Maintenance of airway caliber in isolated airways by deep inspiration and tidal strains

• Published in: Journal of applied physiology (1985) 2008-08, Vol.105 (2), p.479-485
• Main Authors: LaPrad, Adam S, West, Adrian R, Noble, Peter B, Lutchen, Kenneth R, Mitchell, Howard W
• Format: Article
• Language: English
• Subjects: Airway management; Algorithms; Animals; Biological and medical sciences; Bronchi - physiology; Bronchoconstriction - physiology; Bronchoscopy; Carbachol - pharmacology; Data Interpretation, Statistical; Fiber Optic Technology; Fundamental and applied biological sciences. Psychology; Muscarinic Agonists - pharmacology; Optical Fibers; Pressure; Respiratory Mechanics - physiology; Respiratory Physiological Phenomena; Respiratory system; Respiratory System - anatomy & histology; Swine; Tidal Volume - physiology
• ISSN: 8750-7587; 1522-1601
• DOI: 10.1152/japplphysiol.01220.2007

1 Department of Biomedical Engineering, Boston University, Boston, Massachusetts; and 2 Discipline of Physiology, School of Biomedical, Biomolecular, and Chemical Sciences, University of Western Australia, Crawley, Western Australia, Australia Submitted 15 November 2007 ; accepted in final form 6 June 2008 Deep inspirations (DIs) are large periodic breathing maneuvers that regulate airway caliber and prevent airway obstruction in vivo. This study characterized the intrinsic response of the intact airway to DI, isolated from parenchymal attachments and other in vivo interactions. Porcine isolated bronchial segments were constricted with carbachol and subjected to transmural pressures of 5–10 cmH 2 O at 0.25 Hz (tidal breathing) interspersed with single DIs of amplitude 5–20 cmH 2 O, 5–30 cmH 2 O, or 5–40 cmH 2 O (6-s duration) or DI of amplitude 5–30 cmH 2 O (30-s duration). Tidal breathing was ceased after DI in a subset of airways and in control airways in which no DI was performed. Luminal cross-sectional area was measured using a fiber-optic endoscope. Bronchodilation by DI was amplitude dependent; 5–20 cmH 2 O DIs produced less dilation than 5–30 cmH 2 O and 5–40 cmH 2 O DIs ( P = 0.003 and 0.012, respectively). Effects of DI duration were not significant ( P = 0.182). Renarrowing after DI followed a monoexponential decay function to pre-DI airway caliber with time constants between 27.4 ± 4.3 and 36.3 ± 6.9 s. However, when tidal breathing was ceased after DI, further bronchoconstriction occurred within 30s. This response was identical in both the presence and absence of DI ( P = 0.919). We conclude that the normal bronchodilatory response to DI occurs as a result of the direct mechanical effects of DI on activated ASM in the airway wall. Further bronchoconstriction occurs by altering the airway wall stress following DI, demonstrating the importance of continual transient strains in maintaining airway caliber. bronchodilation; airway smooth muscle; bronchial segments Address for reprint requests and other correspondence: A. S. LaPrad, Dept. of Biomedical Engineering, Boston Univ., 44 Cummington St., Boston, MA 02215 (e-mail: alaprad{at}bu.edu )