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[慢性阻塞性肺疾病(COPD)的发病机制]

[Pathogenesis of the chronic obstructive pulmonary disease (COPD)].

作者信息

Musil J

机构信息

Pneumologická klinika 2. lékarské fakulty UK a FN Motol, Praha.

出版信息

Vnitr Lek. 2004 Sep;50(9):663-7.

Abstract

An inflammation in the bronchial wall is usually present already in an early stage of the disease. An inflammatory infiltration cause predominantly mononuclear cells in the mucous membrane and neutrophiles in the phlegm produced by airways. Also eosinophiles can participate in the inflammation. Lymphocytes distribution is different from asthma because there is mainly submucosa infiltrated in COPD. Metaplasia of goblet cells appears. Chronic bronchial obstruction characterizing COPD is induced by conjunction of small airways disease (obstructive bronchiolitis) and a destruction of pulmonary parenchyma (emphysema) which both contribute to an impairment and differ form person to person. Chronic inflammation is a cause of remodeling and narrowing of small airways. Destruction of pulmonary parenchyma and the inflammation cause loss of alveolar connection with small airways and elastic pulmonary stress decreases. Two theories try to explain COPD--a theory of imbalance between proteinases and antiproteinases and a theory of oxidation stress.

摘要

在疾病早期,支气管壁通常就已存在炎症。炎症浸润主要导致黏膜中的单核细胞以及气道产生的痰液中的中性粒细胞增多。嗜酸性粒细胞也可参与炎症反应。淋巴细胞分布与哮喘不同,因为慢性阻塞性肺疾病(COPD)主要是黏膜下层浸润。杯状细胞化生出现。COPD的慢性支气管阻塞是由小气道疾病(阻塞性细支气管炎)和肺实质破坏(肺气肿)共同引起的,这两者都会导致功能损害,且因人而异。慢性炎症是小气道重塑和狭窄的原因。肺实质破坏和炎症导致肺泡与小气道的连接丧失,肺弹性应力降低。有两种理论试图解释COPD——蛋白酶和抗蛋白酶失衡理论以及氧化应激理论。

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