Kaliner M, Marom Z
J Asthma. 1983;20 Suppl 1:9-13. doi: 10.3109/02770908309078047.
To study the hypersecretion of mucus in human airways, an in vitro model was developed. The effect of prostaglandins, nonsteroidal anti-inflammatory drugs, lipoxygenase products of arachidonic acid, and other mucus-stimulating and mucus-inhibiting agents was studied. The data suggest that arachidonic acid metabolized through its lipoxygenase pathway leads to the formation of potent stimulators of mucus release. Among them are the monohydroxyeicosatetraenoic acids, which are produced in large quantities by human airways, and the leukotrienes, which are generated during allergic reactions of the lung. As the lipoxygenase pathway is the only operant metabolic system available for arachidonic acid in the presence of aspirin and non-steroidal anti-inflammatory drugs--and as the nonsteroidal anti-inflammatory drugs themselves stimulate mucus production--it is possible that the mechanism responsible for mucus release in aspirin-sensitive asthmatics is the formation of these lipoxygenase products.
为研究人类气道黏液分泌过多的情况，开发了一种体外模型。研究了前列腺素、非甾体抗炎药、花生四烯酸的脂氧合酶产物以及其他黏液刺激剂和黏液抑制剂的作用。数据表明，通过其脂氧合酶途径代谢的花生四烯酸会导致形成强效的黏液释放刺激剂。其中包括人类气道大量产生的单羟基二十碳四烯酸，以及肺部过敏反应期间产生的白三烯。由于在存在阿司匹林和非甾体抗炎药的情况下，脂氧合酶途径是花生四烯酸唯一可操作的代谢系统，而且非甾体抗炎药本身会刺激黏液产生，因此阿司匹林敏感性哮喘患者中负责黏液释放的机制可能是这些脂氧合酶产物的形成。
