Sheppard D, Saisho A, Nadel J A, Boushey H A
Am Rev Respir Dis. 1981 May;123(5):486-91. doi: 10.1164/arrd.1981.123.5.486.
We undertook a study to determine whether moderate exercise modifies the bronchoconstriction produced by sulfur dioxide (SO2) 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 SO2 alone, and the combination of exercise and SO2. During all studies, a subject breathed SO2 and/or air from a mouthpiece. In 6 additional subjects, we compared the increase in SRaw produced by inhalation of SO2 during exercise with that produced by eucapnic hyperventilation with SO2. Neither inhalation of 0.05 ppm of SO2 at rest nor exercise or hyperventilation alone had any effect on SRaw. Inhalation of SO2 during exercise, however, significantly increased SRaw (from 8.46 +/- 3.58 L x cm H2O/L/s (mean +/- SD) to 18.16 +/- 10.05 at 0.05 ppm and from 8.07 +/- 2.69 to 10.48 +/- 4.49 at 0.25 ppm (p less than 0.05)). In the 2 most responsive subjects, inhalation of 0.10 ppm of SO2 during exercise also significantly increased SRaw. The SRaw increased by the same amount whether SO2 was 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 SO2 during eucapnic hyperventilation to more closely match the volume of the breaths taken after exercise, the time courses of SO2-induced bronchoconstriction after hyperventilation and after exercise were nearly identical. These results suggested that exercise increases the bronchoconstriction produced by a given concentration of SO2 in 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.
我们进行了一项研究,以确定适度运动是否会改变轻度哮喘患者因二氧化硫(SO₂)引起的支气管收缩。在7名受试者中,我们比较了单独进行10分钟运动(在自行车测力计上以400 kpm/min的速度)、单独吸入SO₂以及运动与SO₂联合作用所引起的比气道阻力(SRaw)的变化。在所有研究过程中,受试者通过咬嘴呼吸SO₂和/或空气。在另外6名受试者中,我们比较了运动期间吸入SO₂所引起的SRaw增加与等碳酸过度通气吸入SO₂所引起的SRaw增加。静息时吸入0.05 ppm的SO₂、单独运动或过度通气均对SRaw无任何影响。然而,运动期间吸入SO₂会显著增加SRaw(在0.05 ppm时,从8.46±3.58 L×cmH₂O/L/s(平均值±标准差)增加到18.16±10.05,在0.25 ppm时,从8.07±2.69增加到10.48±4.49(p<0.05))。在2名反应最强烈的受试者中,运动期间吸入0.10 ppm的SO₂也显著增加了SRaw。在相同分钟通气量下,无论运动期间还是等碳酸过度通气期间吸入SO₂,SRaw增加的幅度相同,但SRaw增加的时间进程不同。过度通气后首次测量(30秒)时SRaw达到或接近最大值,而运动后直到2至4分钟才达到。当4名受试者在等碳酸过度通气吸入SO₂后进行更大幅度呼吸,以更接近运动后呼吸的体积时,过度通气后和运动后SO₂诱导的支气管收缩的时间进程几乎相同。这些结果表明,运动通过增加分钟通气量,使哮喘患者因给定浓度的SO₂引起的支气管收缩增强,且运动后支气管收缩延迟是由于恢复过程中持续数分钟的大潮气量所致。