A new model of proliferative vitreoretinopathy

Elizabeth M. Frenzel, Kimberly Neely, Arthur W. Walsh, J. Douglas Cameron, Dale S. Gregerson

Research output: Contribution to journalArticle

53 Citations (Scopus)

Abstract

PURPOSE. To design a new model of proliferative vitreoretinopathy (PVR) that would not rely on the addition of exogenous cells. The release of endogenous cells from surrounding attachments seems to be an early event in the pathogenesis of PVR. Because the proteolytic enzyme dispase dissociates tissues, the hypothesis was that an intraocular injection of dispase could trigger events that would cause PVR. The requirement for a surgical retinal break at the time of dispase injection was also examined. METHODS. One eye of Dutch Belted rabbits was injected with 0.003 U to 1.0 U dispase in the subretinal space or vitreous cavity. Control rabbits received a saline injection. An intentional retinal tear was created in animals in some groups. Observations were made for at least 10 weeks after surgery. RESULTS. Proliferative vitreoretinopathy developed in response to subretinal or intravitreal dispase, with or without creation of a controlled retinal break. Increased severity of PVR correlated with increasing doses of dispase. Evidence of PVR included preretinal membranes, distortion of myelin wings and retinal vessels, fixed retinal folds, and traction retinal detachment. Proliferative vitreoretinopathy did not develop in saline-treated control animals. CONCLUSIONS. Dispase initiated the development of PVR without the addition of exogenous cells, growth factors, or cytokines typically found in PVR membranes. A cascade of events was probably triggered by dispase, causing native cells and factors to produce PVR. The dispase model of PVR was technically easy to perform, permitted a clear view of the retina, and had a high success rate in development of PVR.

Original languageEnglish (US)
Pages (from-to)2157-2164
Number of pages8
JournalInvestigative Ophthalmology and Visual Science
Volume39
Issue number11
StatePublished - Oct 1 1998

Fingerprint

Proliferative Vitreoretinopathy
Retinal Perforations
Intraocular Injections
Rabbits
dispase
Retinal Vessels
Injections
Membranes
Traction
Retinal Detachment
Myelin Sheath
Retina
Intercellular Signaling Peptides and Proteins

All Science Journal Classification (ASJC) codes

  • Ophthalmology
  • Sensory Systems
  • Cellular and Molecular Neuroscience

Cite this

Frenzel, E. M., Neely, K., Walsh, A. W., Cameron, J. D., & Gregerson, D. S. (1998). A new model of proliferative vitreoretinopathy. Investigative Ophthalmology and Visual Science, 39(11), 2157-2164.
Frenzel, Elizabeth M. ; Neely, Kimberly ; Walsh, Arthur W. ; Cameron, J. Douglas ; Gregerson, Dale S. / A new model of proliferative vitreoretinopathy. In: Investigative Ophthalmology and Visual Science. 1998 ; Vol. 39, No. 11. pp. 2157-2164.
@article{a53dea094c354e1c9226f2e15146bdb9,
title = "A new model of proliferative vitreoretinopathy",
abstract = "PURPOSE. To design a new model of proliferative vitreoretinopathy (PVR) that would not rely on the addition of exogenous cells. The release of endogenous cells from surrounding attachments seems to be an early event in the pathogenesis of PVR. Because the proteolytic enzyme dispase dissociates tissues, the hypothesis was that an intraocular injection of dispase could trigger events that would cause PVR. The requirement for a surgical retinal break at the time of dispase injection was also examined. METHODS. One eye of Dutch Belted rabbits was injected with 0.003 U to 1.0 U dispase in the subretinal space or vitreous cavity. Control rabbits received a saline injection. An intentional retinal tear was created in animals in some groups. Observations were made for at least 10 weeks after surgery. RESULTS. Proliferative vitreoretinopathy developed in response to subretinal or intravitreal dispase, with or without creation of a controlled retinal break. Increased severity of PVR correlated with increasing doses of dispase. Evidence of PVR included preretinal membranes, distortion of myelin wings and retinal vessels, fixed retinal folds, and traction retinal detachment. Proliferative vitreoretinopathy did not develop in saline-treated control animals. CONCLUSIONS. Dispase initiated the development of PVR without the addition of exogenous cells, growth factors, or cytokines typically found in PVR membranes. A cascade of events was probably triggered by dispase, causing native cells and factors to produce PVR. The dispase model of PVR was technically easy to perform, permitted a clear view of the retina, and had a high success rate in development of PVR.",
author = "Frenzel, {Elizabeth M.} and Kimberly Neely and Walsh, {Arthur W.} and Cameron, {J. Douglas} and Gregerson, {Dale S.}",
year = "1998",
month = "10",
day = "1",
language = "English (US)",
volume = "39",
pages = "2157--2164",
journal = "Investigative Ophthalmology and Visual Science",
issn = "0146-0404",
publisher = "Association for Research in Vision and Ophthalmology Inc.",
number = "11",

}

Frenzel, EM, Neely, K, Walsh, AW, Cameron, JD & Gregerson, DS 1998, 'A new model of proliferative vitreoretinopathy', Investigative Ophthalmology and Visual Science, vol. 39, no. 11, pp. 2157-2164.

A new model of proliferative vitreoretinopathy. / Frenzel, Elizabeth M.; Neely, Kimberly; Walsh, Arthur W.; Cameron, J. Douglas; Gregerson, Dale S.

In: Investigative Ophthalmology and Visual Science, Vol. 39, No. 11, 01.10.1998, p. 2157-2164.

Research output: Contribution to journalArticle

TY - JOUR

T1 - A new model of proliferative vitreoretinopathy

AU - Frenzel, Elizabeth M.

AU - Neely, Kimberly

AU - Walsh, Arthur W.

AU - Cameron, J. Douglas

AU - Gregerson, Dale S.

PY - 1998/10/1

Y1 - 1998/10/1

N2 - PURPOSE. To design a new model of proliferative vitreoretinopathy (PVR) that would not rely on the addition of exogenous cells. The release of endogenous cells from surrounding attachments seems to be an early event in the pathogenesis of PVR. Because the proteolytic enzyme dispase dissociates tissues, the hypothesis was that an intraocular injection of dispase could trigger events that would cause PVR. The requirement for a surgical retinal break at the time of dispase injection was also examined. METHODS. One eye of Dutch Belted rabbits was injected with 0.003 U to 1.0 U dispase in the subretinal space or vitreous cavity. Control rabbits received a saline injection. An intentional retinal tear was created in animals in some groups. Observations were made for at least 10 weeks after surgery. RESULTS. Proliferative vitreoretinopathy developed in response to subretinal or intravitreal dispase, with or without creation of a controlled retinal break. Increased severity of PVR correlated with increasing doses of dispase. Evidence of PVR included preretinal membranes, distortion of myelin wings and retinal vessels, fixed retinal folds, and traction retinal detachment. Proliferative vitreoretinopathy did not develop in saline-treated control animals. CONCLUSIONS. Dispase initiated the development of PVR without the addition of exogenous cells, growth factors, or cytokines typically found in PVR membranes. A cascade of events was probably triggered by dispase, causing native cells and factors to produce PVR. The dispase model of PVR was technically easy to perform, permitted a clear view of the retina, and had a high success rate in development of PVR.

AB - PURPOSE. To design a new model of proliferative vitreoretinopathy (PVR) that would not rely on the addition of exogenous cells. The release of endogenous cells from surrounding attachments seems to be an early event in the pathogenesis of PVR. Because the proteolytic enzyme dispase dissociates tissues, the hypothesis was that an intraocular injection of dispase could trigger events that would cause PVR. The requirement for a surgical retinal break at the time of dispase injection was also examined. METHODS. One eye of Dutch Belted rabbits was injected with 0.003 U to 1.0 U dispase in the subretinal space or vitreous cavity. Control rabbits received a saline injection. An intentional retinal tear was created in animals in some groups. Observations were made for at least 10 weeks after surgery. RESULTS. Proliferative vitreoretinopathy developed in response to subretinal or intravitreal dispase, with or without creation of a controlled retinal break. Increased severity of PVR correlated with increasing doses of dispase. Evidence of PVR included preretinal membranes, distortion of myelin wings and retinal vessels, fixed retinal folds, and traction retinal detachment. Proliferative vitreoretinopathy did not develop in saline-treated control animals. CONCLUSIONS. Dispase initiated the development of PVR without the addition of exogenous cells, growth factors, or cytokines typically found in PVR membranes. A cascade of events was probably triggered by dispase, causing native cells and factors to produce PVR. The dispase model of PVR was technically easy to perform, permitted a clear view of the retina, and had a high success rate in development of PVR.

UR - http://www.scopus.com/inward/record.url?scp=0031685046&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031685046&partnerID=8YFLogxK

M3 - Article

VL - 39

SP - 2157

EP - 2164

JO - Investigative Ophthalmology and Visual Science

JF - Investigative Ophthalmology and Visual Science

SN - 0146-0404

IS - 11

ER -

Frenzel EM, Neely K, Walsh AW, Cameron JD, Gregerson DS. A new model of proliferative vitreoretinopathy. Investigative Ophthalmology and Visual Science. 1998 Oct 1;39(11):2157-2164.