Oxygen-induced retinopathy: ultrastructure of vitreous new vessels in the kitten model

Abstract

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.

Vitreal macrophages express vascular endothelial growth factor in oxygen‐induced retinopathy

“…For over 20 years putative macrophages have been reported to be in association with proliferating retinal vessels in OIR with the assumption of a phagocytic role. 1 An angiogenic role for macrophages in retinal neovascularization has been suggested 2–4 but the role of the macrophage in retinal neovascularization generally, and in ROP specifically, remains unclear.…”