Raeburn D
Rhone-Poulenc (UK) Ltd., Dagenham Research Centre, Essex, England.
Agents Actions Suppl. 1990;31:259-74. doi: 10.1007/978-3-0348-7379-6_36.
Until recently the contractile actions of asthma mediators have been examined in vitro without consideration of the modulatory role of the associated epithelial cells. Removal of the epithelium in vitro augments contraction and reduces relaxation to several bronchoactive agents and bioassay experiments have shown that the protective effects of the epithelium can be transferred to denuded preparations. It now seems likely that one or more epithelial-associated factors eg EpDRF and PGE2 have a protective role in controlling airway contractility. These findings may be important in asthmatics in vivo since there may be some correlation between epithelial damage/loss and airway hyperreactivity. The identity of EpDRF remains unknown but it does not appear to be a prostanoid and is distinct pharmacologically from EDRF found in blood vessels.
直到最近，哮喘介质的收缩作用都是在体外进行研究的，而没有考虑相关上皮细胞的调节作用。在体外去除上皮会增强收缩并减少对几种支气管活性剂的舒张反应，生物测定实验表明上皮的保护作用可以转移到去上皮的制剂上。现在看来，一种或多种上皮相关因子，如上皮衍生舒张因子（EpDRF）和前列腺素E2（PGE2），在控制气道收缩性方面具有保护作用。这些发现可能对体内的哮喘患者很重要，因为上皮损伤/丧失与气道高反应性之间可能存在某种关联。EpDRF的身份仍然未知，但它似乎不是前列腺素类物质，在药理学上与血管中发现的内皮舒张因子（EDRF）不同。
