Photoreceptor Function in Retinopathy of Prematurity

描述（由申请人提供）：活动性早产儿视网膜病变（ROP），已知是对视网膜缺氧的反应，发生在视杆细胞外段快速发育的年龄。研究人员假设，发育中的视杆细胞的氧气需求迅速增加，导致缺氧，从而引发ROP，并且由于代谢需求未得到满足，视杆细胞功能受损。虽然承认“ROP的光感受器假说”不会被直接测试，但光感受器和ROP的发展知识为该项目创建了一个框架。在足月后年龄的ROP受试者中完成的研究记录了棒损坏的证据。在新项目的目标1中，将在ROP通常活跃的早产年龄测量视杆细胞敏感性Srod。这一点很重要，因为视杆细胞参与主动ROP的证明将保证ROP管理的新视角，其原理将是：满足光感受器的氧气需求。将对早产儿视网膜血管进行数值分析。将分析Srod和血管参数以预测ROP结果、高风险阈值前ROP的概率以及视网膜和视觉功能的后期发展。在健康的ROP受试者中，轻度视力缺陷可能是轻微黄斑病变的常见体征，其为中心凹和中心凹无血管区的神经血管发育改变的残留物。在目标2中，将评价中央视网膜功能（包括ROP婴儿的多焦ERG）并跟踪整个幼儿期。迄今为止的结果表明，杆功能障碍和早期屈光不正的关联，但仍有待发现更多的视网膜机制，在很大比例的ROP儿童谁发展早期屈光不正。因此，目标3的实验将更新屈光测量并分析先前在婴儿期研究的儿童ROP受试者的视网膜机制。对于每组实验，横截面数据的分析将评估视网膜和视觉参数随ROP结果的显著变化。将评价纵向数据随时间的变化以及ROP结局的变化。该项目将获得有关基本疾病过程的新知识，有助于理解ROP中的屈光发展，并为常见视力缺陷的基础提供新的见解。这些信息可能会在未来改变婴儿期和有ROP病史的儿童的ROP管理。

DESCRIPTION (provided by applicant): Active retinopathy of prematurity (ROP), which is known to be a response to retinal hypoxia, occurs at the age of rapid rod outer segment development. The investigators postulate that rapidly increasing oxygen demands of the developing rods contribute to the hypoxia that instigates ROP, and, as a consequence of unmet metabolic needs, rod function is impaired. While acknowledging that the "photoreceptor hypothesis of ROP" will not be put to direct test, knowledge of the development of the photoreceptors and of ROP creates a framework for the project. Completed studies in ROP subjects at post-term ages document evidence of damaged rods. In Aim 1 of the new project, rod cell sensitivity, Srod, will be measured at pre-term ages during which ROP is typically active. This is important because demonstration of rod involvement in active ROP will warrant a new perspective on ROP management, the principle of which will be: Satisfy oxygen needs of photoreceptors. A numeric analysis of preterm retinal blood vessels will be conducted. Srod and blood vessel parameters will be analyzed for prediction of ROP outcome, the probability of high risk pre- threshold ROP, and post-term development of retinal and visual function. In healthy ROP subjects, mild acuity deficits may be the common sign of a subtle maculopathy as residua of altered neural-vascular development of fovea and foveal avascular zone. In Aim 2, central retinal function will be evaluated (including multifocal ERG in ROP infants) and tracked through early childhood. Results to date demonstrate an association of rod dysfunction and early ametropia, but more remains to be discovered about retinal mechanisms in that substantial proportion of ROP children who develop early ametropia. Accordingly, the experiments of Aim 3 will update refractive measurements and analyze retinal mechanisms in child ROP subjects who were previously studied in infancy. For each set of experiments, the analyses of the cross sectional data will evaluate the retinal and visual parameters for significant variation with ROP outcome. The longitudinal data will be evaluated for change over time and for variation with ROP outcome. The project will obtain new knowledge about the fundamental disease process, contribute to the understanding of refractive development in ROP, and provide new insights into the basis of common acuity deficits. This information may, in the future, change management of ROP in infancy and in children with a history of ROP.