Long-lasting impairments in rodent oxygen-induced retinopathy measured by retinal vessel density and visual function
In mild or moderate retinopathy of prematurity (ROP), retinal vessels undergo obliteration, proliferation, and regression. Despite complete regression of vessel abnormalities, a variety of visual impairments have been reported. Rodent oxygen-induced retinopathy (OIR) is widely used as a model to stu...
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Veröffentlicht in: | Science China. Life sciences 2019-05, Vol.62 (5), p.681-690 |
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Sprache: | eng |
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Zusammenfassung: | In mild or moderate retinopathy of prematurity (ROP), retinal vessels undergo obliteration, proliferation, and regression. Despite complete regression of vessel abnormalities, a variety of visual impairments have been reported. Rodent oxygen-induced retinopathy (OIR) is widely used as a model to study ROP. However, the long-term changes of OIR model remain unclear. The aim of this study is to examine long term changes of retinal vessel and visual function in a rodent OIR model resembling human mild or moderate ROP. In this study, after subjecting the animals to 80% oxygen (O
2
) for 5–7 d, the retinal vessel density at postnatal day 12 (P12) was approximately 30% lower than that in the age-matched control, but this difference was not significant between the groups. Vessel abnormalities, such as vessel tortuosity, neovascular tufts, and the number of vessels protruding into the vitreous, peaked between P17 and P20. Despite the regression of many abnormalities, vessel density in the OIR group was 36% and 32% lower than that in the control animals at 6 weeks and 4 months, respectively. The visual acuity and contrast sensitivity were impaired in the OIR group when measured at 2, 3 and 4 months. Therefore, the rodent OIR model exhibited long-lasting reduction in retinal vessel density and visual impairments, similar to those observed in mild or moderate human ROP. This study suggests that the rodent OIR model can be used to explore possible interventions for mild and moderate human ROP. |
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ISSN: | 1674-7305 1869-1889 |
DOI: | 10.1007/s11427-018-9337-0 |