May 2007
Volume 48, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2007
Role of Neuronal Nitric Oxide in Retinal Blood Velocity and Electroretinogram
Author Affiliations & Notes
  • J. J. Kang Derwent
    Dept of Biomedical Eng, Illinois Institute of Technology, Chicago, Illinois
  • S. Tummala
    Dept of Biomedical Eng, Illinois Institute of Technology, Chicago, Illinois
  • K. Triandafilou
    Dept of Biomedical Eng, Illinois Institute of Technology, Chicago, Illinois
  • S. Benac
    Dept of Biomedical Eng, Illinois Institute of Technology, Chicago, Illinois
  • Footnotes
    Commercial Relationships J.J. Kang Derwent, None; S. Tummala, None; K. Triandafilou, None; S. Benac, None.
  • Footnotes
    Support The Whitaker Foundation
Investigative Ophthalmology & Visual Science May 2007, Vol.48, 2281. doi:
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      J. J. Kang Derwent, S. Tummala, K. Triandafilou, S. Benac; Role of Neuronal Nitric Oxide in Retinal Blood Velocity and Electroretinogram. Invest. Ophthalmol. Vis. Sci. 2007;48(13):2281.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose:: The main objective was to determine if neuronal nitric oxide synthase (nNOS) plays a role in control of retinal blood velocity and retinal cellular function, assessed by electroretinogram (ERG).

Methods:: Retinal blood velocity was determined by tracking 1 µm yellow-green fluorescent microspheres (505 nm maximum absorption and 515 nm maximum emission) in anesthetized pigmented adult rats. Using the scanning laser ophthalmoscope, retinal blood velocities were obtained in arteries, veins, and small vessels by recording several 2-min digital movies at each time point. Directional flow of fluorescent microspheres and vessel characterization were determined based on examination of infrared reflectance and fluorescein angiogram images. Post-treatment velocity measurements were obtained every 15 minutes for ~2 hours. In separate experiments, retinal cellular function was assessed by dark-adapted corneal single- and paired-flash ERG. The NO levels were modulated by one 3 µl intravitreal injections of either nitric oxide synthase (NOS) inhibitors, 1-(2-trifluoromethylphenyl) imidazole (TRIM, 2 mM vit. conc, nNOS inhibitor) and NG-nitro-L- arginine methyl ester (L-NAME, 2.5 mM vit. conc, nonselective inhibitor).

Results:: TRIM treatment decreased arterial velocity by ~18%, venous velocity by ~8% and small vessel (diameter < 40µm) velocity by ~5%. After L-NAME treatment, arterial velocity decreased significantly by ~19% and venous velocity decreased by ~33%. Single flash a- and b-wave amplitudes increased ~5% and ~20%, respectively, after the TRIM treatment where both a- and b-wave amplitudes decreased by ~30% after the L-NAME treatment. Time courses obtained through the paired-flash recordings after the TRIM injection were also altered. At a brighter test flash, the recovery of time course was slower compared to the pre- TRIM injection time course.

Conclusions:: These results suggested that nNOS may be involved in both retinal signal processing and retinal blood flow control.

Keywords: nitric oxide • electroretinography: non-clinical • blood supply 
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