Forced expiration and HeO2 response in canine peripheral airway obstruction

We examined the effect of peripheral airway obstruction on parameters of maximum expiratory flow (Vmax) in a canine model of bronchiolitis obliterans (B). B was produced by the repeated intrabronchial instillations of a 1% nitric acid solution in seven dogs (group B). In seven control dogs (group C), a normal saline solution was used. During forced vital capacity deflation, Vmax on air, the relative increase in Vmax on 80% He-20% O2 (delta Vmax), and airway sites of flow limitation "choke points" (CP) were determined at multiple lung volumes (VL). The findings were interpreted in terms of the wave-speed theory of flow limitation. Wave-speed parameters were identified with a pressure-measuring device positioned in the airway. Compared with the findings for group C, Vmax decreased substantially at the lower VL (less than 50% vital capacity) in group B, whereas there were no changes in delta Vmax at any VL. CP were identified in central airways in both groups but were slightly more upstream in group B. Our analysis indicated that the reduction in Vmax in group B was due to an increase in upstream frictional pressure losses (Pfr) that caused a relative reduction in the pressure head, so that choking occurred in slightly upstream airways. delta Vmax did not change in group B because with CP identified in central airways, Pfr were density dependent, and significant differences in head loss on the two gas mixtures did not occur. Choking therefore occurred with similar wave-speed variables on the two gas mixtures, and delta Vmax was maintained.