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HAJIME INOMATA, GEORGE K. SMELSER, FRANK M. POLACK; Corneal Vascularization in Experimental Uveitis and Graft Rejection An Electron Microscopic Study. Invest. Ophthalmol. Vis. Sci. 1971;10(11):840-850.
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Corneal vascularization in rabbit eyes was produced by inducing an anterior uveitis by injection of bovine serum albumin into the vitreous, and by an immunologically provoked graft rejection. Uveitis produced vessels in the peripheral and anterior portions of the corneal stroma. These accompanying graft rejection reached the scar surrounding the graft, and were seen mostly in the middle layers of the corneal stroma. As the vessels approached it, they sent many brush-like branches toward the scar, where they formed a complicated capillary network. The fine structure of the new vessels was essentially the same in the two experiments. The vessels grew by endothelial sprouts from pre-existing vessels. Endothelial cells proliferated near the growing tip of the vessels and migrated toward the very tip of the vascular sprouts, where they penetrated the surrounding tissue as a solid cord of cells joined together with attachment bodies. A lumen developed between the cells later. The endothelial cells had bud-like extensions, suggesting active amoeboid movement. Newly formed vessels leaked. Intramural pericytes were embedded in the basement membrane of relatively mature vessels. An endothelial origin of these pericytes is suggested. Growing vessels in the pathologic corneas were solely of the nonfenestrated type, although pores occurred in the normal limbal vessel from which they were derived. The mechanism of neovasculogenesis in the pathologic cornea is thought to result from complicated processes involving both edema and vasostimulating substances produced by tissue injury.
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