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过度通气诱发的哮喘:两种机制的证据。

Hyperventilation-induced asthma: evidence for two mechanisms.

作者信息

Wilson N M, Barnes P J, Vickers H, Silverman M

出版信息

Thorax. 1982 Sep;37(9):657-62. doi: 10.1136/thx.37.9.657.

Abstract

The mechanism by which airway cooling induces airflow obstruction in asthmatic subjects has not yet been established. Using a pair of isocapnic hyperventilation challenges, with a 40-minute interval, we looked for the presence of a refractory period in 19 asthmatic patients (aged 9-18 years). The subjects fell into two groups. The eight in the "non-refractory" group showed less than a 25% reduction in response to the second challenge, but the 11 in the "refractory" group showed at least a 35% reduction. Twelve subjects also performed a hyperventilation challenge after cholinergic blockade with inhaled ipratropium bromide. In five, in whom no refractoriness after hyperventilation was seen, there was a significant protection from cholinergic blockade (p less than 0.05). In these a vagal (cholinergic) reflex seems likely. The remaining seven, who had a refractory period, received no significant protection from cholinergic blockade and therefore no evidence for the presence of any cholinergic mechanism. We conclude that two mechanisms are responsible for hyperventilation-induced asthma, one of which is a vagal reflex while mediator release may be the other.

摘要

气道冷却导致哮喘患者气流阻塞的机制尚未明确。我们对19名年龄在9至18岁的哮喘患者进行了两项等碳酸血症过度通气激发试验,间隔40分钟,以寻找不应期的存在。受试者分为两组。“非不应期”组的8名患者对第二次激发试验的反应降低不到25%,而“不应期”组的11名患者反应至少降低35%。12名受试者在吸入异丙托溴铵进行胆碱能阻滞之后还进行了过度通气激发试验。在5名过度通气后未见不应期的受试者中,胆碱能阻滞有显著的保护作用(p<0.05)。在这些受试者中,迷走神经(胆碱能)反射似乎是可能的。其余7名有不应期的受试者未从胆碱能阻滞中获得显著保护,因此没有证据表明存在任何胆碱能机制。我们得出结论,过度通气诱发哮喘有两种机制,其中一种是迷走神经反射,另一种可能是介质释放。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2012/459401/af38cdfae1c7/thorax00201-0021-a.jpg

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