November 1995
Volume 36, Issue 12
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Articles  |   November 1995
Effect of nitric oxide synthase inhibition on blood flow after retinal ischemia in cats.
Author Affiliations
  • P Ostwald
    Department of Anesthesia and Critical Care, University of Chicago, IL 60637, USA.
  • I M Goldstein
    Department of Anesthesia and Critical Care, University of Chicago, IL 60637, USA.
  • A Pachnanda
    Department of Anesthesia and Critical Care, University of Chicago, IL 60637, USA.
  • S Roth
    Department of Anesthesia and Critical Care, University of Chicago, IL 60637, USA.
Investigative Ophthalmology & Visual Science November 1995, Vol.36, 2396-2403. doi:
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    • Get Citation

      P Ostwald, I M Goldstein, A Pachnanda, S Roth; Effect of nitric oxide synthase inhibition on blood flow after retinal ischemia in cats.. Invest. Ophthalmol. Vis. Sci. 1995;36(12):2396-2403.

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Abstract

PURPOSE: To determine the effect of nitric oxide synthase inhibition on blood flow in the cat retina and on changes in the electroretinogram after 1 hour of ocular ischemia. METHODS: After the induction of general anesthesia, one eye in each of 18 cats was subjected to 60 minutes of ischemia by raising intraocular pressure above systolic arterial pressure. One group (n = 9) was administered 30 mg/kg L-NG-nitro-arginine-methylester (L-NAME) intravenously 60 minutes before ischemia. The other group (n = 9) was administered an equivalent volume of saline intravenously. Five minutes after the end of ischemia, blood flow in the retina, choroid, and iris-ciliary body was measured using injections of radioactively labeled microspheres. Electroretinographic studies were carried out before, during, and 1, 2, 3, and 4 hours after ischemia ended. Arterial blood gas tension, systemic arterial pressure, hematocrit, and anesthetic levels were controlled in each experiment. RESULTS: Basal blood flow in iris-ciliary body was decreased by L-NAME, whereas retinal and choroidal blood flow was unchanged. Postischemic hyperemia was unaltered in the choroid and reduced in the retina. There was enhancement of postischemic hyperemia in the iris-ciliary body, but this effect may have resulted from a decrease in basal flow in the L-NAME group. Electroretinographic a- and b-wave recoveries were not altered by L-NAME; L-NAME infusion significantly decreased b-wave amplitude. 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 or without nitric oxide synthase inhibition.

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