We conducted an extensive histological study of the retinas of newborn
rats that had been exposed to hyperoxic conditions. Our aim was to ve
rify whether it is possible, using oxygen alone, to induce retinal det
achment, a lesion that is characteristic of the more advanced stages o
f retinopathy of prematurity (ROP). Eight litters (total number of ani
mals: 64) of newborn, albino Wistar rats were used. Four litters (32 r
ats) were exposed to 80% oxygen for the first ten days of life. Some o
f these rats were then removed to room-air environments where they wer
e kept for two, three or four more weeks. The other four litters (32 r
ats) were maintained for the entire period in room-air. On the 11(th),
25(th), 32(nd) and 39(th) days of life rats from both the exposed and
control groups were sacrificed and 5 micron sections of their in tote
eyeballs were submitted to histological evaluation and immunohistoche
mical studies. Folding of the internal retinal layers was observed in
some of the animals exposed to hyperoxia, as well as those kept in roo
m air. These folds did not alter the overall thickness of the retina i
tself and were probably congenital. Retinal folds and microdetachments
were seen in many of the retinas from the exposed group of rats. Exte
nsive detachment was observed in one of the rats sacrificed after two
weeks of room-air recovery, in two of those recovered for three weeks
and in two exposed to four weeks of room air. The sections containing
these areas of retinal detachment showed marked increases in glial fib
rillary acidic protein (GFAP) in immunocytochemical studies, suggestin
g that Muller cells might play a role in the pathogenesis of retinal d
etachment.