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Z. Charara, A.L. Dorfman, S. Joly, J. Racine, S. Chemtob, P. Lachapelle; Oxygen–Induced Retinopathy in Neonatal Rats: How Much Oxygen Do We Need? . Invest. Ophthalmol. Vis. Sci. 2005;46(13):3440.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: Previous studies have shown that the retina of newborn pigmented Long Evans (LE) rats and albino Sprague Dawley (SD) rats exposed to hyperoxia (80% O2) during the second week of life sustain permanent functional and structural damage. The purpose of this study was to find the threshold at which exposure to hyperoxia causes this damage. Methods: Newborn LE (n=35) and SD rats (n=45) were exposed to hyperoxia (40%, 60% and 80%) from birth to postnatal day six and 14, respectively and from postnatal day 6 through 14. Results were compared to control rats raised in room air. Scotopic (intensity: –6.3 to 0.6 log cd.m–2.s; 12 hours dark adaptation) and photopic (intensity: 0.9 log cd.m–2.s, background: 30 cd.m–2) ERGs were recorded at postnatal days 30 and 60. Retinal sections (enucleation at 60 days; 0.5 µm sections, toluidine blue staining) were also analyzed in rats exposed from day 0 to day 14. Results: A typical and predictable (based on a dose–response effect) oxygen induced retinopathy could be evidenced following 60% O2 exposure in SD and LE rats. In contrast, exposure to 40% O2 had no significant detrimental effect on the photopic and scotopic responses of SD rats, while LE rats showed a significant reduction in photopic and scotopic ERG amplitudes following exposure between P6–P14 only. Histological analysis revealed a thinning of the ONL, INL and IPL for LE rats exposed to 40%, 60% and 80% O2, as well as a thinning of the OPL at 40% and a complete destruction of the latter following exposures to 60% and 80% O2. Conclusions:Exposure to 40% O2 is not sufficient to bring about significant functional or structural changes in SD rats, whereas LE rats are already affected at this concentration. Our results would therefore further support our previous demonstration that LE rats are more susceptible than SD rats to postnatal hyperoxia. The reasons for this strain difference remains to be elucidated.
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