title: Clinical and histopathologic features of canine oxygen-induced proliferative retinopathy.
abstract: OBJECTIVE
  In previous studies the morphologic features of the acute vaso-obliterative and vasoproliferative stages of oxygen-induced retinopathy (OIR) were quantified and described in the dog model of retinopathy of prematurity (ROP). In the present study the sequelae of these events were examined using fluorescein angiography and histologic, enzyme, and immunohistochemical techniques.
  
  
  METHODS
  Thirty newborn animals were exposed to 95% to 100% oxygen for 4 days and returned to room air until they were 22 to 45 days of age. Before death some animals were anesthetized, and fluorescein angiography was performed. Retina and vitreous from some animals were processed for adenosine diphosphatase (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 showed dilated and tortuous retinal vessels, pigmentary changes, incomplete vascularization of peripheral retina, vitreous hemorrhage, and persistence of massive intravitreal neovascularization. Full-thickness eyewall sections showed tractional retinal folds, tented intravitreal vascularized membranes, and vitreous synchysis. Immunohistochemical analysis showed inner retinal astrogliosis. Enzyme histochemistry showed high alpha glycerophosphate dehydrogenase activity in poorly differentiated neovascular formations and low activity in formations with mature pericytes and endothelial cells.
  
  
  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.
authors.affiliation: Wilmer Ophthalmological Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
authors.forename: D S
authors.initials: DS
authors.lastname: McLeod
authors.forename: S A
authors.initials: SA
authors.lastname: D'Anna
authors.forename: G A
authors.initials: GA
authors.lastname: Lutty
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D001081:Apyrase / Q000378:metabolism; D001253:Astrocytes / Q000378:metabolism / Q000473:pathology; D004195:Disease Models, Animal; D004285:Dogs; D005451:Fluorescein Angiography; D005654:Fundus Oculi; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D005993:Glycerolphosphate Dehydrogenase / Q000378:metabolism; D006801:Humans; D018496:Hyperoxia / Q000150:complications; D007124:Immunoenzyme Techniques; D007231:Infant, Newborn; D010100:Oxygen / Q000009:adverse effects*; D012160:Retina / Q000378:metabolism / Q000473:pathology; D015861:Retinal Neovascularization / Q000209:etiology / Q000378:metabolism / Q000473:pathology*; D012178:Retinopathy of Prematurity / Q000209:etiology / Q000378:metabolism / Q000473:pathology*; D014823:Vitreous Hemorrhage / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D014841:von Willebrand Factor / Q000378:metabolism
chemical_list: D005904:Glial Fibrillary Acidic Protein; D014841:von Willebrand Factor; D005993:Glycerolphosphate Dehydrogenase; D001081:Apyrase; D010100:Oxygen