Lower threshold and greater bronchomotor responsiveness of asthmatic subjects to sulfur dioxide.
Lower threshold and greater bronchomotor responsiveness of asthmatic subjects to sulfur dioxide.
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DOI：
10.1164/arrd.1980.122.6.873
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发表时间：
2015-05
期刊：
影响因子：
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通讯作者：
D. Sheppard;W. S. Wong;C. Uehara;J. Nadel;H. Boushey
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文献类型：
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作者：
D. Sheppard;W. S. Wong;C. Uehara;J. Nadel;H. Boushey
为了确定患有轻度哮喘或季节性鼻炎的受试者对二氧化硫 (SO2) 的支气管运动反应是否比正常受试者更强，我们对 7 名哮喘受试者、7 名特应性受试者和 7 名正常受试者（年龄为 23 至 37 岁）进行了一项研究。我们在不同的日子（至少相隔 48 小时）测量了通过吸嘴输送 1、3 和 5 ppm SO2 10 分钟引起的比气道阻力 (SRaw) 的变化。为了评估副交感神经通路在支气管运动对 SO2 反应中的重要性，我们还测量了 17 名受试者吸入硫酸阿托品气雾剂 (0.1 mg/kg) 后 5 ppm SO2 引起的 SRaw 的变化。我们发现，在哮喘受试者中，SRaw 仅在 5 ppm 时增加。在哮喘组中，SRaw 在 5 ppm 时比其他组增加更多（p < 0.005），并且有时与需要支气管扩张剂治疗的明显呼吸困难相关。在哮喘和非哮喘受试者中，使用阿托品治疗可以防止吸入 SO2 产生的 SRaw 增加，这表明副交感神经通路的参与。这些结果表明，患有轻度哮喘的受试者在暴露于远低于目前公认的职业暴露标准的 SO2 浓度后会出现支气管收缩，并且 SO2 诱导的支气管收缩是由副交感神经途径介导的。
To determine whether subjects with mild asthma or seasonal rhinitis have greater bronchomotor responses to sulfur dioxide (SO2) than normal subjects, we undertook a study in 7 asthmatic, 7 atopic, and 7 normal subjects, 23 to 37 yr of age. We measured the change in specific airways resistance (SRaw) provoked by 10 min of breathing 1, 3, and 5 ppm of SO2 delivered by mouthpiece on separate days at least 48 h apart. To assess the significance of parasympathetic pathways in the bronchomotor responses to SO2, we also measured the change in SRaw provoked by 5 ppm of SO2 in 17 of the subjects after they inhaled atropine sulfate aerosol (0.1 mg/kg). We found that in the asthmatic subjects, SRaw increased only at 5 ppm. In the asthmatic group, SRaw increased more than in either of the other groups at 5 ppm (p < 0.005), and was sometimes associated with marked dyspnea requiring bronchodilator therapy. The increases in SRaw produced by inhalation of SO2 were prevented by treatment with atropine in asthmatic and nonasthmatic subjects, which suggested the involvement of parasympathetic pathways. These results indicated that subjects with mild asthma develop bronchoconstriction after exposure to concentrations of SO2 well below currently accepted standards for occupational exposure, and that SO2-induced bronchoconstriction is mediated by parasympathetic pathways.