Vascular changes and their mechanisms in the feline model of retinopathy of prematurity.
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.
Chan-Ling
T
T
Department of Anatomy, University of Sydney, Australia.
Tout
S
S
Holländer
H
H
Stone
J
J
D000818:Animals; D002415:Cats; D004195:Disease Models, Animal; D005451:Fluorescein Angiography; D016650:Fluorescein-5-isothiocyanate / Q000378:metabolism; D006735:Horseradish Peroxidase; D006801:Humans; D000860:Hypoxia / Q000503:physiopathology; D007231:Infant, Newborn; D037102:Lectins / Q000378:metabolism; D010101:Oxygen Consumption; D015861:Retinal Neovascularization / Q000378:metabolism / Q000473:pathology; D012171:Retinal Vessels / Q000378:metabolism / Q000648:ultrastructure*; D012178:Retinopathy of Prematurity / Q000378:metabolism / Q000473:pathology*
D037102:Lectins; D006735:Horseradish Peroxidase; D016650:Fluorescein-5-isothiocyanate