Previous attempts to describe the abnormalities of maximum expiratory flow (Vmax) in patients with airflow obstruction have been examined in terms of the equal pressure point theory (EPP) of Mead et al and the "Starling resistor" theory of Pride et al. However, the former remains a conceptual and the latter an intuitive explanation of flow limitation. The recently described wave-speed theory provides a precise mathematical description of Vmax as well as a clear physical basis for understanding flow limitation. This proposal will attempt to relate the specific determinants in the wave-speed theory to Vmax in normal and chemically abnormal lungs. The wave-speed theory states that flow becomes limited when at a point in the airway, the "choke point", flow velocity equals the speed of propagation of pressure pulse waves along the airway wall. This critical velocity is determined by the physical characteristics of the airway and the density of the fluid medium. In the first part of this proposal, "choke points" will be detected in the airways of living dogs using the retrograde catheter technique. The effect of measured changes in elastic recoil pressure (Pel) and airway resistance (RL) on measurements of Vmax and transmural airway pressure at the "choke point" (P*) will be determined. These results will be compared with predictions from the wave-speed theory. Four interventions will be used to alter either Pel or RL: 1) state of lung inflation, 2) partial flow-volume curves with RV and TLC volume history, 3) induced bronchoconstriction and, 4) induced emphysema. The effect of breathing HeO2 on Vmax will also be assessed in protocols #3 and #4. These latter findings will help to determine the wave-speed mechanism accounting for patients who do not increase their Vmax during HeO2 breathing. In the second part of this proposal, morphometrically abnormal excised human lungs will be studied, and measurements of "choke point" location and the variables in the wave-speed equation made at different states of lung inflation. These results will be compared to those in normal excised human lungs and the canine models within the framework of their altered mechanical properties. From these comparisons, deductions of how specific disease entities alter the mechanism of flow limitation will be made.