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色甘酸二钠对哮喘患者二氧化硫诱导的支气管收缩的抑制作用。

Inhibition of sulfur dioxide-induced bronchoconstriction by disodium cromoglycate in asthmatic subjects.

作者信息

Sheppard D, Nadel J A, Boushey H A

出版信息

Am Rev Respir Dis. 1981 Sep;124(3):257-9. doi: 10.1164/arrd.1981.124.3.257.

Abstract

To determine whether disodium cromoglycate (cromolyn) inhibits the bronchoconstriction produced by inhalation of sulfur dioxide (SO2) in people with asthma, we undertook a study of 6 asthmatic subjects. Each subject inhaled 40 mg of cromolyn on one day and lactose placebo on another day 20 min before inhaling SO2 for 10 min while exercising at a moderate rate (400 kpm/min) on a bicycle ergometer. Sulfur dioxide was delivered in humidified air at ambient temperature in concentrations of 0.5 ppm (3 subjects) or 1.0 ppm (3 subjects). Cromolyn and lactose treatments were given to each subject in a randomized sequence and in a double-blind manner. On a third day, each subject exercised at the same work rate breathing humidified air without SO2 at ambient temperature. We measured specific airway resistance (SRaw) in a body plethysmograph every 30 s for 10 min before and after each of the 3 periods of exercise. After treatment with lactose, SO2 inhalation significantly increased SRaw in all 6 subjects (from a baseline of 6.5 +/- 0.9 to 19.0 +/- 4.8 L x cm H2O/L/s (mean +/- SE) after SO2). After treatment with cromolyn, SO2 inhalation caused no increase in SRaw in 4 subjects and a small rise in 2 subjects. The mean increase in SRaw (from a baseline of 7.3 +/- 0.9 to 10.0 +/- 1.5 L x cm H2O/L/s after SO2) was significantly smaller than after lactose treatment (p less than 0.025). Exercise alone had no effect on SRaw in any subject. Thus, cromolyn inhibits SO2-induced bronchoconstriction in subjects with asthma. This finding suggests either that SO2 induces bronchoconstriction by stimulating the release of mediators from mast cells or that cromolyn inhibits bronchoconstriction by a mechanism independent of its effect on mast cells.

摘要

为了确定色甘酸钠(色甘酸)是否能抑制哮喘患者吸入二氧化硫(SO₂)所引起的支气管收缩,我们对6名哮喘受试者进行了一项研究。在吸入SO₂ 10分钟并以适中速率(400 kpm/分钟)在自行车测力计上运动之前20分钟,每位受试者在一天吸入40毫克色甘酸,在另一天吸入乳糖安慰剂。二氧化硫在环境温度下于潮湿空气中以0.5 ppm(3名受试者)或1.0 ppm(3名受试者)的浓度输送。色甘酸和乳糖治疗以随机顺序和双盲方式给予每位受试者。在第三天,每位受试者以相同的工作速率呼吸环境温度下不含SO₂的潮湿空气。在三个运动阶段的每一个阶段之前和之后10分钟内,我们每隔30秒在体容积描记仪中测量比气道阻力(SRaw)。用乳糖治疗后,吸入SO₂使所有6名受试者的SRaw显著增加(SO₂后从基线的6.5±0.9升至19.0±4.8 L×cm H₂O/L/s(平均值±标准误))。用色甘酸治疗后,吸入SO₂在4名受试者中未引起SRaw增加,在2名受试者中引起小幅上升。SRaw的平均增加(SO₂后从基线的7.3±0.9升至10.0±1.5 L×cm H₂O/L/s)显著小于乳糖治疗后(p小于0.025)。单独运动对任何受试者的SRaw均无影响。因此,色甘酸可抑制哮喘受试者中SO₂诱导的支气管收缩。这一发现表明,要么是SO₂通过刺激肥大细胞释放介质来诱导支气管收缩,要么是色甘酸通过一种与其对肥大细胞作用无关的机制来抑制支气管收缩。

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