干空气等渗性高呼吸和高渗生理盐水的咳嗽反应是相互关联的。

Minna Purokivi, Heikki Koskela, John D Brannan, Kirsi Kontra
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引用次数: 15

摘要

背景:哮喘性咳嗽背后的机制在很大程度上是未知的。众所周知,高渗透压刺激会引起哮喘患者咳嗽,但不会引起健康受试者咳嗽。据推测,干空气的异速呼吸急促(IHDA)和高渗气溶胶通过类似的机制在哮喘中引起支气管收缩。我们研究了IHDA诱导的咳嗽反应与高渗盐水(HS)刺激之间是否存在关联。方法:36例哮喘患者和14例健康者分别通过超声雾化器吸入渗透压逐渐升高的HS溶液,记录15次累计咳嗽。IHDA包括三个三分钟的通气步骤:30%、60%和100%的最大自愿通气,终点为30次累计咳嗽。这些挑战分别在不同的日子进行,间隔至少48小时,并在一周内进行。挑战前给予吸入沙丁胺醇(400微克)以防止支气管收缩。咳嗽反应用咳嗽剂量比(CDR)表示,CDR是咳嗽的总次数除以吸入的最大渗透压或达到的最大通气量。结果:咳嗽对IHDA的反应与HS攻击相关(Rs = 0.59, p < 0.001)。咳嗽反应对IHDA在挑战后的第一分钟是最强的。哮喘组咳嗽的CDR(平均±SD)分别为0.464±0.514和0.011±0.024咳嗽/MVV%, p < 0.001。沙丁胺醇能有效防止支气管收缩。结论:哮喘患者对呼吸急促引起咳嗽的反应和对高张力反应一样敏感。IHDA和HS诱导的咳嗽反应具有良好的相关性,表明反应背后的机制相似。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Cough response to isocapnic hyperpnoea of dry air and hypertonic saline are interrelated.

Cough response to isocapnic hyperpnoea of dry air and hypertonic saline are interrelated.

Cough response to isocapnic hyperpnoea of dry air and hypertonic saline are interrelated.

Cough response to isocapnic hyperpnoea of dry air and hypertonic saline are interrelated.

Background: Mechanisms behind asthmatic cough are largely unknown. It is known that hyperosmolar challenges provoke cough in asthmatic but not in the healthy subjects. It has been postulated that isocapnic hyperpnea of dry air (IHDA) and hypertonic aerosols act via similar mechanisms in asthma to cause bronchoconstriction. We investigated whether there is an association between cough response induced by IHDA and hypertonic saline (HS) challenges.

Methods: Thirty-six asthmatic and 14 healthy subjects inhaled HS solutions with increasing osmolalities administered via ultrasonic nebuliser until 15 cumulative coughs were recorded. The IHDA consisted of three three-minute ventilation steps: 30%, 60% and 100% of maximal voluntary ventilation with an end-point of 30 cumulative coughs. The challenges were performed on separate days at least 48 hours between them and within one week. Inhaled salbutamol (400 mcg) was administered before the challenges to prevent bronchoconstriction. The cough response was expressed as the cough-to-dose ratio (CDR) which is the total number of coughs divided by the maximal osmolality inhaled or the maximal ventilation achieved.

Results: Cough response to IHDA correlated with the HS challenge (Rs = 0.59, p < 0.001). Cough response to IHDA was at its strongest during the first minute after the challenge. IHDA induced more cough among asthmatic than healthy subjects CDR being (mean ± SD) 0.464 ± 0.514 and 0.011 ± 0.024 coughs/MVV%, p < 0.001, respectively. Salbutamol effectively prevented bronchoconstriction to both challenges.

Conclusions: Asthmatic patients are hypersensitive to the cough-provoking effect of hyperpnoea, as they are to hypertonicity. Cough response induced by IHDA and HS correlated well suggesting similar mechanisms behind the responses.

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