PATHOGENESIS OF CORNEAL EDEMA AFTER INTRAOCULAR SURGERY

描述（由申请人提供）：本研究的目的是 了解角膜水肿的发病机制，在一些患者中， 眼内手术后。最危险的是糖尿病患者， 有滴眼液、Maltino植入患者和可能长期接触透镜的患者 佩戴者，所有这些人都有严重的内皮细胞多巨体症，特别是 到了做白内障手术的年龄。我们的基本前提是， 这些患者的角膜具有受损的内皮和额外的应力 例如眼内手术、术后炎症和 眼内压会影响代谢泵和屏障功能， 内皮受损导致术后角膜水肿。 这些研究将进一步加深我们对 角膜水肿和术后角膜水肿的预防。我们建议 测试以下关于三个中的每一个的具体影响的假设 影响角膜内皮细胞的因素。(1)角膜 内皮细胞有一个再生区（干细胞）， 提供新细胞，使内皮细胞能够从外周迁移 角膜缘区域到角膜中心区域：这些研究将评估 终末分化的跨膜内皮细胞 细胞，丝裂霉素C的作用，青光眼引流植入物和多巨细胞症 在内皮细胞的三个区域中的内皮细胞群体上： 再生、储存和迁移。(2)谷胱甘肽对角膜有保护作用 内皮细胞抗凋亡和细胞水平的降低 谷胱甘肽（GSH）将调节Fas介导的细胞凋亡。（3）内毒素 (LPS)在存在结合蛋白（LPB）的情况下炎症期间产生 锚定糖蛋白CD-14导致细胞因子从细胞膜释放， 角膜内皮细胞，其可导致角膜水肿。 这些研究的结果应能使人们更好地了解 眼内手术后的角膜内皮反应， 预防术后角膜水肿，这可能发生在应力角膜中 细胞数量低，并伴有革兰氏阴性眼内炎症。

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.