May 2005
Volume 46, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2005
Role of Pars Plana Vitrectomy in Preventing Posterior Neovascularization in a New Experimental Animal Model of Retinal Neovascularization
Author Affiliations & Notes
  • K. Nakata
    Cole Eye Institute, Cleveland Clinic Foundation, Cleveland, OH
  • Q. Ebrahem
    Cole Eye Institute, Cleveland Clinic Foundation, Cleveland, OH
  • B. Anand–Apte
    Cole Eye Institute, Cleveland Clinic Foundation, Cleveland, OH
  • J.G. Hollyfield
    Cole Eye Institute, Cleveland Clinic Foundation, Cleveland, OH
  • H. Lewis
    Cole Eye Institute, Cleveland Clinic Foundation, Cleveland, OH
  • Footnotes
    Commercial Relationships  K. Nakata, None; Q. Ebrahem, None; B. Anand–Apte, None; J.G. Hollyfield, None; H. Lewis, None.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 1407. doi:
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      K. Nakata, Q. Ebrahem, B. Anand–Apte, J.G. Hollyfield, H. Lewis; Role of Pars Plana Vitrectomy in Preventing Posterior Neovascularization in a New Experimental Animal Model of Retinal Neovascularization . Invest. Ophthalmol. Vis. Sci. 2005;46(13):1407.

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

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Abstract

Abstract: : Purpose: Retinal neovascularization (NV) is a significant cause of severe visual loss in patients with proliferative diabetic retinopathy (PDR). Laser photocoagulation to prevent or treat the NV is beneficial only in some patients. Systemic medications to prevent neovascularization are being evaluated but there is no evidence yet of their efficacy, and there are concerns of systemic side effects. We have observed that vitrectomy prevents the development of new posterior NV in patients at high risk for developing PDR. Our purposes are to establish an animal model of NV and evaluate the effect of vitrectomy on its development. Methods: A pig model for NV using intravitreal implantation of sustained–release pellets was established. We divided the pigs into the two groups; one group underwent vitrectomy, and the other was non–vitrectomized. The pellets containing VEGF (vascular endothelial growth factor) and bFGF (basic fibroblast growth factor) was implanted in the right eyes of pigs, following vitrectomy and in the non–vitrectomized eyes. Control pigs received either no pellet or a blank pellet (without VEGF and bFGF). Eyes were inspected by indirect ophthalmoscopy and fluorescein angiography. Histological analysis was performed to confirm the NV, and ELISA analysis was used to measure the concentration of VEGF in the vitreous cavity. Results: In the non–vitrectomy group, the VEGF/bFGF pellets induced NV in all of 7 eyes and tractional retinal detachment and/or vitreous hemorrhage was observed in 6 eyes. However, in the vitrectomy group, NV was inhibited in all eyes which received the pellet. The average concentration of VEGF was 27.2 µg/ml in non–vitrectomized eyes, and 8.8 µg/ml in vitrectomized eyes (p<0.005) Conclusions: NV could be induced in the pigs by intravitreal release of VEGF and bFGF. Vitrectomy could prevent the development of NV in this animal model. This suggests that vitrectomy might be beneficial in patients with progressive DR not responding to laser photocoagulation.

Keywords: diabetic retinopathy • vitreous • retinal neovascularization 
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