PATHOGENESIS OF CORNEAL EDEMA AFTER INTRAOCULAR SURGERY

本研究的目的是了解角膜病变的发病机制。 某些患者在眼内手术后出现的浮肿。在… 风险最大的是糖尿病患者、滴眼液患者、Maltino患者 植入物患者和可能的长期配镜者，他们都有 严重的内皮细胞增多症，特别是在他们接近年龄的时候 做白内障手术。基本的前提是这些人的角膜 患者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 眼压会影响代谢泵和屏障 内皮功能受损导致术后 角膜浮肿。 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的预防 浮肿。PPI建议检验关于以下假设 三种因素对角膜损害的特异性影响 内皮：(1)12(R)HETE及其代谢产物8(R)HHDTrE的产生 经角膜上皮抑制内皮细胞Na+/K+-ATPase 导致内皮细胞增生症和角膜肿胀；(2) 角膜水肿可通过抑制内皮细胞碳水化合物而发生 内皮紧张的角膜中的脱水酶(即，角膜 糖尿病、隐形眼镜佩戴、角膜移植或老化引起的多发性肥大症)。 PI将决定Na+/K+ATPase代谢泵是否处于最大值 在内皮细胞中的效率，因此，缺乏 补偿碳酸酐酶的生理储备 抑制；内毒素(内毒素)在炎症过程中产生 内毒素结合蛋白(LBP)的存在和 锚定糖蛋白(CD-14)导致细胞因子的释放 角膜浮肿。 这些研究将在体外灌流的人和兔身上进行 眼角膜。这些研究的结果应该会提供更好的 对眼内手术后角膜内皮反应的认识 手术和在预防术后角膜水肿方面可以 发生在细胞数较低的压力过大的角膜中 发炎。

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.