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IN human premature infants, prolonged exposure to an oxygen concentration above 30–40 per cent in an incubator tends to produce retinal damage1 (retrolental fibroplasia). A similar disease
has been produced experimentally by oxygen exposure of newborn mice, rats, kittens and other animals, which are relatively immature at birth as compared with full-term human babies2–4. With
the exception of pulmonary injury5, no other pathological alterations have been reported after oxygen exposure of premature infants. As the brain, like the retina, develops considerably
after birth, special attention was paid to the influence of oxygen exposure on the maturation of the brain. No characteristic brain injury has been found in children exposed to oxygen,
though neurologic and mental defects are more common in children with retrolental fibroplasia than in other prematurely born children6. No brain damage in animals after similar treatment has
hitherto been observed3,4.
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