Airway closure and reopening occur during each breath in diseased lungs and are associated with generation of respiratory crackles. The mechanism of airway reopening is under intense investigation. However, the access to the small, non-cartilaginous airways with ordinary mechanical or physiological measuring tools is virtually impossible, without disturbing the local structure and function. In addition, most of the measuring devices that are currently in use have a frequency response that is too slow relative to the dynamics of the opening event. The mechanism of inspiratory crackles is not known. The working assumption that sudden airway reopening is the underlying event is supported by several indirect studies. However, the exact mode by which the airway opening translates into acoustic energy that constitutes the crackles is unknown. Fredberg and Holford [1] invoked the stress-relaxation quadrupole mechanism for crackle generation. One of the specific predictions of this mechanism, namely that the direction of the crackle initial deflection will be predominantly positive, was confirmed in several studies. On the other hand, this mechanism involves tissue motion that may, or may not, be sufficiently quick to produce the crackles' rapid waveform. The competing hypothesis is that crackles are generated when a liquid film in the reopening airway suddenly ruptures (J. B. Grotberg, personal communication). The aim of the present study was to develop a method for measuring the dynamics of airway diameter changes. We used sound waves to track the changes of airway size with minimal disturbance to their mechanics. We applied the method to excised rat lungs and correlated the airway diameter changes to airway opening pressures and lung surface acoustic signals during crackle formation.
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