May 2003
Volume 44, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2003
The Effects on Ocular Growth Rate of Inhibiting Compensatory Choroidal Expansion Using the Nitric Oxide Synthase Inhibitor L-NAME
Author Affiliations & Notes
  • E.C. Wilken
    Bioscience Dept, New England Coll Optometry, Boston, MA, United States
  • D.L. Nickla
    Bioscience Dept, New England Coll Optometry, Boston, MA, United States
  • Footnotes
    Commercial Relationships  E.C. Wilken, None; D.L. Nickla, None.
  • Footnotes
    Support  NIH Grant EY013636
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 2801. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      E.C. Wilken, D.L. Nickla; The Effects on Ocular Growth Rate of Inhibiting Compensatory Choroidal Expansion Using the Nitric Oxide Synthase Inhibitor L-NAME . Invest. Ophthalmol. Vis. Sci. 2003;44(13):2801.

      Download citation file:


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

      ×
  • Supplements
Abstract

Abstract: : Purpose: It is generally accepted that the increase in choroidal thickness in response to myopic defocus in chicks acts as a compensatory mechanism to move the retina towards the image plane (Wallman et al., 1995). It may also however, constitute part of the signal cascade in the visual regulation of eye growth, specifically, to decrease growth rate (Marzani and Wallman, 1997). To test this hypothesis, we used the non-specific nitric oxide synthase inhibitor L-NAME to prevent the transient defocus-induced choroidal thickening (Nickla et al., ARVO 1999) under two visual conditions associated with decreasing eye growth, and looked at the effects on ocular growth rate. Methods: Exp. 1: Chicks were monocularly deprived of form vision with translucent diffusers on day 6. On the following 4 days the diffusers were removed for 2 hrs/day, which normally prevents the development of myopia. One group received an intravitreal injection of 30 µl L-NAME (16 µM; n=7) 1 hr prior to the vision each day, a second received injections of saline (n=7). Exp. 2: Chicks were made myopic by 5 days of form deprivation. On the following 4 days the diffusers were removed for 2 hrs/day to allow 2 daily hrs of myopic defocus. One group received injections of L-NAME prior to vision (n=8), the other group received saline (n=6). Refractive errors were measured with a Hartinger's refractometer at the start and end of the experiment. Ocular dimensions were measured with high-frequency A-scan ultrasonography at various intervals. Results: L-NAME reduced the protective effect of brief daily periods of vision: eyes became significantly more myopic than saline controls (-9D vs –2.5D; p<0.005) and grew faster (change in vitreous chamber: 436 vs 251 µm; p<0.05) over the 4 days. L-NAME also inhibited the recovery from myopia (change in RE: 0D vs +4D; p<0.005); eyes grew faster than saline controls mainly over the initial 48 hrs (119 vs 0 µm/48hr; p<0.05). As expected, L-NAME prevented the transient (2 hr) vision-induced daily choroidal thickening in both experiments (0 vs 78 µm/2hrs; p<0.001). Notably, while the back of the eye grew faster in drug-injected eyes, growth of the anterior chamber was significantly reduced (120 vs 217 µm; p<0.0005). Conclusions: Preventing the daily transient vision-induced increases in choroidal thickness altered ocular growth rate in a consistent manner under two different visual conditions, in both preventing the vision-induced reduction in growth rate. This supports the hypothesis that visually-induced changes in choroidal thickness play a role in the visual regulation of ocular growth even if these changes are only transient.

Keywords: animal model • choroid • myopia 
×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×