Mochizuki H, Shimizu T, Maeda S, Tokuyama K, Morikawa A, Kuroume T
Department of Pediatrics, Gunma University School of Medicine, Maebashi, Japan.
J Allergy Clin Immunol. 1995 Aug;96(2):193-9. doi: 10.1016/s0091-6749(95)70008-0.
Although wheezing and cough are the most common complaints in asthmatic persons, the mechanisms of hyperresponsiveness to bronchoconstriction and cough are nevertheless still unclear.
To investigate the common mechanisms between them, we studied the relationship between ultrasonically nebulized distilled water (UNDW) inhalation challenge and acetic acid (AA) inhalation challenge. In addition, we evaluated the effect of inhaled furosemide on both provocation tests by means of a placebo-controlled study.
In study 1 the UNDW, AA, and histamine inhalation challenges were performed in 40 asthmatic children (26 boys, aged from 7 to 16 years; mean +/- SD, 11.2 +/- 2.0 years). In study 2, 12 of the study 1 subjects (9 boys, 11.3 +/- 2.4 years) were subjected to each challenge test after inhalation of furosemide (10 mg/body square meters), or placebo (0.9% saline solution) on separate days.
There was a good correlation between the provocative dose causing a 20% fall in forced expiratory volume in 1 second in the UNDW inhalation challenge (UNDW-PD20) and threshold dose causing cough in the AA inhalation challenge (R = 0.527; p < 0.001). There was no relationship either between UNDW-PD20 and the provocative concentration causing a 20% fall in the histamine inhalation challenge (histamine-PC20)(R = 0.384; p > 0.1), or between histamine-PC20 and the cough threshold (R = 0.308; p > 0.05). In study 2 neither bronchoconstriction nor bronchodilation after inhalation of furosemide was observed. Inhaled furosemide exerted a protective effect on UNDW-PD20 and cough threshold of the AA inhalation challenge (p < 0.01 and p < 0.01, respectively), but did not attenuate histamine-PC20 (p > 0.1).
These data suggest that a common mechanism may cause hyperresponsiveness against both UNDW-induced bronchoconstriction and AA-induced cough in asthmatic children.
尽管喘息和咳嗽是哮喘患者最常见的症状,但支气管收缩和咳嗽高反应性的机制仍不清楚。
为了研究它们之间的共同机制,我们研究了超声雾化蒸馏水(UNDW)吸入激发试验和醋酸(AA)吸入激发试验之间的关系。此外,我们通过一项安慰剂对照研究评估了吸入速尿对两种激发试验的影响。
在研究1中,对40名哮喘儿童(26名男孩,年龄7至16岁;平均±标准差,11.2±2.0岁)进行了UNDW、AA和组胺吸入激发试验。在研究2中,研究1中的12名受试者(9名男孩,11.3±2.4岁)在不同日期吸入速尿(10mg/体表面积)或安慰剂(0.9%盐水溶液)后,分别接受每种激发试验。
在UNDW吸入激发试验中导致一秒用力呼气量下降20%的激发剂量(UNDW-PD20)与AA吸入激发试验中引起咳嗽的阈值剂量之间存在良好的相关性(R = 0.527;p < 0.001)。UNDW-PD20与组胺吸入激发试验中导致一秒用力呼气量下降20%的激发浓度(组胺-PC20)之间没有关系(R = 0.384;p > 0.1),组胺-PC20与咳嗽阈值之间也没有关系(R = 0.308;p > 0.05)。在研究2中,未观察到吸入速尿后出现支气管收缩或支气管舒张。吸入速尿对UNDW-PD20和AA吸入激发试验的咳嗽阈值有保护作用(分别为p < 0.01和p < 0.01),但未减弱组胺-PC20(p > 0.1)。
这些数据表明,一种共同机制可能导致哮喘儿童对UNDW诱导的支气管收缩和AA诱导的咳嗽产生高反应性。