MECHANISMS OF RECURRENCE OF ANTERIOR UVEITIS OF THE EYE

男性特发性前葡萄膜炎的特征是 血-房水屏障是急性的并且经常复发。 如果不治疗， 它经常会导致继发性青光眼。 当前可用 眼部炎症的客观测量需要不希望的侵入性 例如穿刺术。 因此，严重程度的临床评估 前葡萄膜炎及其对治疗的反应，在很大程度上依赖于 对耀斑和细胞等参数进行主观分级。 的一个主要目的 拟议的研究是适应技术的水 荧光光度法是客观的，但非侵入性的测量前 节段炎症。 最终的直接临床应用 程序是我们的最终目标。 将使用水性荧光光度法测量 细菌内毒素诱导的兔前葡萄膜炎模型， 后来在猴子身上。 通过利用我们开发的新方法， 实验室，我们可以比较荧光光度估计的严重程度与 同一只眼睛的超微结构示踪研究结果。 的能力 区分有助于和不有助于水的部位 在葡萄膜炎严重程度的每个阶段的荧光提供了有价值的工具， 用来完善解释 临床环境中的荧光光度数据。 使用相同的程序， 结合冷冻断裂技术，我们将检查 消退期间血-房水屏障的重建过程 前葡萄膜炎，无论是否使用类固醇治疗， 非甾体抗炎药。 将特别强调 紧密连接重组的机制， 构成血-房水屏障的解剖学等价物。 葡萄膜炎后，屏障重建不完全或错误， 到复发。 因此，屏障改造过程的知识可能是 这对了解人类复发性前葡萄膜炎至关重要。 血-房水屏障渗透性增加的其他动物模型 如果没有明显的炎症细胞反应， 了解耀斑和荧光光度之间的关系 测量水性荧光。 最后，对兔子的研究将确定眼内 由炎症引起的压力是由大小的变化或 这些眼睛的睫状上皮中的缝隙连接的数量。

Idiopathic anterior uveitis in man is characterized by a breakdown of the blood-aqueous barrier which is acute and often recurrent. Left untreated, it can frequently lead to secondary glaucoma. Currently available objective measures of ocular inflammation necessitate undesirable invasive procedures such as paracentesis. Thus, clinical assessment of the severity of anterior uveitis and its response to therapy, has relied heavily upon subjective grading of such parameters as flare and cells. A major aim of the proposed studies is adaptation of the technique of aqueous fluorophotometry to the objective, but non-invasive measure of anterior segment inflammation. Eventual direct, clinical application of the procedure is our ultimate goal. Aqueous fluorophotometry will be used to measure the changes in severity of a bacterial endotoxin-induced model of anterior uveitis in rabbits and later in monkeys. By taking advantage of a new method developed in our laboratory, we can compare fluorophotometric estimates of severity with results of ultrastructural tracer studies on the same eyes. The ability to distinguish between sites which do and do not contribute to aqueous fluorescence at each stage of uveitis severity provides a valuable tool with which to refine pharmacokinetic models necessary to interpret fluorophotometric data in a clinical setting. Using the same procedures, in conjunction with the freeze-fracture technique, we will examine the process of re-establishment of the blood-aqueous barrier during resolution of anterior uveitis, both with and without treatment using steroidal and non-steroidal anti-inflammatory agents. Particular emphasis will be given to the mechanisms involved in the reassembly of tight junctions, which constitute the anatomic equivalent of the blood-aqueous barrier. Incomplete or faulty barrier reformation, after uveitis, could contribute to recurrence. Thus knowledge of the process of barrier reformation may be critical to an understanding of recurrent anterior uveitis in man. Additional animal models of increased blood-aqueous barrier permeability without appreciable inflammatory cell responses will be exploited to better understand the relationship between flare and fluorophotometrically measured aqueous fluorescence. Finally, studies in rabbits will determine if changes in intraocular pressure caused by inflammation are paralleled by changes in the size or number of gap junctions in the ciliary epithelium of these eyes.