Newborn mice exposed to high (greater than 98%) ambient oxygen during the newborn period and subsequently removed to room air will develop a proliferative retinopathy which mimics the neovascular component of acute retinopathy of prematurity. In this paper, we report preliminary ultrastructural findings on the vitreous new vessels in the mouse model of oxygen-induced retinopathy, and argue that the model is appropriate for research on non surgical treatments for ROP in particular and angiogenesis in general.

Within the central nervous system, pericyte degeneration in diabetes mellitus occurs only in the retinal microcirculation and is not seen in the brain. This study sought to elucidate differences between bovine retinal and brain pericytes. When pairs of retinal and brain pericytes from individual calves were cultured in vitro, the morphological organisation of early post-confluent retinal pericyte cultures was consistently different from that of brain pericyte cultures. When retinal and brain pericyte cultures were grown to second passage in high or normal glucose medium supplemented with fetal calf serum, brain pericyte cultures grew significantly faster than retinal pericytes in either medium (p less than 0.0001). Brain pericytes thus appeared to grow intrinsically faster than retinal pericytes and this effect was largely independent of glucose concentration. Brain pericytes also grew faster than retinal pericytes in high glucose medium containing human diabetic or control serum (p less than 0.002). The proliferative effect of serum from diabetic patients with non-proliferative diabetic retinopathy on pericytes grown in high glucose medium was not significantly different from that of control serum. Both brain and retinal pericytes showed variation in their ability to replicate in high concentrations of glucose. The selectivity of pericyte degeneration to the retinal circulation does not appear to be due to changes in the mitogenic activity of diabetic serum for retinal pericytes, but may relate to the intrinsic relative inability of the retinal pericyte to reproliferate in response to the metabolic injury of diabetes mellitus.

Oxygen-induced retinopathy was produced by exposing 3-day-old kittens to 80% oxygen between 60 and 105 hours. They were then allowed to survive in room air until day 15, 21 or 28 when they were sacrificed after perfusion with colloidal carbon. Specimens were prepared for transmission electron microscopy. Ninety separate vitreous capillaries from oxygen-treated animals were examined. A total of 235 intercellular junctions were examined, 116 of them from the 15-day old animals. In the 15-day old animals, five junctions of 116 were open and the remainder were tight. No open junctions were seen in 21- or 28-day-old animals. In one capillary from a 15-day animal, fenestrated endothelium was seen in an aberrant, intraluminal loop of endothelium which formed no part of the blood/tissue barrier. The wall thickness of the vitreous new vessels seemed to decrease and the number of vesicles and vacuoles appeared to increase with increasing age. The basement membrane of the vitreous new vessels was scanty. In some sections, cells, presumably macrophages, were seen outside the new vessels. It is concluded that the increased permeability of the vitreous new vessels in 15-day-old animals can be explained by, and is possibly totally due to, the presence of open endothelial junctions.