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(Investigative Ophthalmology and Visual Science. 2001;42:1111-1118.)
© 2001 by The Association for Research in Vision and Ophthalmology, Inc.

Graded Contribution of Retinal Maturation to the Development of Oxygen-Induced Retinopathy in Rats

Olga Dembinska1, Luz Marina Rojas2, Daya R. Varma3,4,5, Sylvain Chemtob6 and Pierre Lachapelle1,7

1 From the Departments of Neurology and Neurosurgery, 6 Pharmacology and Therapeutics, and 7 Ophthalmology, McGill University, Montreal, Quebec, Canada; 2 Instituto de Investigaciones en Biomedicina y Ciencias Aplicadas, Universidad de Oriente, Sucre, Venezuela; and the 3 Departments of Pediatrics, 4 Ophthalmology, and 5 Pharmacology, University of Montreal, Quebec, Canada.

PURPOSE. Newborn rats exposed to hyperoxia during the first days of life have been shown to exhibit not only vasculopathy but also permanent changes in the structure and function of the retina. Given that the rat retina is immature at birth and that the maturation process continues until the opening of the eyes at 14 days of life, this study was conducted to investigate the susceptibility of the retina to oxygen toxicity as a function of the degree of retinal maturity reached at the time of oxygen exposure.

METHODS. Newborn rats were exposed to hyperoxia during selected postnatal day intervals. Scotopic electroretinograms were recorded at 30 and 60 days of age, and retinal histology was obtained at the end of the study.

RESULTS. There was a strong correlation between the duration of the hyperoxic event and the structural and functional consequences in the retina. However, the repercussions were significantly more profound when the exposure to oxygen occurred within the second week of life (6–14 days), compared with earlier (0–6 days) or later periods (14–28 days).

CONCLUSIONS. The results strongly suggest that the structural and functional retinal changes secondary to postnatal hyperoxia are not only the direct consequence of exposure to high levels of oxygen (i.e., free radicals), but also are determined by the level of retinal maturity reached at the time of oxygen exposure. The results also indicate that the structural anomalies precede the functional impairments.




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