April 2010
Volume 51, Issue 13
ARVO Annual Meeting Abstract  |   April 2010
A Porcine Model of Proliferative Vitreoretinopathy
Author Affiliations & Notes
  • A. S. Bansal
    Ophthalmology, Emory University, Atlanta, Georgia
  • H. E. Grossniklaus
    Ophthalmology, Emory University, Atlanta, Georgia
  • T. W. Olsen
    Ophthalmology, Emory University, Atlanta, Georgia
  • Footnotes
    Commercial Relationships  A.S. Bansal, None; H.E. Grossniklaus, None; T.W. Olsen, None.
  • Footnotes
    Support  Unrestricted Grant from Research to Prevent Blindness
Investigative Ophthalmology & Visual Science April 2010, Vol.51, 6085. doi:
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      A. S. Bansal, H. E. Grossniklaus, T. W. Olsen; A Porcine Model of Proliferative Vitreoretinopathy. Invest. Ophthalmol. Vis. Sci. 2010;51(13):6085.

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

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Purpose: : Proliferative vitreoretinopathy (PVR) is the principle cause for failed retinal detachment (RD) surgery. Frenzel et al. (IOVS 1998) developed a dispase-based model of experimental PVR in rabbits. The rabbit model has limitations. A large animal pig model of PVR has several advantages: 1) Larger eye that allows for surgical intervention, 2) a holangiotic retina, 3) has scleral anatomy similar to humans, 4) has an area centralis, 5) has a choroid-Bruch’s-retinal pigment epithelial complex similar to humans. The aim of our study is to develop a large animal model of PVR using dispase in pigs that allows for surgical manipulation and intervention that is not possible in other models.

Methods: : We adapted the model of Frenzel et al. to the pig (n=10). The pigs weighed 10-15 Kg. All pigs were anesthetized prior to intervention. The first four received an intravitreal injection of dispase (0.3 units/0.3cc) and two received intravitreal saline (controls). None developed PVR or RD. Therefore, a ‘transequator’ group of four pigs were injected using a 25-guage sharp needle extending through the equator to the opposite equator in order to create a tear in the retina. Dispase (1.5 units/0.1cc) was injected as the needle was withdrawn. All animals were examined using indirect ophthalmoscopy and ultrasound at 1, 3, and 6 weeks post-injection. PVR was graded according to standard clinical definitions. All pigs were euthanized at 6 weeks and eyes were enucleated and examined histologically with H&E stain.

Results: : Three of four eyes injected intravitreally using 0.3 units/0.3cc dispase showed only vitreous haze and/or hemorrhage at 1 week. The vitreous and retina were normal in both saline control eyes. With the high-dose dispase, transequatorial injection, three of four eyes developed PVR at 6 weeks. One eye developed a classic PVR related RD, one eye had an open-anterior, closed posterior funnel RD, and one eye had surface fibrosis and no RD. Histopathology of the enucleated specimens confirmed the presence of PVR.

Conclusions: : The porcine model using a transequatorial injection of high-dose dispase described represents a new model system to study surgical and pharmacotherapeutic intervention for PVR. This large animal model closely replicates the human condition.

Keywords: proliferative vitreoretinopathy • retinal detachment 

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