Identification of a suitable animal model is essential for the continued study of retinopathy of prematurity (ROP). Since 1984 we have used the newborn rat for the study of oxygen-induced retinopathy (OIR). The rat retina is highly immature at birth. Like those of humans, the retinal vessels arise from mesenchymal precursors, but contrary to that which occurs in humans, canalization of the rats inner retinal vessels is not related to the presence of cystoid spaces. In addition, only immature Stage I photoreceptors are present around the optic disk at birth. This extreme immaturity makes the rat retina highly susceptible to direct damage from oxygen. Oxygen-induced retinopathy can be produced by exposing the newborn rat to 80% oxygen for the first 7-10 days of life. We have demonstrated that OIR does not develop when oxygen is administered under conditions of moderate hyperbarism (+1.8 atm). It is possible that hyperbarism exerts a protective effect on the immature retinal vessels by inducing a vasoconstrictive response which reduces the amount of oxygen transported from the choroid to the inner retina during hypoxia. I recently hypothesized that this vasoconstriction might also affect the ciliary body, thus reducing the quality of aqueous produced, and we are currently studying the relationship between development of the immature retinal vessels in the rat and production and drainage of the aqueous. The question we are attempting to answer is whether a condition of relatively increased intraocular pressure is capable of promoting the development of OIR.