Page C P, Coyle A J
Dept of Pharmacology, King's College, Chelsea Campus, University of London, U.K.
Eur Respir J Suppl. 1989 Jun;6:483s-487s.
Many mediators have been proposed to be important in the pathogenesis of bronchial asthma based solely on their ability to elicit airway smooth muscle contraction. However, such an approach fails to appreciate the underlying pathological changes as being central to the aetiology of the disease. Platelet activating factor (PAF) has been demonstrated to mimic many of the features of asthma including bronchial hyperreactivity, eosinophil recruitment, mucus secretion and smooth muscle hyperplasia. The recent availability of selective PAF antagonists has demonstrated the central role of PAF in allergic responses in experimental animals and at least in the skin of man. The precise mechanism by which PAF and antigen induce BHR is not completely understood but may involve an interaction between platelets and eosinophils. It is anticipated that further investigation into the relationship between PAF, platelets and eosinophils may provide a greater insight into the pathogenesis of the disease.
仅基于其引发气道平滑肌收缩的能力，许多介质被认为在支气管哮喘的发病机制中起重要作用。然而，这种方法未能认识到潜在的病理变化是该疾病病因的核心。血小板活化因子（PAF）已被证明可模拟哮喘的许多特征，包括支气管高反应性、嗜酸性粒细胞募集、黏液分泌和平滑肌增生。最近选择性PAF拮抗剂的出现证明了PAF在实验动物的过敏反应中以及至少在人类皮肤中的核心作用。PAF和抗原诱导支气管高反应性的确切机制尚不完全清楚，但可能涉及血小板和嗜酸性粒细胞之间的相互作用。预计对PAF、血小板和嗜酸性粒细胞之间关系的进一步研究可能会为该疾病的发病机制提供更深入的见解。
