May 2008
Volume 49, Issue 13
ARVO Annual Meeting Abstract  |   May 2008
Vascular-Induced Retinal Degradation
Author Affiliations & Notes
  • A. D. Springer
    Cell Biology & Anatomy, New York Medical College, Valhalla, New York
  • Footnotes
    Commercial Relationships  A.D. Springer, None.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science May 2008, Vol.49, 5897. doi:
  • Views
  • Share
  • Tools
    • Alerts
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      A. D. Springer; Vascular-Induced Retinal Degradation. Invest. Ophthalmol. Vis. Sci. 2008;49(13):5897.

      Download citation file:

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

  • Supplements

Purpose: : The objective was to evaluate the changing position of the inner retinal vasculature as the eye develops and ages. Retinal laminar deformation by inner retinal vessels was examined in a developmental series of macaque retinas. A hypothesis is presented that explains how the inner retinal vasculature is destined to damage the retina slowly over a prolonged period. Such degradation would be exacerbated when fluid flow across the retina is elevated as sometimes occurs in glaucoma.

Methods: : Paraffin sections through 13 macaque retinas varying in age from 73 - 4,189 days post-conception (dpc) were used to quantify the progressive sclerad displacement of inner retinal vessels. Sections were examined to determine the number of outward displacements of the inner nuclear layer (INL) caused by outward movement of large vessels in the underlying optic fiber and ganglion cell (GCL) layers.

Results: : Mean frequency of INL indentations/section (INLi) was initially 0-0.4 between 73-95 dpc and began rising rapidly thereafter. INLi rose to 6.2 just after birth at 180 dpc. INLi rose more slowly after birth and asymptoted at 5 months postnatal to 10.9. The onset of INLi was correlated with the development of retinal structures associated with intraocular pressure (IOP) (i.e., ciliary processes and Schlemm’s canal). Additional material revealed that INLi also occur in human retina.

Conclusions: : Hydrostatic pressure on the inner retina, in conjunction with the pumping of fluid by the pigment epithelium, causes slow outward fluid movement across the retina (Bill, 1976). Since arteries are stiffer and less permeable to fluids than retina, the continuous and slow movement of fluid across the retina gradually pushes the larger inner retinal arteries outwardly. Smaller vessels are displaced less. Over a prolonged period, such movements, by themselves, could damage retinal cells and axons by compressing them. Chronic elevation of IOP, as in glaucoma, would exacerbate the effect of outward arterial displacement in two additional ways. The arteries would be driven deeper into the retina, further compressing retinal tissue and the vessels would autoregulate and dilate in response to increased IOP. A 50% reduction in blood flow would produce a compensatory 19% increase in arterial diameter, further exacerbating the mechanical compressive effects of arteries on the inner retina.

Keywords: retinal development • pathology: human • anatomy 

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.