Open AccessExperimental corneal neovascularisation using sucralfate and basic fibroblast growth factor
Author(s) -
Loughnan Michael S.,
Chatzistefanou Klio,
Gonzalez Evelyn M.,
Flynn Evelyn,
Adarnis Anthony P.,
Shing Yuen,
D'Amato Robert J.,
Folkman Judah
Publication year - 1996
Publication title -
australian and new zealand journal of ophthalmology
Language(s) - English
Resource type - Journals
eISSN - 1440-1606
pISSN - 0814-9763
DOI - 10.1111/j.1442-9071.1996.tb01596.x
Subject(s) - sucralfate , basic fibroblast growth factor , fibroblast growth factor , medicine , angiogenesis , neovascularization , cornea , inflammation , immunology , ophthalmology , growth factor , receptor
Purpose: To develop a non‐inflammatory model of both acute and chronic angiogenesis in the rabbit cornea using a known directly angiogenic cytokine. Methods: Pellets made of the slow‐release polymer Hydron (polyhydroxyethylmethacrylate) and containing sucralfate and/or basic fibroblast growth factor (basic‐FGF) were implanted into rabbit corneas. The neovascular response to the implantation of pellets containing basic‐FGF alone, sucralfate alone or a titration of basic‐FGF in the presence of a constant amount of sucralfate was measured. The role of inflammation in the neovascular response was also investigated. Results: The addition of sucralfate to the pellets led to the sustained release of basic‐FGF resulting in a predictable and aggressive neovascular response with a low dose of basic‐FGF that by itself was unable to elicit neovascularisation. At a dose of 500ng per pellet, approximately one‐third of the surface area of the cornea was vascularised within eight days of implantation. Minimal or no vascularisation occurred with the same dose of basic‐FGF without sucralfate. While this dose of basic‐FGF induced corneal oedema, only minimal inflammation was observed and the response was unaffected by ionising radiation. A less aggressive though still robust neovascular response with no or only minimal oedema was observed when the dose was lowered to 50ng of basic‐FGF per pellet. Some induced vessels persisted for more than three months. Conclusion: This is an inexpensive in vivo model of angiogenesis with the advantages of the neovascularisation being aggressive, predictable, persistent, unassociated with an obvious inflammatory response and induced by the sustained release of an agent known to have a direct stimulatory action on endothelial cells.