May 2005
Volume 46, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2005
Laser–Induced Models of Choroidal Neovascularization in Rabbits Associated With Sustained Suprachoroidal and Episcleral Delivery of VEGF and bFGF
Author Affiliations & Notes
  • G.G. Gum
    Biological Test Center, Irvine, CA
  • C.G. Wong
    SCLERA LLC, Laguna Beach, CA
  • R.P. de Carvalho
    Wilmer Eye Institute, The Johns Hopkins Univ., Baltimore, MD
  • Footnotes
    Commercial Relationships  G.G. Gum, None; C.G. Wong, SCLERA LLC P; R.P. de Carvalho, SCLERA LLC P.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 1422. doi:
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      G.G. Gum, C.G. Wong, R.P. de Carvalho; Laser–Induced Models of Choroidal Neovascularization in Rabbits Associated With Sustained Suprachoroidal and Episcleral Delivery of VEGF and bFGF . Invest. Ophthalmol. Vis. Sci. 2005;46(13):1422.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Abstract: : Purpose: Choroidal neovascularization (CNV) can be induced by traumatic rupture of Bruch’s membrane (BM) or sustained delivery of growth factors. This study aims to characterize the association of laser–induced models of CNV with sustained release of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) through different delivery methods. We hypothesize that sustained release of VEGF and bFGF can prolong the viability of CNV after laser injury to the BM. Methods: Dutch Belted rabbits (n=9) were assigned to have laser injury of BM (n=2); episcleral delivery of VEGF/bFGF (n=2); episcleral delivery of VEGF/bFGF associated with laser injury of BM (n=2); or suprachoroidal sustained release of VEGF/bFGF associated with laser injury of BM (n=3). Laser–treated eyes received a total of 24 single laser spots. The development of CNV was assessed and monitored by fluorescein angiography at 1, 2, 3, 4 and 8 weeks after the procedures. At 8 weeks, optical coherence tomography (OCT) was performed on representative laser lesions, animals were euthanized and the enucleated eyes were evaluated histologically. Results: CNV could be demonstrated by fluorescein angiography in all eyes exposed to laser injury of BM. OCT demonstrated the presence of a rim of fibrovascular tissue around the laser injury site below and above the retinal pigment epithelium. OCT correlated to fluorescein angiography in all studied lesions. CNV remained prominent at 8 weeks in eyes exposed to the laser in association with sustained release of the growth factors. CNV was predominately extinguished at 8 weeks in eyes exposed to the laser injury only. Conclusions: Sustained release of growth factors can prolong the viability of CNV induced by the laser injury of BM. Suprachoroidal and episcleral delivery of growth factors was demonstrated to enhance the CNV response to laser–induced BM damage. OCT and fluorescein angiography can be used to monitor in vivo the progression of CNV.

Keywords: neovascularization • growth factors/growth factor receptors • laser 
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