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Panitan Yossuck, Yun Yan, Misrak Tadesse, Rosemary D. Higgins; Dexamethasone and Critical Effect of Timing on Retinopathy. Invest. Ophthalmol. Vis. Sci. 2000;41(10):3095-3099.
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purpose. Administration of corticosteroids soon after birth has been reported to
have deleterious, protective, and no effect on retinopathy of
prematurity. Conflicting results may be due to timing of corticosteroid
administration. The goal of this study was to determine effects of
pretreatment and late dexamethasone on retinopathy in a mouse model.
methods. The C57BL6 mouse model of oxygen-induced retinopathy (by placing
animals in 75% oxygen from postnatal days 7 through 12) was used to
create retinal neovascularization. Dexamethasone at 0.5 mg/kg per day
was administered from day 1 through day 5 in the pretreatment group.
The late-treatment group received 5 days of dexamethasone at the same
dose beginning on day 12. Mice were killed at days 17 through
20, and retinal vasculature was assessed by a retinal scoring system of
wholemount preparation after high-molecular-weight fluorescein-labeled
dextran perfusion. In addition, retinal neovascularization was assessed
by quantification of extraretinal neovascular nuclei in retinal
sections. Statistical significance was defined as P < 0.05 and was determined by the Kruskal–Wallis test, Mann–Whitney
test, and Student’s t-test.
results. Oxygen-exposed animals that received treatment with dexamethasone
before oxygen exposure had an improvement in retinopathy, with a median
score of 6 (5,7; 25th,75th quartiles) compared with 10 (8,11) in the
untreated oxygen-exposed (P < 0.05). The group
treated late (after oxygen exposure) with dexamethasone had a median
score of 10 (9,11). Pretreatment reduced extraretinal vascularization,
when assessed by quantification of neovascular nuclei, to a mean ± SEM of 19 ± 9, significantly less than in the untreated
oxygen-exposed group (55 ± 12; P < 0.05). No
difference was observed in the late-treatment group when compared with
the untreated oxygen-exposed group. Significant growth retardation,
indicated by body weight, was observed in the pretreatment
(P < 0.01) and late-treatment
(P < 0.05) groups when compared with the control
conclusions. Timing of dexamethasone administration was critical to the inhibition
of development of retinopathy in the mouse model. Degree of growth
retardation, measured by body weight, also appeared to be time
dependent. These data may explain the different results of clinical
observations with respect to corticosteroid treatment, timing, and
development of retinopathy.
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