THERE is convincing clinical evidence that retrolental fibroplasia is the result of a disturbance of the oxygen conditions to which an infant is normally exposed. Direct experimental evidence of this was supplied by Ashton and others (1953), the anatomical studies of Michaelson (1948) and the physiological studies of Campbell (1951) having previously suggested the significance of the role of oxygen in the development of the retinal vessels. Ashton and his co-workers found occlusion of the retinal blood vessels in new-born kittens who were exposed to hyperoxic conditions. When the animals were returned to normal atmospheric or hypo-oxic conditions there was a subse- quent disturbance of vessel growth and also new vessel ingrowth into the vitreous body. The following work had been planned in order to test the effect of hyperoxia on the developing vessels of the mouse retina. This animal was chosen because the development of the retinal vessels is confined almost completely to the period between the first and eleventh day of life, and because the mode of retinal vessel development and the definitive vessel pattern are very similar to those occurring in the human retina. A description of the normal development of the retinal vessels in the mouse followed by a descrip- tion of their development after the animal had been for some time in an incubator at' high oxygen concentrations.
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Michaelson et al. (1954) studied this question.