ANIMAL MODEL FOR RETINOPATHY OF PREMATURITY

现代新生儿重症监护提高早产儿存活率 护理单位引起早产儿视网膜病（ROP）的复发。 有理由认为，随着越来越多、越来越小的早产儿存活下来， ROP视力丧失的发生率将继续增加，除非 40年前， 新生儿吸入的氧气水平与 ROP。 然而，关于心脏病的病理生理学的基本问题仍然存在。 条件 它似乎涉及两个典型事件： 早产儿视网膜血管的衰减 正在接受氧气治疗，视网膜血液增生 这是通过移除到室内空气呼吸来促进的血管。 最终 本研究的目的是充分表征ROP的这两个方面 并开始制定预防方法， 从大鼠模型的研究中获得的理解。 为此，四 提出了相关的研究项目：1）试图减少 通过补充抗氧化剂使视网膜对氧的敏感性; 2） 试图减少视网膜对异常血管的倾向， 通过补充抗血管生成因子的增殖; 3） 试图确定缺血诱导的缺氧在 血管增生反应;和4）试图详细描述 正常视网膜血管形成过程，特别强调 梭形细胞分化的动力学。 对ROP动物模型的批评集中在它们不能 会导致视网膜脱落，这是婴儿的关键晚期。 我们 尽管有这个缺点，但使用大鼠的策略是建立在 以下前提：如果药物手段阻止早期 在动物中可以发现氧诱导的视网膜病变的表现， 通过使用相同的药剂，我们可能会提供有效的 治疗婴儿。 新生儿对这些早期事件的抑制可能 通过消除刺激来消除视网膜脱离。

The increased survival of premature infants in modern neonatal intensive care units has caused a resurgence of retinopathy of prematurity (ROP). It is reasoned that as more and smaller premature babies survive, the incidence of visual loss from ROP will continue to increase unless effective treatments are found. Four decades ago, a high correlation was found between inspired levels of oxygen by neonates and development of ROP. Yet, basic questions remain about the pathophysiology of the condition. It appears to involve two characteristic events: an attenuation of retinal blood vessels that occurs while a premature infant is undergoing oxygen therapy, and a proliferation of retinal blood vessels that is promoted by removal to room air breathing. The ultimate goal of this research is to fully characterize these two aspects of ROP and to begin to develop methods for their prevention based on understanding gained from studies of a rat model. To this end, four interrelated research projects are proposed: 1) an attempt to reduce retinal susceptibility to oxygen through antioxidant supplementation; 2) an attempt to reduce the propensity of the retina for abnormal vascular proliferation through supplementation with antiangiogenic factors; 3) an attempt to determine the role of ischemia-induced hypoxia in the vasoproliferative response; and 4) an attempt to describe in detail the normal retinal vasoformation process, with particular emphasis on the dynamics of spindle-cell differentiation. Criticism of animal models of ROP has focused on their inability to produce retinal detachment, the critical end-stage in infants. Our strategy for using rats in spite of this drawback is built upon the following premise: If a pharmacologic means of arresting the early manifestations of oxygen-induced retinopathy can be found for animals, it is possible that by applying the same agents, we will provide effective therapy to infants. The repression of these early events in neonates may eliminate retinal detachment by removing its stimulus.