February 1994
Volume 35, Issue 2
Free
Articles  |   February 1994
Subretinal neovascularization after naphthalene damage to the rabbit retina.
Author Affiliations
  • N Orzalesi
    Eye Clinic, University of Milan, H. S. Paolo, Italy.
  • L Migliavacca
    Eye Clinic, University of Milan, H. S. Paolo, Italy.
  • S Miglior
    Eye Clinic, University of Milan, H. S. Paolo, Italy.
Investigative Ophthalmology & Visual Science February 1994, Vol.35, 696-705. doi:
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      N Orzalesi, L Migliavacca, S Miglior; Subretinal neovascularization after naphthalene damage to the rabbit retina.. Invest. Ophthalmol. Vis. Sci. 1994;35(2):696-705.

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

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Abstract

PURPOSE: To examine the retinotoxic effect of naphthalene, a powerful oxidative agent and a well-known cataractogenic agent. METHODS: A 10% solution of naphthalene dissolved in paraffin oil was given every other day by gavage to 31 pigmented rabbits for 5 weeks, at a dose of 1 g/kg body weight. Four rabbits who received only paraffin oil served as controls. The eyes were clinically followed up by means of ophthalmoscopy and retinal fluorangiography. At selected intervals, the eyes were examined with light microscopy and transmission electron microscopy. RESULTS: The first lesions were focal and appeared in the periphery of the fundus about 3 weeks after the beginning of treatment and tended to spread over the entire retina. Histologically, there was a degeneration of photoreceptors, accompanied by a reaction and proliferation of retinal pigment epithelium (RPE) that phagocytized the damaged visual cells. After about 3 months, the proliferation of RPE was followed by subretinal neovascularization (SRN). Both mature fenestrated and thick-walled non-fenestrated capillaries penetrated Bruch's membrane, enveloped by abundant fibrous extracellular matrix and accompanied by pericytes. As a consequence of this process, the retina was focally transformed into a "neovascular complex" in which a vascular plexus was intermingled with pseudo-acinar cavities lined by RPE. There were no signs of SRN at retinal fluorangiography, possibly because of the dense microenvironment of extracellular matrix and RPE cells of the neovascular complexes. CONCLUSIONS: Naphthalene degeneration of the rabbit retina appears to be a simple model of photoreceptor vulnerability in the first stages of SRN thereafter. The close chronologic and topographic relationship between the appearance of the anomalous vessels and RPE alteration and the close resemblance with previous models of experimental SRN may support the hypothesis of an experimental model of SRN triggered by the RPE.

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