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ADENOSINE AND RETINAL ISCHEMIA

ADENOSINE AND RETINAL ISCHEMIA
腺苷和视网膜缺血
批准号:
2164154
负责人:
STEVEN ROTH
金额:
$20.21万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
1994
资助国家:
美国
项目状态:
已结题
起止时间:
1994-01-01 至 1997-12-31

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中文摘要
翻译
视网膜缺血发生时,氧气和葡萄糖供应到视网膜 被打断了 这种情况可能发生在视网膜血管疾病 例如视网膜动脉阻塞,或由于系统性疾病 例如糖尿病。 视网膜损伤的病理生理学 缺血后似乎涉及兴奋性氨基酸, 血流紊乱。 腺苷的局部浓度 在脑缺血时大量增加, 在局部缺血之前或之后给予动物的类似物产生了 改善效果。 一种腺苷类似物可以减弱 视网膜缺血性损伤,腺苷似乎是一个 参与视网膜血管对血液减少的反应的因子 氧含量 本研究的总体假设是腺苷 是视网膜对氧气条件反应的关键因素 和/或葡萄糖向视网膜的输送减少。 基于该 腺苷的功能,使用选择性腺苷对抗,或 内源性腺苷浓度的调节,可以允许操纵 关键事件(兴奋性氨基酸浓度或血流量 在视网膜缺血期间或之后的改变)。 评价的作用 腺苷在视网膜缺血中,将测量腺苷浓度 在缺氧和缺血的视网膜中。 腺苷的用途 在这些条件下的拮抗剂将允许评估的影响, 腺苷对视网膜血流的影响 在另一系列的 实验中,我们将使用选择性腺苷激动剂之前或 在视网膜缺血后检查腺苷是否可以提供 减轻视网膜损伤。 这些研究将提供新的 信息的作用,腺苷在代偿机制, 以及视网膜缺血后的潜在治疗方法, 预防或改善视网膜缺血性损伤和视力丧失。
英文摘要
Retinal ischemia occurs when the oxygen and glucose supply to the retina is interrupted. This condition may occur in retinal vascular diseases such as retinal artery occlusion, or as a result of systemic diseases such as diabetes mellitus. The pathophysiology of retinal injury following ischemia appears to involve excitatory amino acids and disturbances in blood flow. The local concentration of adenosine increases massively during cerebral ischemia, and exogenous adenosine analogues administered to animals before or after ischemia have produced ameliorative effects. An adenosine analogue has been found to attenuate retinal ischemic injury in rabbits, and adenosine appears to be one factor involved in the retinal vascular response to decreased blood oxygen content. The overall hypothesis of this study is that adenosine is a critical factor in the retinal response to conditions where oxygen and./or glucose delivery to the retina is diminished. Based upon this function of adenosine, the use of selective adenosine against, or modulation of endogenous adenosine concentration, may allow manipulation of critical events (excitatory amino acid concentration or blood flow alterations) during or after retinal ischemia. To evaluated the role of adenosine in retinal ischemia, adenosine concentration will be measured in the retina during hypoxic and ischemia. The use of adenosine antagonists under these conditions will allow evaluation of the influence of adenosine on blood flow in the retina. In another series of experiments, we will use selective adenosine agonists either before or after retinal ischemia to examine whether adenosine can provide an attenuation of retinal injury. These studies will provide new information on the role of adenosine in compensatory mechanisms during and after retinal ischemia and potential therapeutic approaches to prevent or ameliorate retinal ischemic injury and visual loss.
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