PATHOGENESIS OF CORNEAL EDEMA AFTER INTRAOCULAR SURGERY

本研究的目的是了解角膜上皮细胞增生的发病机制， 在某些患者中，眼内手术后会发生水肿。 在 最大的风险是糖尿病患者，有滴状，Maltino 植入患者和可能的长期透镜配戴者，所有这些人都有 严重的内皮细胞增生症，特别是当他们接近 做白内障手术 基本前提是，这些人的角膜 患者具有受损的内皮和额外的压力， 眼内手术，术后炎症和增加 眼压会影响代谢泵和屏障 内皮功能受损导致术后 角膜水肿 建议的研究应可加深我们对 角膜水肿的发病机制及术后角膜水肿的预防 水肿 PI建议检验以下关于 三个因素中的每一个对受损角膜的特定影响 内皮：（1）12（R）HETE和代谢物8（R）HHDTrE产生 抑制内皮细胞Na+/K+ ATP酶 导致内皮细胞增生和角膜肿胀;（2） 角膜水肿可以通过抑制内皮细胞的碳 具有受压内皮的角膜中的脱水酶（即，角膜， 糖尿病、接触透镜佩戴、角膜移植术或衰老引起的多肥大症）。 PI将确定Na+/K+ ATP酶代谢泵是否处于最大值 在内皮细胞中的效率，因此，缺乏 用于补偿碳酸酐酶的生理储备 抑制;在炎症过程中产生内毒素（LPS）， 脂多糖结合蛋白（LBP）和 锚定糖蛋白（CD-14）引起细胞因子的释放， 角膜水肿 这些研究将在体外灌注的人和兔中进行 角膜 这些研究的结果应该提供更好的 对眼内植入后角膜内皮反应的理解 手术和预防术后角膜水肿， 发生在细胞数量低的应激角膜中， 炎症

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 lens wearers, all of whom have severe endothelial polymegathism, particularly as they approach the age for cataract surgery. The 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. The PI proposes to test the following hypothesis about the specific effects of each of three factors on the compromised corneal endothelium: (1) that 12(R)HETE and the metabolite 8(R)HHDTrE produced by the corneal epithelium can inhibit endothelial Na+/K+ ATPase resulting in endothelial polymegathism and corneal swelling; (2) that corneal edema can occur by the inhibition of endothelial carbonic anhydrase in corneas with a stressed endothelium (i.e., corneas with polymegathism from diabetes, contact lens wear, keratoplasty or aging). ThePI will determine if the Na+/K+ ATPase metabolic pumps are at maximum efficiency in the endothelial cells, and therefore, lack the physiological reserve to compensate for the carbonic anhydrase inhibition; that endotoxin (LPS) produced during inflammation in the presence of the lipopolysaccharide binding protein (LBP) and the anchoring glycoprotein (CD-14) causes the release of cytokines resulting corneal edema. These studies will be performed on in vitro perfused human and rabbit corneas. 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 inflammation.