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，在某些患者中， 在眼内手术后。风险最大的是糖尿病患者，患者 使用滴眼液、Maltino植入物的患者，可能还会长期戴隐形眼镜 佩戴者，所有人都有严重的内皮细胞增多症，特别是当 他们快到做白内障手术的年龄了。我们的基本前提是 这些患者的角膜有内皮受损和额外的压力。 如眼内手术、术后炎症和术后并发症增加 眼压会影响机体的代谢泵和屏障功能 内皮受损导致术后角膜水肿。 拟议中的研究将进一步加深我们对糖尿病发病机制的理解。 角膜水肿与术后角膜水肿的预防。我们建议 测试以下关于三种药物的具体效果的假设 影响角膜内皮受损的因素。(1)角膜 内皮细胞有一个再生区(干细胞)，维持恒定的 供应新细胞以使内皮细胞能够从外周迁移 角膜缘区域到中央区域：这些研究将评估 内皮细胞是终末分化的转运性两极化细胞 细胞、丝裂霉素C的作用、青光眼引流植入物和多发性增生症 关于三个内皮细胞区内皮细胞的数量： 再生、存储和迁移。(2)谷胱甘肽保护角膜 抗内皮细胞凋亡和细胞水平的降低 谷胱甘肽(GSH)可调节Fas介导的细胞凋亡。以及(3)内毒素 在结合蛋白(LPB)存在的情况下，炎症过程中产生的(LP) 而锚定糖蛋白CD-14导致细胞因子从 可导致角膜水肿的角膜内皮细胞。 这些研究的结果应该会让我们更好地理解 眼内手术后的角膜内皮反应 应激性角膜术后角膜水肿的预防 细胞数量低，继发革兰氏阴性眼内炎。

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.