title: Ciliary tissue transplantation in the rabbit.
abstract: Irreversible damage of the ciliary body can be responsible for prolonged ocular hypotony and phthisis bulbi, which, currently, cannot be treated. The aim of this study was to achieve survival of morphologically normal ciliary tissue (CT) transplants in the anterior chamber of a rabbit's eye. Outbred female New Zealand albino rabbits received CT allografts, which were placed on to the surface of the host iris. We evaluated the influence of ciclosporin (CsA), VEGF and donor perfusion on graft survival. Operated eyes were assessed clinically and histologically, and revascularization of the grafts was determined by fluorescein angiography. All grafts became dark and ischemic during the first five to seven days after transplantation. Reperfusion of the grafted tissue was complete at approximately ten days after transplantation. In untreated animals, transplants became infiltrated by inflammatory cells, which led to destruction of the tissue. This was prevented by systemic use of CsA. Transplants treated with VEGF prior to transplantation had fewer ischemic areas but epithelial cell survival was not improved. Whole body donor perfusion prior to preparation of the grafts resulted in less inflammation and, histologically, in a better quantity and quality of the epithelial cells in the CT transplants. Ciliary tissue can be successfully transplanted but the ciliary epithelium suffers from ischemia and in untreated animals the whole transplant is rejected in the classical fashion. If the donor is perfused and the host immunosuppressed, histologically normal ciliary epithelium can be preserved together with rapid revascularization, minimal inflammation and good survival of the transplant, although fibrosis continued to occur during the two months after transplantation.
authors.affiliation: Department of Ophthalmology J3-S, Leiden University Medical Center, P.O. Box 9600, 2333 ZA Leiden, The Netherlands. l.j.pandova-jovanovik@lumc.nl
authors.forename: L
authors.initials: L
authors.lastname: Jovanovik-Pandova
authors.forename: P G
authors.initials: PG
authors.lastname: Watson
authors.forename: C
authors.initials: C
authors.lastname: Liu
authors.forename: W Y
authors.initials: WY
authors.lastname: Chan
authors.forename: D
authors.initials: D
authors.lastname: de Wolff-Rouendaal
authors.forename: E R
authors.initials: ER
authors.lastname: Barthen
authors.forename: K
authors.initials: K
authors.lastname: Emmanouilidis-van der Spek
authors.forename: M J
authors.initials: MJ
authors.lastname: Jager
mesh_terms: D000818:Animals; D002924:Ciliary Body / Q000098:blood supply / Q000473:pathology / Q000637:transplantation*; D016572:Cyclosporine / Q000627:therapeutic use; D005260:Female; D005355:Fibrosis; D006085:Graft Survival; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D007511:Ischemia / Q000473:pathology / Q000628:therapy; D010477:Perfusion; D011817:Rabbits; D015424:Reperfusion; D013997:Time Factors; D014184:Transplantation, Homologous; D042461:Vascular Endothelial Growth Factor A / Q000627:therapeutic use
chemical_list: D007166:Immunosuppressive Agents; D042461:Vascular Endothelial Growth Factor A; D016572:Cyclosporine