Confidential Information About CAPNS1 Made Obtainable

Матеріал з HistoryPedia
Версія від 21:12, 26 травня 2017, створена Bumper0hook (обговореннявнесок) (Створена сторінка: Asthma is a common, chronic respiratory disease with a high personal, social, and economic impact. It is characterized by airway obstruction and an inflammatory...)

(різн.) ← Попередня версія • Поточна версія (різн.) • Новіша версія → (різн.)
Перейти до: навігація, пошук

Asthma is a common, chronic respiratory disease with a high personal, social, and economic impact. It is characterized by airway obstruction and an inflammatory process that affects the whole respiratory tract, from the central to peripheral airways [1]. In recent years, there has been an emerging interest in the role of the small airways, and there is increasing evidence that they contribute significantly to the clinical expression of asthma. Furthermore, new inhaler devices have become available that enable a higher drug deposition in the small airways. The aim of this manuscript is to review the clinical relevance of small airway disease and the implications for the treatment of asthma. The small airways are defined by an internal airway diameter of CAPNS1 of the total lung volume (compared to a lung volume of 50?ml in the large airways) [2]. Because the small airways contain little or no cartilage, they are easily collapsible, for example, during forced expiration and/or smooth muscle contraction. With a higher generation number, the airway diameter gradually decreases. This might suggest that obstruction increases with a higher generation. However, the opposite is true: The cumulative cross-sectional area of the airways increases exponentially, and therefore, Microbiology inhibitor the overall resistance of nondiseased small airways is very low [2]. Historically, the small airways have been called ��the quiet zone��, because of their large reserve capacity and the notion that a high level of disease activity would be necessary before they cause a drop in lung function or an increase in symptoms [3]. This concept was challenged for the first time by the landmark study of Wagner et?al. [4]. Using a wedged bronchoscope with a diameter of 5.5?mm, they demonstrated a striking difference in peripheral airway resistance between asthmatics and healthy individuals, which was sevenfold higher in patients with mild asthma, despite the fact that forced expiratory volume in 1-s Talazoparib manufacturer (FEV1) was similar between the two groups. Moreover, a higher peripheral airway resistance was associated with a more severe bronchial hyper-responsiveness to methacholine [4]. Such observations have been confirmed in later studies. Using the same wedged bronchoscope technique, Kraft et?al. [5] demonstrated that patients with nocturnal asthma have a higher peripheral airway resistance at night than during daytime, a phenomenon not observed in patients without nocturnal asthma. In another study, Kaminsky et?al. showed that after a challenge with cool, dry air, baseline peripheral airway resistance increases to a significantly higher extent in patients with asthma when compared with healthy controls.