Exercise increases sulfur dioxide-induced bronchoconstriction in asthmatic subjects.

Exercise increases sulfur dioxide-induced bronchoconstriction in asthmatic subjects.
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运动会增加哮喘患者二氧化硫引起的支气管收缩。

DOI:
10.1164/arrd.1981.123.5.486
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发表时间:
1981
期刊:
The American review of respiratory disease
影响因子:
--
通讯作者:
Boushey,HA
Boushey,HA
中科院分区:
--
文献类型:
--
作者:
Sheppard,D;Saisho,A;Nadel,JA;Boushey,HA

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我们进行了一项研究,以确定适度运动是否能改变轻度哮喘受试者中二氧化硫(S02)引起的支气管收缩。在7名受试者中,我们比较了单独运动10分钟(在循环计力器上400 kpm/min)、单独吸入S02以及运动和S02结合产生的特定气道阻力(SRaw)的变化。在所有的研究中,受试者从口腔口吸入二氧化硫和/或空气。在另外6名受试者中,我们比较了运动期间吸入S02所产生的SRaw的增加与吸入S02所产生的SRaw的增加。在休息时吸入0.50 ppm的二氧化硫、单独运动或过度通气对SRaw都没有任何影响。然而,运动时吸入二氧化硫显著增加了SRaw (0.50 ppm时从8.46±3.58 L × cm H20/L/s (mean±SD)增加到18.16±10.05,0.25 ppm时从8.07±2.69增加到10.48±4.49 (p < 0.05))。在2名反应最灵敏的受试者中,在运动期间吸入0.10 ppm的二氧化硫也显著增加了SRaw。运动时吸入s02与呼吸过度通气时吸入s02均可使SRaw增加相同量,但SRaw增加的时间过程不同。在过度通气后第一次测量时(30秒),SRaw达到或接近最大值,但直到运动后2至4分钟才达到或接近最大值。当4例患者在过度通气时吸入s02后呼吸量增大,使其与运动后呼吸量更接近时,过度通气后与运动后s02所致支气管收缩的时间过程几乎相同。这些结果表明,在给定浓度的so02下,运动通过增加通气的分钟量而增加哮喘患者的支气管收缩,运动后支气管收缩的延迟是由于在恢复过程中持续几分钟的大潮汐量。
We undertook a study to determine whether moderate exercise modifies the bronchoconstriction produced by sulfur dioxide (S02) in subjects with mild asthma. In 7 subjects, we compared the changes in specific airway resistance (SRaw) produced by 10 min of exercise alone (400 kpm/min on a cycle ergometer), inhalation of S02alone, and the combination of exercise and S02. During all studies, a subject breathed S02and/or air from a mouthpiece. In 6 additional subjects, we compared the increase in SRaw produced by inhalation of S02during exercise with that produced by eucapnic hyperventilation with S02. Neither inhalation of 0.50 ppm of S02at rest nor exercise or hyperventilation alone had any effect on SRaw. Inhalation of S02during exercise, however, significantly increased SRaw (from 8.46 ± 3.58 L × cm H20/L/s (mean ± SD) to 18.16 ± 10.05 at 0.50 ppm and from 8.07 ± 2.69 to 10.48 ± 4.49 at 0.25 ppm (p < 0.05)). In the 2 most responsive subjects, inhalation of 0.10 ppm of S02during exercise also significantly increased SRaw. The SRaw increased by the same amount whether S02was inhaled during exercise or during eucapnic hyperventilation at the same minute ventilation, but the time course of the increase in SRaw was different. The SRaw was at or near maximal values at the first measurement (30 s) after hyperventilation but not until 2 to 4 min after exercise. When 4 subjects took larger breaths after inhaling S02during eucapnic hyperventilation to more closely match the volume of the breaths taken after exercise, the time courses of S02-induced bronchoconstriction after hyperventilation and after exercise were nearly identical. These results suggested that exercise increases the bronchoconstriction produced by a given concentration of S02in subjects with asthma by increasing the minute volume of ventilation and that the delay in bronchoconstriction after exercise is due to the large tidal volumes that persist for some minutes during recovery.
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