Perinatal ocular physiology and ROP in the experimental animal model.

In order to overcome the scarcity of premature human ocular tissues and the enormous obstacles to direct examination of immature human ocular vasculatures, a number of animal models have been employed by investigators in order to study various aspects of ROP. A variety of factors may influence selection of the particular model used, but ultimately it is the faithfulness with which the model mimics human ROP that is most important. The validity of the models has been and remains a controversial subject, but evidence appears strong in favor of the beagle puppy model for studying physiology of the ocular vasculatures during perinatal development. Human ROP pathology usually is defined in terms of static morphological state, physiological dysfunction being considerably more difficult to assess. Most of the animal models fall short of mimicking the pathological lesions found in human eyes, especially those associated with severe, or end-stage ROP, yet they do fairly well in terms of mimicking the retinal vascular physiological changes associated with onset of the disease. Unfortunately, where the physiological aspects of ROP are concerned, focus is primarily on the effects of hyperoxia; other physiological factors as well as the potential role of the choroid are essentially ignored. This paper discusses the potential of physiological changes which occur during the perinatal period to play a role in ROP pathogenesis.