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支气管对冷空气激发试验的反应:正常人和哮喘患者不同机制的证据。

The bronchial response to cold air challenge: evidence for different mechanisms in normal and asthmatic subjects.

作者信息

Heaton R W, Henderson A F, Gray B J, Costello J F

出版信息

Thorax. 1983 Jul;38(7):506-11. doi: 10.1136/thx.38.7.506.

Abstract

We have investigated possible mechanisms of response to airway cooling by studying the effects of sodium cromoglycate and ipratropium bromide on the changes in airways resistance that followed eucapnic hyperventilation with subfreezing air in a group of 12 patients with mild asthma and 10 normal subjects. We have also studied the period of refractoriness to repeated challenge. Maximum bronchoconstriction was not reduced after the second challenge, but in the asthmatics the one-second forced expiratory volume recovered more rapidly after the second challenge. The response in normal subjects was completely abolished by ipratropium bromide (p less than 0.0005) whereas sodium cromoglycate was without effect. In the asthmatics both ipratropium and cromoglycate were effective in attenuating the response (p less than 0.005). These results suggest that in normal subjects the response to airway cooling is produced predominantly via neural mechanisms, whereas in asthmatics there is an additional mechanism which can be abolished by sodium cromoglycate.

摘要

我们通过研究色甘酸钠和异丙托溴铵对一组12例轻度哮喘患者和10例正常受试者在使用低于冰点的空气进行等碳酸过度通气后气道阻力变化的影响,探讨了气道冷却反应的可能机制。我们还研究了对重复激发的不应期。第二次激发后最大支气管收缩未减轻,但在哮喘患者中,第二次激发后一秒用力呼气量恢复得更快。异丙托溴铵可完全消除正常受试者的反应(p<0.0005),而色甘酸钠则无作用。在哮喘患者中,异丙托溴铵和色甘酸钠均可有效减轻反应(p<0.005)。这些结果表明,在正常受试者中,对气道冷却的反应主要通过神经机制产生,而在哮喘患者中,存在一种可被色甘酸钠消除的额外机制。

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