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Study on the Mechanism of Increased Vascular Permeability in Pulmonary Edema

肺水肿血管通透性增加的机制研究

基本信息

批准号：
06454443
负责人：
SHIMADA Yasuhiro
金额：
$ 4.54万
依托单位：
Nagoya University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B)
财政年份：
1994
资助国家：
日本
起止时间：
1994 至 1996
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-06454443/
关键词：
pulmonary edema neurogenic pulmonary edema vascular permeability neurotransmitter ARDS neuropeptide Y peptide YY pulmonary circulation neuropeptide Y Paptide YY Peptide YY neuroPeptide Y

项目摘要

We investigated the role of neurotransmitters on the mechanism of pulmonary vascular permeability, and the following results were obtained in terms of the role of neuropeptide Y (NPY), which co-exists with norepinephrine in the sympathetic nervous system, on the development of pulmonary edema.1)We studied the effect of sympathetic nerve stimulation on lung vascular permeability on isolated perfused lung model. Electrical stimulation increased the lung weight, suggesting an increase in lung vascular permeability. The increase in lung weight occurred in the presence of norepinephrine blockers, suggesting the presence of vasoactive substances other than norepinephrine.2)By using the isolated perfused lung model, NPY and neurokinin A (NKA) showed an increase in capillary permeability coefficient (Kfc), and calcitonin-gene related protein (CGRP) showed a decrease.3)Lung vascular permeability can be elucidated by injecting carbon particlesinto the perfusate of the lung model and microscopically calculate the carbon particles present in the alveoli. Administration of NPY into the trachea caused a significant increase in the number of carbon particlesin the alveoli in a dose-dependent manner.4)Pretreatment with NPY_<18-36>, which is a partial antagonist of NPY Y_3 receptor, elongated the time required for edema formation and reduced the protein concentration ratio of alveolar fluid to serum in the fibrin pulmonary edema model.5)Pretreatment with NPY_<18-36> reduced the number of carbon particlesin the alveoli in the animals treated with NPY intratracheally.

本研究探讨了神经递质在肺血管通透性机制中的作用，并就交感神经系统中与去甲肾上腺素共存的神经肽Y（neuropeptide Y，NPY）在肺水肿发生中的作用进行了研究。结果如下：1）在离体肺灌流模型上研究了交感神经刺激对肺血管通透性的影响。电刺激增加肺重量，表明肺血管通透性增加。在去甲肾上腺素阻断剂存在的情况下，肺重量增加，表明存在除去甲肾上腺素以外的血管活性物质。2）通过使用离体灌注肺模型，NPY和神经激肽A（NKA）显示毛细血管通透性系数（Kfc）增加，降钙素基因相关蛋白（CGRP）水平降低肺血管通透性可以通过将碳颗粒注入肺模型的灌流液中并在显微镜下计算肺泡中存在的碳颗粒来阐明。气管内注射NPY可使肺泡内碳颗粒数明显增加，并呈剂量依赖性。4）<18-36>NPY Y_3受体部分拮抗剂NPY_预处理可延长纤维蛋白肺水肿模型的水肿形成时间，降低肺泡液/血清蛋白浓度比。5）气管内注射NPY_预处理可<18-36>降低肺泡内碳颗粒数。