title: Supplemental oxygen therapy. Basis for noninvasive treatment of retinopathy of prematurity.
abstract: OBJECTIVE
  To determine the effectiveness of supplemental oxygen therapy (SOT) in ameliorating the proliferative vasculopathy characteristic of the feline model of retinopathy of prematurity (ROP).
  
  
  METHODS
  Kittens were exposed to high (70% to 80%) oxygen for the first 4 days of life to induce obliteration of the retinal circulation. The level of inspired oxygen at successive stages after hyperoxia were varied systematically, and the retinas were examined for the extent of revascularization, astrocyte survival, intactness of the blood-retinal barrier, and extent of preretinal vessels.
  
  
  RESULTS
  The level of inspired oxygen required to protect the retina from hypoxic damage and yet provide a stimulus for growth of the vasculature varied during a 6-week period. The rate of revascularization of the retina increased as the oxygen content of the inspired gas mixture decreased, with a consequential increase in the pathology observed. However, a regimen that produced a quicker rate of revascularization with a slightly higher level of pathology actually offered the retina greater protection in the long term. The formation of preretinal vessels was effectively prevented by SOT. Supplemental oxygen therapy could be terminated once a significant portion of the retina was revascularized.
  
  
  CONCLUSIONS
  The proliferative vasculopathy of a kitten model of ROP can be significantly reduced by a regimen of SOT, which attempts to mimic physiological levels of hypoxia in the retina during its revascularization. Optimal revascularization requires a balance between the rate and quality of vessel growth. With further refinement of the protocol, SOT could provide noninvasive treatment of ROP in neonates.
authors.affiliation: Department of Anatomy and Histology, University of Sydney, Australia.
authors.forename: C L
authors.initials: CL
authors.lastname: Tailoi
authors.forename: B
authors.initials: B
authors.lastname: Gock
authors.forename: J
authors.initials: J
authors.lastname: Stone
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D001253:Astrocytes / Q000502:physiology; D001813:Blood-Retinal Barrier / Q000502:physiology; D001973:Bromodeoxyuridine; D002415:Cats; D002470:Cell Survival / Q000502:physiology; D004195:Disease Models, Animal; D005904:Glial Fibrillary Acidic Protein; D006801:Humans; D018496:Hyperoxia / Q000473:pathology / Q000503:physiopathology; D000860:Hypoxia / Q000473:pathology / Q000503:physiopathology; D007150:Immunohistochemistry; D007231:Infant, Newborn; D037102:Lectins; D010102:Oxygen Inhalation Therapy; D015861:Retinal Neovascularization / Q000473:pathology / Q000517:prevention & control; D012171:Retinal Vessels / Q000473:pathology / Q000502:physiology; D012178:Retinopathy of Prematurity / Q000473:pathology / Q000503:physiopathology / Q000628:therapy*
chemical_list: D005904:Glial Fibrillary Acidic Protein; D037102:Lectins; D001973:Bromodeoxyuridine