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Experimental Approach to the Pathogenesis of Retrolental Fibroplasia: I. Changes of the Eye Induced by Exposure of Newborn Mice to Concentrated Oxygen
Author(s) -
GYLLENSTEN LARS J.,
HELLSTRÖM BO E.
Publication year - 1954
Publication title -
acta pædiatrica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.772
H-Index - 115
eISSN - 1651-2227
pISSN - 0803-5253
DOI - 10.1111/j.1651-2227.1954.tb15463.x
Subject(s) - medicine , retinal , retina , ophthalmology , retinopathy of prematurity , atrophy , oxygen , pathology , biology , chemistry , pregnancy , genetics , organic chemistry , neuroscience , gestational age
Summary 1. Newborn, full‐term mice were subjected to exposures in 98–100 per cent oxygen,(a) intermittently, (b)continuously, or (c)for five days followed by rapid transfer to, and stay in, normal atmosphere. The development of the eyes was followed histologically for 38, 16, and 15 days after birth, respectively. 2. Intermittent exposures to oxygen caused a high frequency of persistence, proliferation and dilatation of the retrolental hyaloid vessels with hemorrhages in the primary vitreous body. Eetinal folds were occasionally found. 3. Continuous exposures to oxygen caused a persistence and proliferation of the retrolental hyaloid vessels and a retarded formation of retinal vessels. Small intraocular blecdings occurred occasionally. 4. Continuous exposures to oxygen followed by rapid transfer to, and stay in, normal atniosphere caused a dilatation and a progressive proliferation of the retrolental hyaloid vessels and of retinal vessels with capillary buddings from the retinal vessels into the vitreous body. Hemorrhages from both retinal and hyaloid vessels occurred frequently. The retina showed progressive irregularities, proliferations and foldings. 5. netinal atrophy after longer periods of observation since the transfer from oxygen to normal air is preliminarily reported. 6. The experimental changes of the eyes after oxygen exposures are discussed with regard to the patliogenesis of human retrolental fibroplasia.