NEW STRATEGY BASED ON REGULATION OF OXTPATIVE STRESS IN TREATMENT OF BRONCHIAL ASTHMA

基于过度应激调节的支气管哮喘治疗新策略

基本信息

  • 批准号:
    13670611
  • 负责人:
  • 金额:
    $ 1.73万
  • 依托单位:
  • 依托单位国家:
    日本
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
  • 财政年份:
    2001
  • 资助国家:
    日本
  • 起止时间:
    2001 至 2002
  • 项目状态:
    已结题

项目摘要

We have previously found that higher levels of nitrogen oxides in exhaled air and in induced sputum were found in asthmatics compared to normal control subjects, and that nitrogen oxides altered β_2 -adrenoceptor (β_-AR) function in an experimental animal model. Therefore, this study was designed to determine whether nitrogen oxides influence the bronchodilating activity of β_2-AR agonists in asthmatic patients. We simultaneously measured the levels of nitrogen oxides in exhaled air and in induced sputum in 20 asthmatic patients. The bronchodilating activity of β_2-AR agonists was expressed as a spontaneous recovery (pre- raethacholine) and recovery from the lowest value in FEV1 evoked by methacholine challenge (post-methacholine). For 1-week after the first study, 400 μg of beclomethasone dipropionate (BDP) twice daily was administered for all patients, and the above mentioned protocols were repeated. Recovery in FEV1 (pre-methacholine) after β_2-AR agonists was not significantly correlated with any baseline FEV1 and PC20 methacholine. Moreover, recovery in FEV1 (post-methacholine) after β_2-AR agonists was not also significantly correlated with maximal fall in FEV1 after methacholine challenge and PC20 methacholine. However, recovery in FEV1 after β_2-AR agonists was inversely correlated with NO levels in exhaled air, and concentration of nitrite and nitrate in induced sputum. After treatment with inhaled BDP for 1-week, there was no significant change in baseline FEV1. However, there was a significant decrease in the concentration of nitrite and nitrate in induced sputum. We found that change of nitrite and nitrate levels in induced sputum after 1-week BDP therapy was significantly correlated with change in bronchodilating activity of β_2-AR agonists between pre- and post-BDP therapy. We determined that nitrogen oxides in the airways reduced β_2-AR agonists-induced brochodilation in asthmatics.
我们先前发现,哮喘患者呼出的空气和诱导痰中的氮氧化物含量高于正常对照组,并且在实验动物模型中,氮氧化物改变了β_2 -肾上腺素能受体(β_-AR)的功能。因此,本研究旨在确定氮氧化物是否影响哮喘患者β_2-AR激动剂的支气管扩张活性。我们同时测量了20名哮喘患者呼出空气和诱导痰中的氮氧化物水平。β_2-AR激动剂的支气管扩张活性表现为自发恢复(乙酰胆碱前)和从乙酰胆碱激发引起的FEV1最低值恢复(乙酰胆碱后)。在第一次研究后的1周内,所有患者均给予400 μg二丙酸倍氯米松(BDP),每日2次,并重复上述方案。β_2-AR激动剂后FEV1(前甲胆碱)的恢复与任何基线FEV1和PC20甲胆碱均无显著相关。此外,β_2-AR激动剂后FEV1的恢复与乙酰胆碱刺激后FEV1的最大下降和乙酰胆碱PC20的最大下降也没有显著相关。然而,β_2-AR激动剂后FEV1的恢复与呼出空气中NO水平以及诱导痰中亚硝酸盐和硝酸盐浓度呈负相关。吸入BDP治疗1周后,基线FEV1无显著变化。诱导痰中亚硝酸盐和硝酸盐浓度明显降低。我们发现,BDP治疗1周后诱导痰中亚硝酸盐和硝酸盐水平的变化与BDP治疗前后β_2-AR激动剂支气管扩张活性的变化显著相关。我们确定气道中的氮氧化物降低了哮喘患者β_2-AR激动剂诱导的心肌舒张。

项目成果

期刊论文数量(18)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Hiroshi Kanazawa et al.: "Nitrogen oxides reduce albuterol-induced bronchodilation in patients with b ronchial asthma"Respiration. (In press).
Hiroshi Kanazawa 等人:“氮氧化物可减少支气管哮喘患者沙丁胺醇诱导的支气管扩张”呼吸。
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    0
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Kanazawa H, et al.: "Nitrogen oxides reduce albuterol-induced bronchodilator in patients with bronchial asthma"Respiration. 69. 490-495 (2002)
Kanazawa H 等人:“氮氧化物可减少支气管哮喘患者沙丁胺醇诱导的支气管扩张剂”呼吸。
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    0
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Kanazawa H, et al.: "Vascular involvement in exercise-induced airway narrowing in patients with bronchial asthma"chest. 122. 166-170 (2002)
Kanazawa H 等人:“支气管哮喘患者运动引起的气道狭窄中的血管受累”胸部。
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    0
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Kanazawa H, Hirata K, Yoshikawa J: "Nitrogen oxides reduce albuterol-induced bronchodilation in patients with bronchial asthma"Respiration. 69. 490-495 (2002)
Kanazawa H、Hirata K、Yoshikawa J:“氮氧化物可减少支气管哮喘患者沙丁胺醇诱导的支气管扩张”呼吸。
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
  • 作者:
  • 通讯作者:
Hiroshi Kanazawa et al.: "Vascular involvement in exercise-induced airway narrowing in patients with bronchial asthma"Chest. (In press).
Hiroshi Kanazawa 等人:“支气管哮喘患者运动引起的气道狭窄中的血管受累”胸部。
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KANAZAWA Hiroshi其他文献

KANAZAWA Hiroshi的其他文献

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{{ truncateString('KANAZAWA Hiroshi', 18)}}的其他基金

Elucidation of the pathophysiology of intractable asthma from the view-point of aging of airway tissues and establishment of new treatment strategy
从气道组织老化角度阐明难治性哮喘的病理生理并建立新的治疗策略
  • 批准号:
    26461166
  • 财政年份:
    2014
  • 资助金额:
    $ 1.73万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
pH regulation of organelles and its physiological role and molecular mechanism
细胞器的pH调节及其生理作用和分子机制
  • 批准号:
    21370055
  • 财政年份:
    2009
  • 资助金额:
    $ 1.73万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Elucidation of molecular mechanisms of angiogenesis mediated by angiopoietins and its application for asthma therapy
阐明血管生成素介导的血管生成的分子机制及其在哮喘治疗中的应用
  • 批准号:
    20590901
  • 财政年份:
    2008
  • 资助金额:
    $ 1.73万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Molecular basis for regulation of intracellular environment and function of ion transporting proteins
调节细胞内环境和离子转运蛋白功能的分子基础
  • 批准号:
    17370046
  • 财政年份:
    2005
  • 资助金额:
    $ 1.73万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Adaptation of cells to high salinity conditions and basic mechanisms of ion transport in biological membranes
细胞对高盐条件的适应和生物膜中离子传输的基本机制
  • 批准号:
    15370054
  • 财政年份:
    2003
  • 资助金额:
    $ 1.73万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
A NON-INVASIVE METHOD FOR EVALUATING PULMONARY ENDOTHELIAL CELL APOPTOSIS AND ITS APPLICATION TO THERAPY IN CHRONIC OBSTRUCTIVE PULMONARY DISEASE
一种评估肺内皮细胞凋亡的非侵入性方法及其在慢性阻塞性肺疾病治疗中的应用
  • 批准号:
    15590820
  • 财政年份:
    2003
  • 资助金额:
    $ 1.73万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Unity and diversity of ion transport mechanisms and regulation of Na+/H+ antiporters
离子转运机制的统一性和多样性以及Na /H反向转运蛋白的调节
  • 批准号:
    13142207
  • 财政年份:
    2001
  • 资助金额:
    $ 1.73万
  • 项目类别:
    Grant-in-Aid for Scientific Research on Priority Areas
Structure, function and regulation of Na^+/H^+ antiporters and intracellular localization mechanism.
Na^/H^反向转运蛋白的结构、功能和调控以及细胞内定位机制。
  • 批准号:
    13680689
  • 财政年份:
    2001
  • 资助金额:
    $ 1.73万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Molecular structure of H^+ transporting ATPase and its rotation mechanisms in the catalysis
H^转运ATP酶的分子结构及其催化旋转机制
  • 批准号:
    09680622
  • 财政年份:
    1997
  • 资助金额:
    $ 1.73万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Art as Cultural Identity in Modern Nation-States
艺术作为现代民族国家的文化身份
  • 批准号:
    08301004
  • 财政年份:
    1996
  • 资助金额:
    $ 1.73万
  • 项目类别:
    Grant-in-Aid for Scientific Research (A)

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呼吸鞘脂合成参与气道高反应性和病毒引发的哮喘
  • 批准号:
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  • 财政年份:
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巨噬细胞在有机磷农药引起的气道高反应性中的作用
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巨噬细胞在有机磷农药引起的气道高反应性中的作用
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    8663694
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新型吸入麻醉药地氟烷对气道高反应性的影响
  • 批准号:
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Role of NKT cells in airway hyperreactivity & tolerance
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