Lars Gyllensten

Experimental Approach to the Pathogenesis of Retrolental Fibroplasia: I. Changes of the Eye Induced by Exposure of Newborn Mice to Concentrated Oxygen

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.

Retrolental Fibroplasia - Animal Experiments| The effect of the eyes of fullterm mice. A preliminary report

The following changes have been found in the eyes of 1–3 weeks old fullterm mice, who were exposed to pure oxygen intermittingly from birth: haemorrhages, retinal folding and formation of a vascular, cellular and fibrons tissue in the Vitreous body.

Experimental Approach to the Pathogenesis of Retrolental Fibroplasia III. Changes in the Eye induced by Exposure of Newborn Mice to General Hypoxia

A VAST literature has accumulated on the strong correlation between exposure to high concentrations of oxygen during the postnatal care of premature babies and the development of retrolental fibroplasia (for reviews of the literature see Francois and others, 1954; Gordon and others, 1954; Henry, 1954; Ingalls, 1954; Lanman and others, 1954; Patz, 1954). Changes in the eye, similar to those seen in human retrolental fibroplasia, have also been produced experimentally by exposing young animals to high concentrations of oxygen (Gyllensten and Hellstrom, 1952, 1954, 1955; Ashton and others, 1953, 1954; Patz and others, 1953). The role of oxygen, however, is not yet clear, and oxygen cannot be the only cause of the disease. Exline and Harrington (1951), Lelong and others (1952), and Zacharias and others (1954) found no obvious correlation between oxygen treatment and subsequent retrolental fibroplasia. A few cases are known of retrolental fibroplasia in stillborn infants (Reese and others, 1952) and in children who were never given any extra oxygen (Coxon, 1951; Bembridge and others, 1952). These objections to the theory of oxygen poisoning as the only cause of retrolental fibroplasia would be explained if it could be demonstrated that oxygen is not the immediate cause of the disease but acts by way of an intermediate mechanism that can be provoked in exceptional cases by other agents. Clinical observations (Szewczyk, 1951) tended to demonstrate that in the early stages of retrolental fibroplasia oxygen-induced changes in the eye develop after the transfer from a high concentration of oxygen to normal air, and that the changes regress if the child is given oxygen again. Szewczyk (1951, 1952, 1953) suggested that the disease depended on relative anoxia, which is supposed to occur as a sort of adaption disease when the child is rapidly transferred to normal air. Similar views have been propounded by many workers, including Jefferson (1952), Crosse and Evans (1952),