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of circumstances might be accounted for merely by the combination of a diffuse homogeneous increase in the resistance of peripheral airways in the presence of normally compliant central airway walls (4, 16, 28). According to this model, as the frequency of oscillation is increased a progressively larger proportion of flow delivered at the airway opening expands central airways rather than lung parenchyma. These frequency-dependent serial shifts in flow distribution bween the airways and the alveolar zone, in turn, lead to the observed frequency-dependent alterations of and CL. On the other hand this hypothesis does not preclude the alternate possibility that frequency-dependent alterations of flow distribution could occur among parallel pathways of gas conduction and thereby account for the observed changes in and CL, as suggested much eaier by Otis and co-workers (20). There is reason to believe that the to might be . First, the tissues themselves might possess intrinsic differences in responsiveness to that agent (23,24, 26), and second, in the case of inhaled , the distribution of aerosol deposition among lung regions could be (2). Thus both serial and parallel nonhomogeniesâ could contribute to the frequency-dependent behavior observed in dog lungs after aerosol exposure. The relative
Journal of Applied Physiology – The American Physiological Society
Published: Jun 1, 1985
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