Pathophysiology of specific bronchial hyperresponsiveness
特定支气管高反应性的病理生理学
基本信息
- 批准号:07670662
- 负责人:
- 金额:$ 1.6万
- 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:1995
- 资助国家:日本
- 起止时间:1995 至 1997
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
1. Alcohol-induced bronchoconstriction in guinea pigs(1) Acetaldehyde, a metabolite of ethanol, causes bronchoconstriction but ethanol does not.(2) The acetaldehyde-induced bronchoconstriction is mediated via histamine release.(3) A low dose of acetaldehyde, which does not cause bronchoconstriction, enhances non-specific bronchial responsiveness.(4) Thromboxane A2 is involved in the acetaldehyde-induced non-specific bronchial hyperresponsiveness.2. A guinea big model of propranolol-induced bronchoconstriction and the role of autonomic nerve system, chemical mediators and neuropeptides(1) An inhalation of propranolo causes bronchoconstriction when it is inhaled 20 minutes after an aerosolized antigen provocation in passively sensitized guinea pigs.This is the first animal model or propranolol-induced bronchoconstriction.(2) Parasympathctic or alpha-adrenergic nerve activity is not involved in this response.(3) Ncuropeptides such as substance P and neurokinin A do not take a part in this … More response.(4) Lipid mediators, especially thromboxane A2, have an important role in this response.3. A guinea-pig model of untrasonically nebulized distillled water (UNDW) -induced bronchoconstriction and the role of autonomic nerve system, chemical mediators and neuropeptides(1) An inhalation of UNDW produces acute bronchoconstriction when it is inhaled 20 mimutes after an aerosolized antigen provocation in passively sensitized guinea pigs.This is the first animal model of UNDW-induced bronchoconstriction.(2) Parasympathetic nerve activity is not involved in this response.(3) Histamine and substance P,but not neurokinin A,take a large part in this response.(4) Thromboxane A2 does not have a role in this response.4. ConclusionForm these results, it is suggested that allergic airway response, or allergic airway inflammatory process, is important in development of specific bronchial responsiveness. Furthermore, the mechanism of specific bronchial hyperresponsiveness may be different each other, suggesting heterogeneity of contributing factors between several specific bronchial hyperresponsiveness in asthma. Less
1. 豚鼠酒精诱导的支气管收缩(1) 乙醛是乙醇的代谢产物,会引起支气管收缩,但乙醇不会。(2) 乙醛诱导的支气管收缩是通过组胺释放介导的。(3) 低剂量的乙醛不会引起支气管收缩,但会增强非特异性。 (4)血栓素A2参与乙醛诱导的非特异性支气管高反应性。2.普萘洛尔诱导的支气管收缩几内亚大模型以及自主神经系统、化学介质和神经肽的作用(1) 在被动致敏的豚鼠中,雾化抗原激发后20分钟吸入普萘洛尔,会引起支气管收缩。这是第一个普萘洛尔诱导的动物模型 (2) 副交感神经或 α-肾上腺素能神经活动不参与这种反应。(3) P 物质和神经激肽 A 等神经肽不参与这种反应。(4) 脂质介质,特别是血栓素 A2,在这种反应中具有重要作用。3。非超声雾化蒸馏水(UNDW)诱导的支气管收缩豚鼠模型以及自主神经系统、化学介质和神经肽的作用(1)被动致敏的豚鼠在雾化抗原激发后20分钟吸入UNDW会产生急性支气管收缩。这是第一个动物模型 UNDW诱导的支气管收缩。(2)副交感神经活动不参与这种反应。(3)组胺和P物质,但不是神经激肽A,在这种反应中起很大作用。(4)血栓素A2在这种反应中不起作用。4.结论这些结果表明,过敏性气道反应或过敏性气道炎症过程在特定支气管反应性的发展中很重要。此外,特定支气管高反应性的机制可能彼此不同,这表明哮喘中几种特定支气管高反应性之间的影响因素存在异质性。较少的
项目成果
期刊论文数量(54)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Myou S,Fujimura M,Nishi K,Ohka T,Matsuda T.: "Inhibitory effect of terfenadine, a selective H1-histamine antagonist, on alcoholic beverage-induced bronchoconstriction in asthmatic patients." Eur Respir J. 8 (4). 619-623 (1995)
Myou S、Fujimura M、Nishi K、Ohka T、Matsuda T.:“特非那定(一种选择性 H1-组胺拮抗剂)对哮喘患者酒精饮料引起的支气管收缩的抑制作用。”
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- 影响因子:0
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Songur N,Fujimura M,Mizuhashi K,Saito M,Matsuda T.: "Effect of AL-3264 on propranolol-induced bronchoconstriction in guinea pigs." J Lipid Mediators Cell Signaling. 11 (2). 175-185 (1995)
Songur N、Fujimura M、Mizuhashi K、Saito M、Matsuda T.:“AL-3264 对豚鼠心得安引起的支气管收缩的影响。”
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- 影响因子:0
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Fujimura M,Amemiya T,Myou S,Mizuguchi M,Matsuda T.: "A guinea-pig model of ultrasonically nebulized distillled water-induced bronchoconstriction." Eur Respir J. 10. 2237-2242 (1997)
Fujimura M、Amemiya T、Myou S、Mizuguchi M、Matsuda T.:“超声波雾化蒸馏水诱导支气管收缩的豚鼠模型。”
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- 影响因子:0
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Fujimura M,et al: "Inhibitory effects of indomethacin on tachyphylaxis in response to acetaldehyde-induced bronchoconstriction in asthmatic patients." J Allergy Clin Immunol. 99(5). 620-623 (1997)
Fujimura M 等人:“吲哚美辛对哮喘患者乙醛引起的支气管收缩的快速耐受的抑制作用。”
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- 影响因子:0
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Fujimura M,et al.: "Role of sensory neuropeptides in post-allergic propranolol-induced bronchoconstriction in guinea pigs in vivo." Clin Exp Allergy. 26(12). 1428-1435 (1996)
Fujimura M 等人:“感觉神经肽在豚鼠体内过敏后普萘洛尔诱导的支气管收缩中的作用。”
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- 影响因子:0
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FUJIMURA Masaki其他文献
FUJIMURA Masaki的其他文献
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{{ truncateString('FUJIMURA Masaki', 18)}}的其他基金
To overcome intractable chronic cough: disclosure of mechanism of cough response to bronchoconstiction to conrol of the cough
攻克顽固性慢性咳嗽:揭示支气管收缩咳嗽反应机制控制咳嗽
- 批准号:
23591142 - 财政年份:2011
- 资助金额:
$ 1.6万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
To overcome the intractable chronic cough : mechanism of cough and development of therapy
克服顽固性慢性咳嗽:咳嗽机制及治疗进展
- 批准号:
20590916 - 财政年份:2008
- 资助金额:
$ 1.6万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Importance of environmental fungi and IgE non-mediated mechanism in atopic eough
环境真菌和 IgE 非介导机制在特应性发作中的重要性
- 批准号:
17607003 - 财政年份:2005
- 资助金额:
$ 1.6万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
DEVELOPMENT OF DIAGNOSIS AND TREATMENT BASED ON PATHOPHYSIOLOGY OF CHRONIC COUGH
基于慢性咳嗽病理生理学的诊断和治疗进展
- 批准号:
14570546 - 财政年份:2002
- 资助金额:
$ 1.6万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Investigation of Biological Behavior and Treatment Modality for Ovarian Clear Cell Adenocarcinoma
卵巢透明细胞腺癌的生物学行为和治疗方式的研究
- 批准号:
09671667 - 财政年份:1997
- 资助金额:
$ 1.6万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Involvement of Enteric Nervous System in the Regulation of Gastrointestinal Motility
肠神经系统参与胃肠动力的调节
- 批准号:
07671384 - 财政年份:1995
- 资助金额:
$ 1.6万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Mechanisms of heightened airway cough receptor sensitivity in eosinophilic bronchitis (atopic cough : eosinophilic bronchitis without asthma).
嗜酸性粒细胞性支气管炎气道咳嗽受体敏感性升高的机制(特应性咳嗽:不伴哮喘的嗜酸性粒细胞性支气管炎)。
- 批准号:
04807055 - 财政年份:1992
- 资助金额:
$ 1.6万 - 项目类别:
Grant-in-Aid for General Scientific Research (C)
相似海外基金
Molecular biological mechanism of alcohol-induced asthma
酒精诱发哮喘的分子生物学机制
- 批准号:
12670563 - 财政年份:2000
- 资助金额:
$ 1.6万 - 项目类别:
Grant-in-Aid for Scientific Research (C)














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