End stage disease in the dog model of oxygen-induced retinopathy

D. S. McLeod, S. A. D'Anna, G. A. Lutty

Research output: Contribution to journalArticlepeer-review


Purpose. We have previously described the vaso-obliterative and vasoproliferative stages of oxygen-induced retinopathy (OIR), in the dog model of retinopathy of prematurity (ROP). In this study we examined the end stage disease in this model using fluorescein angiography, histology and enzyme and immunohistochemical techniques. Methods. Nine newborn animals were exposed to 95-100% oxygen for 4 days and returned to room air for periods ranging from 22-45 days of age. Prior to sacrifice, animals were anesthetized and fluorescein angiography performed. Retina and vitreous from some animals were processed for ADPase flat-embedding. In other cases, eyes were prepared for full thickness eyewall sectioning or frozen for histochemical analysis. Results. Fluorescein angiography, funduscopic examination and ADPase preparations revealed dilated and tortuous retinal vessels, pigmentary changes, incomplete vascularization of peripheral retina, vitreous hemorrhage and persistence of massive preretinal neovascularization. Full thickness eyewall sections demonstrated fractional retinal folds, tented preretinal vascularized membranes and severe vitreous synchysis. Immunohistochemical analysis revealed inner retinal astrogliosis. Enzyme histochemistry demonstrated impaired retinal oxidative metabolism despite normal neuronal and photoreceptor differentiation. Conclusions. End stage OIR in the neonatal dog shares many features with the chronic human disease. These results provide additional support for the use of this model in experimental studies of ROP.

Original languageEnglish (US)
Pages (from-to)S132
JournalInvestigative Ophthalmology and Visual Science
Issue number3
StatePublished - Feb 15 1996

ASJC Scopus subject areas

  • Ophthalmology
  • Sensory Systems
  • Cellular and Molecular Neuroscience


Dive into the research topics of 'End stage disease in the dog model of oxygen-induced retinopathy'. Together they form a unique fingerprint.

Cite this