BRAIN IMAGING IN ALTITUDE ILLNESS

高原疾病的脑成像

• 批准号: 7627712
• 负责人: ROBERT C ROACH
• 金额: $ 0.5万
• 依托单位: UNIVERSITY OF CALIFORNIA LOS ANGELES
• 依托单位国家: 美国
• 财政年份: 2007
• 资助国家: 美国
• 起止时间: 2007-09-30 至 2008-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7627712
• 关键词: Acute; Altitude; Altitude Sickness; Blood - brain barrier anatomy; Blood Plasma Volume; Blood Volume; Brain; Brain Edema; Brain imaging; Cerebral perfusion pressure; Cerebrum; Computer Retrieval of Information on Scientific Projects Database; Drops; Exercise; Functional disorder; Funding; Genotype; Goals; Grant; Heat-Shock Response; Human; Hypoxia; Institution; Intracranial Pressure; Liquid substance; Magnetic Resonance Imaging; Measurement; Molecular Genetics; Nitric Oxide; Oxygen; Peptidyl-Dipeptidase A; Permeability; Physiological; Production; Research; Research Personnel; Resources; Role; Severities; Source; Study of magnetics; Symptoms; United States National Institutes of Health; Vascular Endothelial Growth Factors; Water; extracellular; innovation; innovative technologies; response

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. 'The goal of this proposal is to determine the role of brain swelling in the pathophysiology of acute mountain sickness (AMS). We recently showed that exercise caused a >3 fold rise in AMS symptom severity, a drop in arterial oxygen saturation (SaO2) during exercise, and slight fluid retention. We also recently showed that subjects ill with AMS had a small drop in plasma volume and a large rise in extracellular water compared to those that remained free of AMS. In further studies, magnetic resonance imaging revealed that most brains swell when humans ascend to high altitude. Our overall hypothesis is that brain swelling, which can include elevated brain water and blood volume, causes the symptoms of AMS. Our approach is to use several new and innovative technologies to dissect the role of cellular, molecular, genetic and physiological responses in the pathophysiology of AMS. The new and innovative approaches include measurement in humans acutely deprived of oxygen of 1) nitric oxide (NO) production; 2) vascular endothelial growth factor (VEGF); 3) heat shock factor/heat shock protein72 (HSF/HSP72); and 4) angiotensin converting enzyme (ACE) genotype. We will also make the first noninvasive measurements of cerebral perfusion pressure (eCPP), intracranial pressure (eICP), cerebral blood volume (CBV), blood-brain barrier (BBB) permeability, brain water and craniospinal volumes in humans exposed to acute hypoxia for 9 hrs.

该子项目是利用该技术的众多研究子项目之一 资源由 NIH/NCRR 资助的中心拨款提供。子项目及 研究者 (PI) 可能已从 NIH 的另一个来源获得主要资金， 因此可以在其他 CRISP 条目中表示。列出的机构是 对于中心来说，它不一定是研究者的机构。 “该提案的目标是确定脑肿胀在急性高山病（AMS）病理生理学中的作用。我们最近发现，运动导致 AMS 症状严重程度增加 3 倍以上、运动期间动脉血氧饱和度 (SaO2) 下降以及轻微的液体潴留。我们最近还发现，与未患有 AMS 的受试者相比，患有 AMS 的受试者的血浆体积略有下降，而细胞外水则大幅上升。在进一步的研究中，磁共振成像显示，当人类登上高海拔地区时，大多数大脑都会肿胀。我们的总体假设是，脑肿胀（包括脑水和血容量升高）会导致 AMS 症状。我们的方法是使用多种创新技术来剖析细胞、分子、遗传和生理反应在 AMS 病理生理学中的作用。新的创新方法包括测量严重缺氧的人体 1) 一氧化氮 (NO) 的产生； 2）血管内皮生长因子（VEGF）； 3)热休克因子/热休克蛋白72(HSF/HSP72)； 4) 血管紧张素转换酶（ACE）基因型。我们还将首次对受暴露人体的脑灌注压（eCPP）、颅内压（eICP）、脑血容量（CBV）、血脑屏障（BBB）渗透性、脑水和颅脊髓容量进行无创测量 急性缺氧9小时。