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A Study of the Nuclear Magnetic Resonance (NMR) Relaxation Times to Characterize the Pathophysiology of Lung Injuries.

核磁共振 (NMR) 弛豫时间表征肺损伤病理生理学的研究。

基本信息

批准号：
01480237
负责人：
YAMABAYASHI Hajime
金额：
$ 3.01万
依托单位：
Tokai University Shool of Medicine
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (B)
财政年份：
1989
资助国家：
日本
起止时间：
1989 至 1990
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-01480237/
关键词：
Lung Injury Nuclear magnetic Resonance Relaxation Time 核磁気共鳴法(NMR)核磁気共鳴

项目摘要

We previously found that the nuclear magnetic resonance (NMR) relaxation times T_1 and T_2 characterized various lung injuries (1). The present project investigated the pathophysiology of lung injury through the NMR relaxation behavior of water molecules in lung tissue.1. Two T_2 components (T_2 fast : T_<2f> and T_2 slow : T_<2s>) have been observed for peripheral lung tissue (1-3). We analyzed the origin of water for these components and found that the T_<2f> component related to the water in alveolar walls, mainly the intracellular water of alveolar epithelial cells, and the T_<2s> component related to the interstitium (4).2. We developed a motion insensitive NMR imaging technique which we call Interleaved Line Scan (ILS) and measured the two components of T_2 for peripheral lung tissue in living spontaneously breathing rats (5). With this technique, we demonstrated the time course of T_2 in endotoxin lung injury using living animals (6). We are now to develop a method to measure the in-vivo relaxation times of lung tissue using a surface coil.3. The changes in T_1 and T_2 of lung injuries reflect the interactions between water molecules and tissue's macromolecules (1-3). We measured the temperature dependence of T_1 and T_2 for experimental lung injuries to investigate the state of water in the tissue. The results suggest that the changes in activation energy of water molecules is different for the normal and injured lung tissues. With the calculated activation energy of water molecules, it would be possible to understand the damages of tissue macromolecules in various stages and types of lung injury.

我们以前发现，核磁共振（NMR）弛豫时间T_1和T_2表征了各种肺损伤（1）。本课题通过对肺组织中水分子的核磁共振弛豫行为的研究，探讨了肺损伤的病理生理机制.在外周肺组织中观察到两个T_2分量（T_2快：T_<2f>和T_2慢：T_<2s>）（1-3）。我们分析了这些成分的水分来源，发现T_<2f>成分与肺泡壁中的水有关，主要是肺泡上皮细胞内的水，T_<2s>成分与肺泡上皮细胞内的水有关（4）.我们开发了一种对运动不敏感的核磁共振成像技术，我们称之为交错线扫描（ILS），并测量了活体自发呼吸大鼠外周肺组织的T_2的两种成分（5）。利用该技术，我们用活体动物证明了内毒素肺损伤中T_2的时间过程（6）。我们现在正在开发一种方法来测量在体内使用表面线圈的肺组织的弛豫时间。肺损伤T_1和T_2的变化反映了水分子与组织大分子之间的相互作用（1-3）。本实验测定了实验性肺损伤T_1和T_2的温度依赖性，以探讨肺组织中水分的状态。结果表明，正常肺组织和损伤肺组织水分子活化能的变化是不同的。通过计算水分子的活化能，可以了解肺损伤不同阶段和不同类型时组织大分子的损伤情况。