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慢性阻塞性肺疾病小气道的病理生理学。

Pathophysiology of the small airways in chronic obstructive pulmonary disease.

机构信息

Department of Cardiac, Thoracic and Vascular Sciences, Respiratory Diseases Clinic, University of Padova, Padua, Italy.

出版信息

Respiration. 2012;84(2):89-97. doi: 10.1159/000341382. Epub 2012 Aug 6.

DOI:10.1159/000341382
PMID:22868355
Abstract

Chronic obstructive pulmonary disease (COPD) is characterized by a persistent airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases. From a pathological point of view, COPD is characterized by two distinct and frequently coexisting aspects: small airway abnormalities and parenchymal destruction (or emphysema). When pathological changes are localized in lung parenchyma, they will contribute to airflow limitation by reducing the elastic recoil of the lung through parenchymal destruction, as well as by reducing the elastic load applied to the airways through destruction of alveolar attachments. Conversely, when pathological changes involve the small airways, they will contribute to airflow limitation by narrowing and obliterating the lumen and by actively constricting the airways, therefore increasing the resistance. In this article we will review the structural abnormalities in small airways and their relationship with the disordered pulmonary function in COPD, in the attempt to disentangle the mechanisms contributing to the development and progression of airflow limitation in smokers. We will start by describing the normal structure of the small airways, and then observe the main pathological alterations that accumulate in this site and how they parallel pulmonary function derangement.

摘要

慢性阻塞性肺疾病(COPD)的特征是持续的气流受限,通常呈进行性发展,并伴有气道和肺部对有害颗粒或气体的慢性炎症反应增强。从病理学角度来看,COPD 的特征是两个明显且经常同时存在的方面:小气道异常和肺实质破坏(或肺气肿)。当病理变化局限于肺实质时,通过破坏肺实质减少肺的弹性回缩,以及通过破坏肺泡附着减少施加到气道的弹性负荷,将导致气流受限。相反,当小气道发生病变时,通过缩小和闭塞管腔以及主动收缩气道,从而增加阻力,导致气流受限。在本文中,我们将回顾小气道的结构异常及其与 COPD 中肺功能障碍的关系,试图阐明导致吸烟者气流受限发展和进展的机制。我们将首先描述小气道的正常结构,然后观察在该部位积聚的主要病理改变以及它们如何与肺功能障碍平行。

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