PATHOGENESIS OF CORNEAL EDEMA AFTER INTRAOCULAR SURGERY

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DESCRIPTION (provided by applicant): The objective of this study is to understand the pathogenesis of corneal edema which occurs, in some patients, following intraocular surgery. At greatest risk are diabetic patients, patients with guttata, maltino implant patients and possibly long-term contact lens wearers, all of whom have severe endothelial polymegathism, particularly as they approach the age for cataract surgery. Our basic premise is that the cornea of these patients have a compromised endothelium and additional stress such as intraocular surgery, postoperative inflammation and increases in intraocular pressure will affect the metabolic pump and barrier functions of the compromised endothelium resulting in postoperative corneal edema. The proposed studies should further our understanding of the pathogenesis of corneal edema and the prevention of postsurgical corneal edema. We propose to test the following hypothesis about the specific effects of each of three factors on the compromised corneal endothelium. (1) that the corneal endothelium has a regeneration zone (stem cells) that maintains a constant supply of new cells to enable endothelial cell migration from the peripheral limbal region to the central region of the cornea: these studies will evaluate endothelial cells that are transit amphifying cells, terminally differential cells, the effect of mitomycin C, glaucoma drainage implants and polymegathism on the endothelial cell population in the three zones of endothelial cells: regenerative, storage and migration. (2) that glutathoine will protect corneal endothelial cells against apoptosis and that the cellular levels of reduced glutathione (GSH) will modulate Fas-mediated apoptosis. And (3) that endotoxin (LPS) produced during inflammation in the presence of the binding protein (LPB) and the anchoring glycoprotein CD-14 causes the release of cytokines from the corneal endothelial cells which can result in corneal edema. The results of these studies should provide a better understanding of the corneal endothelial response following intraocular surgery and in the prevention of postoperative corneal edema that can occur in stressed corneas with low cell numbers and following gram negative intraocular inflammation.