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Related Experiment Videos

Experimental corneal neovascularisation using sucralfate and basic fibroblast growth factor

M S Loughman1, K Chatzistefanou, E M Gonzalez

  • 1Department of Surgery, Harvard Medical School, Children's Hospital, Boston, Massachusetts 02115, USA.

Australian and New Zealand Journal of Ophthalmology
|August 1, 1996
PubMed
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This study presents a novel, non-inflammatory rabbit cornea model for studying angiogenesis. The model uses sustained release of basic fibroblast growth factor (basic-FGF) with sucralfate, enabling predictable and persistent neovascularization for research.

Area of Science:

  • Ophthalmology
  • Vascular Biology
  • Biomaterials Science

Background:

  • Angiogenesis, the formation of new blood vessels, is crucial in various physiological and pathological processes.
  • Developing reliable in vivo models for studying angiogenesis is essential for understanding disease mechanisms and testing therapies.
  • Existing models may involve significant inflammation or lack predictability, limiting their utility.

Purpose of the Study:

  • To establish a non-inflammatory in vivo model of acute and chronic angiogenesis in the rabbit cornea.
  • To utilize a known angiogenic cytokine, basic fibroblast growth factor (basic-FGF), for controlled neovascularization.
  • To investigate the role of sucralfate in modulating the release and efficacy of basic-FGF.

Main Methods:

  • Slow-release Hydron polymer pellets containing sucralfate and/or basic-FGF were implanted into rabbit corneas.

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  • Neovascular responses were measured for pellets with basic-FGF alone, sucralfate alone, or varying concentrations of basic-FGF with a constant amount of sucralfate.
  • The influence of inflammation on the neovascular response was assessed.
  • Main Results:

    • Sucralfate enabled sustained release of basic-FGF, leading to predictable and aggressive corneal neovascularization, even at low doses.
    • A dose of 500 ng basic-FGF/pellet with sucralfate vascularized one-third of the cornea within eight days, with minimal inflammation.
    • Lowering the basic-FGF dose to 50 ng/pellet resulted in robust neovascularization with minimal edema, and some vessels persisted for over three months.

    Conclusions:

    • A cost-effective in vivo model for angiogenesis was developed.
    • The model demonstrates aggressive, predictable, and persistent neovascularization.
    • The model is characterized by minimal inflammation and is induced by sustained release of basic-FGF, a direct endothelial cell stimulant.