Jeffery P
Lung Pathology Unit, Imperial College School of Medicine, Royal Brompton Hospital, London, UK.
Int J Clin Pract Suppl. 1998 Sep;96:5-14.
The structural and inflammatory changes occurring in the bronchi of asthmatics have been examined in specimens from subjects dying in status asthmaticus and from bronchial biopsies of subjects with mild asthma. Histological changes in the bronchi of asthmatics include shedding and damage of the airway surface epithelium and thickening of the reticular basement membrane. Exposure of an asthmatic subject to an allergen results in an immediate allergic response characterised by mast cell degranulation. This may be followed by a late-phase response involving eosinophil degranulation and differentiation of a myofibroblast phenotype which may be the precursor of increased amounts of bronchial smooth muscle present in chronic severe asthma. These changes are accompanied by vasodilatation, vascular congestion and consequent oedema, and result in thickening of the airway wall and reduction of the airway lumen. Mucus secretion further increases airflow resistance and, in conjunction with an inflammatory exudate, forms tenacious airway plugs which are characteristic of severe life-threatening attacks.
对死于哮喘持续状态患者的标本以及轻度哮喘患者的支气管活检标本进行了研究,以观察哮喘患者支气管发生的结构和炎症变化。哮喘患者支气管的组织学变化包括气道表面上皮脱落和损伤以及网状基底膜增厚。哮喘患者接触过敏原会引发以肥大细胞脱颗粒为特征的即刻过敏反应。随后可能会出现迟发反应,涉及嗜酸性粒细胞脱颗粒和肌成纤维细胞表型分化,而肌成纤维细胞表型可能是慢性重度哮喘中支气管平滑肌增多的前体。这些变化伴有血管扩张、血管充血及随之而来的水肿,导致气道壁增厚和气道管腔变窄。黏液分泌进一步增加气流阻力,并与炎性渗出物一起形成黏稠的气道栓子,这是严重危及生命发作的特征。