in the regulation of uveal circulation and may contribute to the regulation of retinal, but not choroidal, blood flow after ischemia. The authors could not detect a difference in outcome by electroretinography with o r without nitric oxide synthase inhibition.