June 1992
Volume 33, Issue 7
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Articles  |   June 1992
Vascular changes and their mechanisms in the feline model of retinopathy of prematurity.
Author Affiliations
  • T Chan-Ling
    Department of Anatomy, University of Sydney, Australia.
  • S Tout
    Department of Anatomy, University of Sydney, Australia.
  • H Holländer
    Department of Anatomy, University of Sydney, Australia.
  • J Stone
    Department of Anatomy, University of Sydney, Australia.
Investigative Ophthalmology & Visual Science June 1992, Vol.33, 2128-2147. doi:
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      T Chan-Ling, S Tout, H Holländer, J Stone; Vascular changes and their mechanisms in the feline model of retinopathy of prematurity.. Invest. Ophthalmol. Vis. Sci. 1992;33(7):2128-2147.

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      © 2016 Association for Research in Vision and Ophthalmology.

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Abstract

This study documents changes to retinal vasculature during the feline form of retinopathy of prematurity (ROP). The authors describe the closure and obliteration of retinal vessels during exposure to high oxygen, the pattern and tempo of growth of proliferative vasculature, which, after the return of the animal to room air, extends from the optic disc in a spectacular "rosette" pattern, the formation of preretinal vascular growths, and an initial lack of barrier properties in the new vessels. Finally, the response of the vasculature to the relief of hypoxia is reported, including the gradual establishment of barrier properties in the intraretinal vessels, the partial normalization of the proliferative vessels, and the abnormalities that persist. It is suggested that the vascular changes occur in successive stages: closure and obliteration during hyperoxia, vasoproliferation induced by hypoxia, and normalization after the relief of hypoxia with distinct cellular mechanisms and stimuli. It is argued that the same stages can be seen in the human form of ROP; two possible stimuli for the fibroplasia that damages the retina in human ROP are discussed.

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