The James Hogg iCAPTURE Center for Cardiovascular and Pulmonary Research, Providence Health Care/St. Paul's Hospital, Department of Medicine, Respiratory Division, University of British Columbia, Vancouver, BC.
Annu Rev Physiol. 2010;72:437-62. doi: 10.1146/annurev-physiol-021909-135851.
To achieve gas exchange, inspired air must pass through an intricate and dynamic tracheobronchial tree. The tree offers resistance to airflow, and increased resistance is the most important functional change in lung disease. Numerous mechanisms contribute to increased resistance by causing airway narrowing, closure, occlusion, and/or obliteration. Although airway smooth muscle (ASM) contraction and shortening are an important cause of increased resistance, non-ASM elements can also contribute. Nonmuscle elements can modify the amount of airway narrowing for any given level of ASM shortening and the amount of shortening for a given level of ASM activation. In this review, we outline the physiological basis for airflow resistance and describe how changes in the lung parenchyma, the airways, and their luminal contents can contribute to increased airflow resistance. A detailed understanding of the mechanisms and consequences of increased airway resistance is vital to our attempts to alleviate the enormous burden of suffering caused by obstructive lung diseases.
为了实现气体交换，吸入的空气必须通过错综复杂且不断变化的气管支气管树。该树对气流产生阻力，阻力增加是肺部疾病最重要的功能变化。许多机制通过引起气道狭窄、关闭、阻塞和/或闭塞来增加阻力。尽管气道平滑肌（ASM）收缩和缩短是增加阻力的重要原因，但非 ASM 元素也可能起作用。非肌肉元素可以改变任何给定的 ASM 缩短程度下气道狭窄的程度，以及任何给定的 ASM 激活程度下的缩短程度。在这篇综述中，我们概述了气流阻力的生理学基础，并描述了肺实质、气道及其管腔内容物的变化如何导致气流阻力增加。详细了解气道阻力增加的机制和后果对于我们减轻由阻塞性肺部疾病引起的巨大痛苦负担至关重要。
