Walden S M, Bleecker E R, Chahal K, Britt E J, Mason P, Permutt S
Am Rev Respir Dis. 1984 Sep;130(3):357-62. doi: 10.1164/arrd.1984.130.3.357.
Cooling and drying of the intrapulmonary airways have been shown to be important stimuli for the development of bronchospasm induced by exercise and isocapnic cold air hyperventilation. It has also been suggested that alpha-adrenergic receptor activity is increased at lower temperatures. To evaluate the role of alpha-adrenergic activity in the development of bronchoconstriction during airway cooling, we examined the effects of alpha-adrenergic blockade with phentolamine on bronchospasm induced by exercise and isocapnic cold air hyperventilation in 8 asthmatics. Exercise consisted of 6 min of steady-state exercise at 90% predicted maximal heart rate breathing compressed air at 0% humidity and 21 +/- 1 degrees C (mean +/- SD). During baseline exercise studies, FEV1 fell 41.6 +/- 15.8%, but only 12.8 +/- 8.5% during alpha-adrenergic blockade (p less than 0.001). Isocapnic cold air challenge consisted of breathing compressed cold air (0% humidity, -17 +/- 4 degrees C) for 3-min periods, with stepwise increases in minute ventilation (Ve) until the FEV1 fell at least 20%. During baseline cold air challenges, FEV1 fell 20% (PD20 FEV1) at a Ve of 48.8 +/- 21 L/min. However, during alpha-adrenergic blockade 6 asthmatics were able to achieve much higher levels of VE (86.6 +/- 22.7 L/min) before FEV1 fell 20% (p less than 0.01), and 2 asthmatics did not decrease their FEV1 by 20%, despite reaching maximal levels of ventilation of 132 and 108 L/min, respectively. Alpha-adrenergic blockade did not affect airways responses to histamine or ragweed antigen (p greater than 0.1).(ABSTRACT TRUNCATED AT 250 WORDS)
肺内气道的冷却和干燥已被证明是运动和等碳酸冷血空气过度通气诱发支气管痉挛的重要刺激因素。也有人提出,在较低温度下α-肾上腺素能受体活性会增加。为了评估α-肾上腺素能活性在气道冷却期间支气管收缩发展中的作用,我们研究了酚妥拉明阻断α-肾上腺素能对8名哮喘患者运动和等碳酸冷血空气过度通气诱发的支气管痉挛的影响。运动包括在90%预计最大心率下进行6分钟的稳态运动,呼吸湿度为0%、温度为21±1℃(平均±标准差)的压缩空气。在基线运动研究期间,第一秒用力呼气量(FEV1)下降了41.6±15.8%,但在α-肾上腺素能阻断期间仅下降了12.8±8.5%(p<0.001)。等碳酸冷血空气激发包括呼吸压缩冷空气(湿度0%,-17±4℃)3分钟,分钟通气量(Ve)逐步增加,直到FEV1至少下降20%。在基线冷空气激发期间,当Ve为48.8±21升/分钟时,FEV1下降20%(PD20 FEV1)。然而,在α-肾上腺素能阻断期间,6名哮喘患者在FEV1下降20%之前能够达到更高的Ve水平(86.6±22.7升/分钟)(p<0.01),2名哮喘患者尽管分别达到了132和108升/分钟的最大通气水平,但FEV1并未下降20%。α-肾上腺素能阻断对气道对组胺或豚草抗原的反应没有影响(p>0.1)。(摘要截断于250字)