Mechanism of exsecise-induced astham in an animal model
动物模型中运动诱发哮喘的机制
基本信息
- 批准号:06670624
- 负责人:
- 金额:$ 1.22万
- 依托单位:
- 依托单位国家:日本
- 项目类别:Grant-in-Aid for General Scientific Research (C)
- 财政年份:1994
- 资助国家:日本
- 起止时间:1994 至 1995
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
We reported that release of Substance-P from C-fiber of bronchial nerves has an important role in the mechanisms of the exercise-induced asthma (EIA).This time, therefore, we examined the effect of leukotrien C4, D4, E4 antagonist (ONO-1078) on the EIA in order to determine the role leukotrien to cause EIA.Futhermore, to clarify the involvement of Substance-P and leukotriene released by mast cell, we take the NK1 receptor antagonist (FK888), NK1 and NK2 receptor antagonist (FK224) and Leukotriene C4, D4, E4 antagonist (ONO-1078) to EIA in guinea pig immunized byOA.And to determine the effect of probocation of cold air to hyperresponsiveness, we measured the Rr and airway responsiveness to histamine and investigated the histamine and Substnace-P level in BALF in guinea pig immunized by OA after cold air porbocation.It is recognized that Rr in guinea pig dosen't increase 5 minutes after exercise, but increased significantly 15 minutes after exercise. Histamine concentration in BAlF of guinea pig 15 minutes after exercise was higher than before, but not significantly. Substance-P level were significantly higher than before. Proportion do neutrophiles in BALF increase 15 minutes after exerciase. ONO-1078 inhibited EIA and so did FK888 and FK224. Although the Rr increased and threshhold to histamined decrease 15 minutes after inhalation of cold air (-10゚C), histamine and Substance-P level in BALF didn't significantly change respectively.It is suggested that activation of mast cell and releasebility of C-fiber in the bronchus were induced after hyperventilation, mediators from mast cells and C-fiber play an important role in mechanisms of EIA.
我们研究了运动性哮喘(exercise-induced asthma,EIA)时支气管神经C纤维释放P物质的作用,探讨了白三烯C4、D4、E4拮抗剂对EIA的影响(ONO-1078)对EIA的影响,以确定白三烯在引起EIA. Fuketin中的作用,以阐明肥大细胞释放的P物质和白三烯的参与,采用NK_1受体拮抗剂(FK 888)、NK_1和NK_2受体拮抗剂(FK 224)和白三烯C_4、D_4、E_4拮抗剂(ONO-1078)对OA免疫豚鼠EIA的影响,并观察冷空气对OA高反应性的影响,我们测量了呼吸率和气道对组胺的反应性,并研究了组胺和基质-结果表明,OA免疫豚鼠在运动后5分钟,呼吸速率(Rr)不增加,但在运动后15分钟,Rr显著增加。运动后15分钟,豚鼠BAlF中组胺含量较运动前升高,但无显著性差异。P物质水平明显高于治疗前。运动后15分钟BALF中嗜酸性粒细胞比例增加。ONO-1078抑制EIA,FK 888和FK 224也是如此。吸入冷空气(-10 ℃)15分钟后,支气管肺泡灌洗液中组胺和P物质含量无明显变化,但呼吸速率增加,组胺阈值降低,提示过度换气引起支气管肥大细胞活化和C纤维释放,肥大细胞和C纤维介导的介质在EIA的发生机制中起重要作用。
项目成果
期刊论文数量(8)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
前田志津子,小林仁: "運動誘発喘息動物モデルの作成とこの気道収縮における化学伝達物質の検討" 岩手医誌. 46. 451-459 (1994)
Shizuko Maeda、Hitoshi Kobayashi:“运动诱发哮喘动物模型的创建以及气道收缩中化学介质的研究”《岩手医学杂志》46. 451-459 (1994)。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
前田志津子、小林仁: "運動誘発喘息モデルの作製とこの気道収縮における化学伝達物質の検討" 岩手医学会誌. 46. 451-459 (1994)
Shizuko Maeda、Hitoshi Kobayashi:“运动诱发哮喘模型的创建以及气道收缩中化学介质的研究”岩手医学会杂志 46. 451-459 (1994)。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
Shiduko Maeda and Hitoshi Kobayashi: "Evaluation of bronchoconstrictive mediators in an animal model of exercise-induced asthma." J.Iwate med.Ass.Vol.46. 451-459 (1994)
Shiduko Maeda 和 Hitoshi Kobayashi:“运动诱发哮喘动物模型中支气管收缩介质的评估。”
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
前田志津子、小林仁: "運動誘発喘息動物モデルの作成とこの気道収縮における化学伝達物質の検討" 岩手医誌. 46. 451-459 (1994)
Shizuko Maeda、Hitoshi Kobayashi:“运动诱发哮喘的动物模型的创建以及气道收缩中化学介质的研究”《岩手医学杂志》46. 451-459 (1994)。
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- 影响因子:0
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KOBAYASHI Hitoshi其他文献
KOBAYASHI Hitoshi的其他文献
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{{ truncateString('KOBAYASHI Hitoshi', 18)}}的其他基金
Development of a Target System for Compact Neutron Source using 8-10 MeV Proton Beam for Medical and Industry Application
使用 8-10 MeV 质子束开发用于医疗和工业应用的紧凑型中子源目标系统
- 批准号:
23340080 - 财政年份:2011
- 资助金额:
$ 1.22万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Synthetic Studies on Tomb Figurines in the Sui and Tang Dynasties
隋唐墓俑综合研究
- 批准号:
19672001 - 财政年份:2007
- 资助金额:
$ 1.22万 - 项目类别:
Grant-in-Aid for Young Scientists (S)
Development of computerized programer education and job assignment system for social recoverage of the heavily handicapped.
开发计算机化程序员教育和工作分配系统,以促进重度残疾人的社会康复。
- 批准号:
62580251 - 财政年份:1987
- 资助金额:
$ 1.22万 - 项目类别:
Grant-in-Aid for General Scientific Research (C)
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