This proposed research is aimed at understanding airflow and resistance in the nasal airways. To this end, experiments will be conducted in scaled nasal airway models, nose casts, animals and human subjects. Knowledge of fluid mechanics as well as techniques of system identification will be employed to design the experiments, analyze the data, and interpret the results. Mainly but not exclusively to answer questions of """"""""What"""""""" and """"""""how"""""""" rather than """"""""why"""""""", this research consists of three parts, each having three specific aims. Part 1 deals with flow dynamics in the nose. Idealized nasal airway models of 3:1 scale will be constructed out of clear acrylic plastic and transparent casts of the nose will also be made. The flow visualization results obtained in the casts will serve as a guide to design flow visualization in the clear models by laser sheet scanning. Detailed velocity measurement in the models will be made using Laser Doppler Anemometry. Pressure-flow relationships in the casts will be obtained and the factors governing their main features investigated. Part 2 of the research seeks to establish two new methods of measuring nasal airflow resistance. A non-invasive forced oscillation method is based on the fact that the nasal and lower airways form parallel paths for air entering from the mouth. A second method consists of a few sniffs by the subject wearing a face mask. These techniques will yield nasal impedance from which resistance can be identified. Both will be tested in normal subjects as well as patients. Part 3 consists of animal experiments designed to understand three aspects of nasal physiology. Three working hypotheses regarding flow and resistance in the nose are used for this experiment: (1) it is easier to ventilate a paranasal sinus by high-frequency oscillating air current than by steady flow through the nasal chamber; (2) the wave-speed theory of flow limitation applies to maximal nasal inspiratory flow; and (3) severely increased nasal resistance causes an increase in pulmonary resistance, due mainly to an augmentation of lung tissue resistance.
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