SODIUM MRI & CSI OF EXPERIMENTAL DIABETIC RETINOPATHY

拟议研究的具体目的是使用钠磁 核磁共振成像（23 Na MRI）和钠化学位移成像（23 Na CSI） 在两种动物模型中表征玻璃体的状态， 糖尿病视网膜病变 糖尿病视网膜病变是糖尿病的一种并发症， 25岁至35岁人群新失明的主要原因 多年来，随着医学进步， 糖尿病患者的长寿 越来越多的糖尿病失明者， 特别是在青少年发病类别，提供了一个明确的挑战， 制定有效的战略，基本的理解，诊断和 治疗这种疾病。 磁共振已被证明是一个很好的工具，为研究 钠，因为在23 Na磁共振中可获得高对比度 图像，这个四极核的固有敏感性， 环境，以及生物体内相对高浓度的钠 系统. 在这项工作中，我们将使用钠磁共振成像， 化学位移成像技术由首席研究员 和她的学生及合作者研究糖尿病患者 玻璃体视网膜病变： 1. 在玻璃体内局部测量钠自旋-自旋 弛豫时间和钠的“可见度”; 2. 评估血液成分穿过血视网膜的渗漏 通过监测静脉内施用的顺磁性物质的流动来建立屏障 将试剂转移到玻璃体中。 糖尿病视网膜病变将通过激光光凝法模拟。 视网膜和通过四氧嘧啶诱导糖尿病。 我们预计血迹- 视网膜屏障功能障碍将导致视网膜的化学位移图像。 与正常玻璃体不同的玻璃体区域。 我们也 预计钠自旋-自旋弛豫时间和可见度值 当玻璃体的状态通过渗漏而改变时， 视网膜血管的血液成分。 这些参数将 提供了对玻璃体凝胶性质变化的洞察， 糖尿病视网膜病变

The specific aim of the proposed research is to use sodium magnetic resonance imaging (23Na MRI) and sodium chemical shift imaging (23Na CSI) to characterize the state of the vitreous body in two animal models of diabetic retinopathy. Diabetic retinopathy, a complication of diabetes, is the major cause of new blindness in persons between the ages of 25 and 35 years, and continues to grow in importance as medical advances extend the longevity of diabetics. The increasing number of diabetic blind, especially in the juvenile onset category, offers a clear challenge to develop effective strategies for the basic understanding, diagnoses and treatment of this disorder. Magnetic resonance has proven to be an excellent tool for the study of sodium because of the high contrast obtainable in 23Na magnetic resonance images, the inherent sensitivity of this quadrupolar nucleus to its environment, and the relatively high concentration of sodium in biological systems. In this work we will use sodium magnetic resonance imaging and chemical shift imaging techniques developed by the principal investigator and her students and collaborators to investigate the effects of diabetic retinopathy on the vitreous body by: 1. measuring, on a local basis within the vitreous, sodium spin-spin relaxation times and sodium "visibility"; 2. assessing leakage of blood constituents across the blood-retinal barrier by monitoring the flow of intravenously administered paramagnetic shift reagent into the vitreous. Diabetic retinopathy will be modeled by laster photocoagulation of the retina and by alloxan induction of diabetes. We anticipate that blood- retinal barrier dysfunction will result in chemical shift images of the regions of the vitreous distinct from those of normal vitreous. We also anticipate that sodium spin-spin relaxation times and visibility values will change as the state of the vitreous is altered through the leakage of blood constituents from retinal blood vessels. These parameters will provide insight into the changing nature of the vitreous gel associated with diabetic retinopathy.