Schiffman P L, Ryan A, Whipp B J, Hansen J E, Wasserman K
J Clin Invest. 1979 Jan;63(1):30-7. doi: 10.1172/JCI109274.
To investigate the mechanism of exercise-induced bronchospasm, we measured specific airway conductance before and after exercise in 7 healthy normals, 12 asthmatics with intact carotid bodies, and 5 asthmatics who had had bilateral carotid body resection. The subjects breathed either air or oxygen (randomly assigned) during cycle ergometer exercise. Post-exercise bronchodilation was the usual pattern in normals, whereas post-exercise bronchospasm occurred in all asthmatics who breathed air during exercise. Oxygen breathing during exercise markedly attenuated the post-exercise bronchospasm in those asthmatics with intact carotid bodies, but had no significant effect in those without effect in those without carotid bodies. The attenuation of the bronchospasm with oxygen occurred with either incremental or constant load exercise of high intensity. The degree of attenuation did not correlate significantly with changes in end-tidal PCO2, maximum work rate, maximum exercise ventilation, or maximum heart rate. These studies indicate that oxygen attenuates exercise-induced bronchospasm in asthmatics through its action on the carotid bodies.
为了研究运动诱发支气管痉挛的机制,我们测量了7名健康正常人、12名颈动脉体完整的哮喘患者和5名双侧颈动脉体切除的哮喘患者运动前后的气道比传导率。受试者在进行蹬车运动时随机吸入空气或氧气。运动后支气管扩张是正常人的常见模式,而运动时吸入空气的所有哮喘患者均出现运动后支气管痉挛。运动时吸氧可显著减轻颈动脉体完整的哮喘患者运动后的支气管痉挛,但对无颈动脉体的患者无显著影响。高强度递增或持续负荷运动时,吸氧均可减轻支气管痉挛。支气管痉挛的减轻程度与呼气末二氧化碳分压、最大工作率、最大运动通气量或最大心率的变化无显著相关性。这些研究表明,氧气通过作用于颈动脉体减轻哮喘患者运动诱发的支气管痉挛。