阿托品、色甘酸钠和百里胺在前列腺素F2α诱发的外源性哮喘支气管收缩中的作用
Atropine, sodium cromoglycate, and thymoxamine in PGF2 alpha-induced bronchoconstriction in extrinsic asthma.
作者信息
Patel K R
出版信息
Br Med J. 1975 May 17;2(5967):360-2. doi: 10.1136/bmj.2.5967.360.
Abstract
In six patients with extrinsic bronchial asthma the inhalation of prostaglandin (PG) F2 alpha in a small dosage produced significant bronchoconstriction, whereas PGE2 produced bronchodilatation. In these patients cholinergic blockade with atropine partially inhibited the PGF2 alpha-induced bronchoconstriction, but the alpha-receptor-blocking drug thymoxamine and sodium cromoglycate did not. These results suggest that the effect of PGF2 alpha is mediated through cholinergic receptors in the airways, and this effect is grossly exaggerated in asthma. The failure to inhibit PGF2 alpha-induced bronchoconstriction with sodium cromoglycate and the observation of an inhibitory effect of sodium cromoglycate in both allergic and exercise asthma suggest that locally formed PGF2 alpha may not be the main factor in the pathogenesis of bronchial asthma.
摘要
在6例外源性支气管哮喘患者中，吸入小剂量前列腺素（PG）F2α会引起明显的支气管收缩，而PGE2则会引起支气管扩张。在这些患者中，用阿托品进行胆碱能阻滞可部分抑制PGF2α诱导的支气管收缩，但α受体阻断药百里胺和色甘酸钠则不能。这些结果表明，PGF2α的作用是通过气道中的胆碱能受体介导的，并且这种作用在哮喘中被严重夸大。色甘酸钠未能抑制PGF2α诱导的支气管收缩，以及色甘酸钠在过敏性哮喘和运动性哮喘中均有抑制作用，这表明局部生成的PGF2α可能不是支气管哮喘发病机制中的主要因素。
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