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A. L. Dorfman, A. Polosa, S. Chemtob, P. Lachapelle; Retinal Maturity at Birth Predicts the Outcome of Oxygen Induced Retinopathy (OIR). Invest. Ophthalmol. Vis. Sci. 2010;51(13):5590.
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© ARVO (1962-2015); The Authors (2016-present)
Previous studies of ours showed that pigmented Long Evans (LE) rats react more severely to postnatal hyperoxia compared to albino Sprague Dawley (SD) rats. The purpose of this study was to examine if a previously reported difference in retinal maturation at birth, between the two strains, could explain this discrepency.
LE and SD rats were exposed to 80% O2 for 22.5 hours from P0-P14. Scotopic (intensity: -6.3 to 0.6 log cd.sec.m-2; 12 hrs dark adaptation) and photopic (intensity: 0.9 log cd.sec.m-2; background: 30cd.m-2) ERGs were recorded at P15, P16, P17, P19, P30 and P60. Retinal cytoarchitecture was evaluated in whole eyes at P60.
Maturation of most of the ERG components occured by P19 in control LE rats and 5 days later (P24) in SD rats. While the ERG maturation process was initiated in exposed SD rats to reach a maximum obtained at P17 in control, it failed to do so in exposed LE rats. Interestingly, the degree of ERG attenuation (a-wave: 85%, rod-cone b-wave: 33% and photopic b-wave: 23% of control) measured in LE rats exposed from P0-P9 was almost identical to that reached in SD rats exposed for a longer period of time (P0-P14: 80%, 37% and 27% of control, respectively). LE rats exposed from P0-P14 developed an OIR significantly more severe than that of SD rats exposed for the same time. Retinal histology of exposed SD rats reveals that most of the posterior pole is devoid of an OPL and only a peripheral ring of intact OPL remains, the thickness (measured from the ora serata) of which is 1447.1 µm ± 137.4 in the inferior retina (IR) and 1019.2 µm ± 252.2 in the superior retina (SR). In comparison, exposed LE rats reveal a significantly (p<.05) thinner ring of intact OPL measuring 7.7 µm ± 3.3 and 7.5 µm ± 0.1 in the IR and SR, respectively (p>0.05).
Based on ERG analysis, our results would suggest that the retina of the LE rat matures approximately 5 days sooner than that of the SD rat. If the latter finding can also be interpreted as indicative that LE rats are born with a more mature retina compared to SD rats, it would explain why LE rats react so strongly to postnatal hyperoxia. The latter claim also finds support in our demonstration of a near equivalent OIR in LE rats exposed from P0-P9 and SD rats exposed from P0-P14. To our knowledge this is the first animal demonstration that retinal maturity at birth plays a critical role in determining the severity of the resulting OIR.
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