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Updated: Jun 16, 2026

Utilizing the Precision-Cut Lung Slice to Study the Contractile Regulation of Airway and Intrapulmonary Arterial Smooth Muscle
Published on: May 5, 2022
It's not all smooth muscle: non-smooth-muscle elements in control of resistance to airflow
Ynuk Bossé1, Erik P Riesenfeld, Peter D Paré
1The 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. ybosse@mrl.ubc.ca
Abstract:
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.
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