Pavord I D, Tattersfield A E
Division of Respiratory Medicine, Nottingham University, City Hospital, UK.
Lancet. 1995 Feb 18;345(8947):436-8. doi: 10.1016/s0140-6736(95)90409-3.
The possibility that impaired production of bronchoprotective factors contributes to the pathogenesis of asthma cannot be excluded. Prostaglandin E2 (PGE2) could be such a factor. It is a dominant cyclo-oxygenase product of airway epithelium and smooth muscle; it has inhibitory effects on inflammatory cells and pathways involved in bronchoconstriction at concentrations known to occur in the airway; inhalation of PGE2 has considerable bronchoprotective effects in patients with asthma; and manoeuvres that increase or decrease endogenous production of PGE2 have beneficial and deleterious effects on airway function.
支气管保护因子生成受损促成哮喘发病机制的可能性不能排除。前列腺素E2(PGE2)可能就是这样一种因子。它是气道上皮和平滑肌主要的环氧化酶产物;在已知存在于气道中的浓度下,它对参与支气管收缩的炎症细胞和途径具有抑制作用;吸入PGE2对哮喘患者有相当大的支气管保护作用;增加或减少内源性PGE2生成的操作对气道功能有有益和有害影响。