Agrawal K P, Reed C E, Hyatt R E, Imber W E, Krell W S
Mayo Clin Proc. 1986 Oct;61(10):778-84. doi: 10.1016/s0025-6196(12)64816-2.
Challenges with ouabain and histamine were performed a week apart in 10 patients with asthma and 5 normal subjects. Concentrations were increased cumulatively until specific airway conductance decreased by 30% or the maximal concentration of 1.0% was reached. At low concentrations, ouabain induced bronchodilatation in six patients who had asthma. Bronchodilatation gradually decreased with increasing concentrations and was followed by bronchoconstriction in two patients with asthma who had high airway sensitivity to histamine. Ouabain caused only bronchoconstriction in three patients with severe asthma. The normal subjects showed mild bronchodilatation or no response to ouabain. Several possible biochemical mechanisms may be responsible for the bronchodilatory response to low doses of ouabain, such as stimulation of adenylate cyclase or (Na+,K+)-adenosine triphosphatase. The absence of a bronchodilatory response to ouabain in patients with severe asthma suggests an impairment in the activity of these enzymes.
在10例哮喘患者和5名正常受试者中，分别在相隔一周的时间进行哇巴因和组胺激发试验。浓度逐步递增，直至比气道传导率下降30%或达到1.0%的最大浓度。在低浓度时，哇巴因使6例哮喘患者出现支气管扩张。随着浓度增加，支气管扩张逐渐减弱，随后2例对组胺气道敏感性高的哮喘患者出现支气管收缩。哇巴因仅使3例重度哮喘患者出现支气管收缩。正常受试者对哇巴因表现为轻度支气管扩张或无反应。低剂量哇巴因引起的支气管扩张反应可能有几种潜在的生化机制，如刺激腺苷酸环化酶或（钠，钾）-三磷酸腺苷酶。重度哮喘患者对哇巴因无支气管扩张反应提示这些酶的活性受损。
