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吸入沙丁胺醇不能预防非哮喘运动员的臭氧毒性。

Inhaled albuterol does not protect against ozone toxicity in nonasthmatic athletes.

作者信息

Gong H, Bedi J F, Horvath S M

机构信息

Department of Medicine, UCLA Medical Center.

出版信息

Arch Environ Health. 1988 Jan-Feb;43(1):46-53. doi: 10.1080/00039896.1988.9934373.

Abstract

We evaluated the acute prophylactic efficacy of albuterol aerosol in protecting nonasthmatic athletes from the untoward effects of 0.21 ppm ozone (O3) on symptoms, pulmonary function, exercise performance, and post-exposure histamine bronchoprovocation. Fifteen trained competitive cyclists participated in a randomized crossover study consisting of double-blinded inhalations of albuterol (180 micrograms) and placebo approximately 30 min prior to heavy continuous exercise (minute ventilation, [VE] greater than or equal to 80 L/min) for 60 min, followed by a maximal sprint (peak VE greater than 140 L/min) until exhaustion. Each subject was exposed randomly to either 0.21 ppm O3 or filtered air (FA) during the four single-blinded exposure sessions. Albuterol pretreatment resulted in modest but significant bronchodilation as compared to placebo. However, albuterol did not prevent O3-induced respiratory symptoms, decrements in forced vital capacity (FVC), forced expired volume in one second (FEV1.0), and maximum midexpiratory flow rate (FEF25-75%), and positive histamine challenges as compared to that with placebo/O3. There were no statistically significant differences in the metabolic data or ride times across all drugs and exposures, although the peak VE was significantly lower with O3 than FA (142.3 vs. 150.7 L/min, respectively) regardless of drug. The results indicate that acute pretreatment with inhaled albuterol is unable to prevent or ameliorate O3-induced symptoms and alterations in pulmonary function and exercise performance. The contribution of beta-adrenergic mechanisms in the acute airway responses to O3 appears to be minimal.

摘要

我们评估了沙丁胺醇气雾剂对非哮喘运动员的急性预防效果,以保护他们免受0.21 ppm臭氧(O3)对症状、肺功能、运动表现和暴露后组胺支气管激发试验的不良影响。15名训练有素的竞技自行车运动员参与了一项随机交叉研究,该研究包括在剧烈持续运动(分钟通气量,[VE]大于或等于80 L/min)60分钟前约30分钟进行双盲吸入沙丁胺醇(180微克)和安慰剂,随后进行最大冲刺(峰值VE大于140 L/min)直至精疲力竭。在四个单盲暴露阶段,每个受试者随机暴露于0.21 ppm O3或过滤空气(FA)中。与安慰剂相比,沙丁胺醇预处理导致了适度但显著的支气管扩张。然而,与安慰剂/O3相比,沙丁胺醇并不能预防O3诱导的呼吸道症状、用力肺活量(FVC)、一秒用力呼气量(FEV1.0)和最大呼气中期流速(FEF25-75%)的下降以及组胺激发试验阳性。尽管无论使用何种药物,O3组的峰值VE均显著低于FA组(分别为142.3 vs. 150.7 L/min),但所有药物和暴露条件下的代谢数据或骑行时间均无统计学显著差异。结果表明,吸入沙丁胺醇进行急性预处理无法预防或改善O3诱导的症状以及肺功能和运动表现的改变。β-肾上腺素能机制在对O3的急性气道反应中的作用似乎很小。

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