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许多炎症介质都在哮喘中起一定作用,但其作用的确切证据尚不足。每种介质有使呼吸道平滑肌收缩、粘液分泌增加和炎症细胞趋化性等作用,从而引起支气管阻塞。炎症细胞在介质的作用下又可释放多种介质。但各种介质的细胞来源常不肯定,肥大细胞、巨噬细胞、嗜酸细胞和中性白细胞可能均参与介质的释放。气道炎症细胞的浸润作用可使支气管收缩加剧,反应增强,此为哮喘的一个特征。介质通过激活呼吸道靶细胞上的特异受体而起作用。目前已有几种特异的拮抗剂,由于哮喘有许多介质参与,单一的拮抗剂效果不佳。介质之间存在着相互作用,如PGD_2可增强组胺和胆碱能促效药的作用,由于PGD_2和组胺均由肺肥
Many inflammatory mediators play a role in asthma, but the exact evidence for its effects is not yet sufficient. Each medium has to make respiratory smooth muscle contraction, mucus secretion and inflammatory cell chemotaxis and other effects, causing bronchial obstruction. Inflammatory cells can release a variety of media under the action of the medium. However, the sources of cells in various media are not always sure. Mast cells, macrophages, eosinophils and neutrophils may all participate in the release of the mediators. Infiltration of airway inflammatory cells can exacerbate bronchoconstriction, increased response, this is a feature of asthma. The mediator works by activating specific receptors on respiratory target cells. There are several specific antagonists currently available, and as a single mediator, the asthma has many mediators involved. There are interactions between the media, such as PGD_2 can enhance the role of histamine and choline can promote drug action, as both PGD_2 and histamine by the lung fat