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支气管哮喘患者抗原特异性支气管激发试验后β受体的减少

Decrease of beta-receptors after the antigen-specific bronchial provocation test in bronchial asthma.

作者信息

Gamboa P M, de la Cuesta C G, Sanz M L, García B E, Oehling A

机构信息

Departamento de Alergología, Facultad de Medicina, Universidad de Navarra, Pamplona, Spain.

出版信息

Allergol Immunopathol (Madr). 1990 May-Jun;18(3):115-9.

PMID:2174641
Abstract

Airway hyperreactivity to different stimuli is a characteristic feature of bronchial asthma. The beta-adrenergic theory, as proposed by Szentivanyi in 1968, tried to explain with beta-adrenergic dysfunction, the cause not only of bronchial hyperreactivity but of all atopic diseases. In a previous work, we found that asymptomatic asthmatic patients presented a number of beta-receptors similar to that of a normal control group, while symptomatic asthmatic patients presented a significantly decreased number when compared to both groups (40% decrease). In view of these results, we proposed to study the possible changes in the number of beta-receptors in asymptomatic asthmatic patients after a bronchial provocation test. Fifteen patients, diagnosed of bronchial asthma and sensitive to the house dust mite, D. pteronyssinus, were studied. All were free of medication and asymptomatic at least 90 days before the study. A test of specific bronchial provocation was performed on 10 patients, determining the number of beta-receptors in basal conditions, after 30 minutes and 24 hours. The other five patients underwent an unspecific provocation test with methacholine, with determination of the beta-receptor number at basal conditions, and 24 hours later. Only a significant decrease (30.4%) was found in the beta-receptor numbers, 24 hours after specific bronchial provocation with p less than 0.025 with the Student test for paired data. With regards the beta-adrenergic theory of atopy, in our opinion our results show that the detected decrease of beta-receptors would be the consequence and not the cause of atopic diseases.

摘要

气道对不同刺激的高反应性是支气管哮喘的一个特征。1968年,森蒂瓦尼提出的β-肾上腺素能理论试图用β-肾上腺素能功能障碍来解释支气管高反应性以及所有特应性疾病的病因。在之前的一项研究中,我们发现无症状哮喘患者的β受体数量与正常对照组相似,而有症状的哮喘患者与两组相比,β受体数量显著减少(减少40%)。鉴于这些结果,我们提议研究无症状哮喘患者在支气管激发试验后β受体数量的可能变化。研究了15名被诊断为支气管哮喘且对屋尘螨(粉尘螨)敏感的患者。所有患者在研究前至少90天未用药且无症状。对10名患者进行了特异性支气管激发试验,分别在基础状态、30分钟后和24小时后测定β受体数量。另外5名患者用乙酰甲胆碱进行了非特异性激发试验,在基础状态和24小时后测定β受体数量。在进行特异性支气管激发试验24小时后,仅发现β受体数量显著减少(30.4%),配对数据的学生检验显示p值小于0.025。关于特应性的β-肾上腺素能理论,我们认为我们的结果表明,检测到的β受体减少是特应性疾病的结果而非病因。

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Decrease of beta-receptors after the antigen-specific bronchial provocation test in bronchial asthma.支气管哮喘患者抗原特异性支气管激发试验后β受体的减少
Allergol Immunopathol (Madr). 1990 May-Jun;18(3):115-9.
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