The pathophysiology of reduced maximum expiratory flow in a canine model of pulmonary emphysema was studied, and the results interpreted in terms of the wave-speed theory of flow limitation. According to this theory, maximum expiratory flow is related both to the cross-sectional area and compliance at an airway site where a critical gas velocity is first reached ("choke-point") and to gas density. Pulmonary emphysema was produced by the repeated instillations of the enzyme papain into the airways of six dogs. In five control dogs, a saline solution was instilled. During forced vital capacity deflation, in an open-chest preparation, maximum expiratory flow, choke-point locations, and the response to breathing an 80:20 helium/oxygen gas mixture were determined at multiple lung volumes. To locate choke-points, a pressure measuring device was positioned in the airway to measure lateral and end-on intrabronchial pressures, from which the relevant wave-speed parameters were obtained. In general, the reduced maximum expiratory flow in emphysema can be explained by diminished lung elastic recoil pressure and by altered bronchial pressure-area behavior, which results in a more peripheral location of choke-points that have smaller cross-sectional areas than controls. With respect to the density dependence of maximum expiratory flow, this response did not differ from control values in four dogs with emphysema in which frictional pressure losses upstream from choke-points did not differ on the two gas mixtures. In two dogs with emphysema, however, upstream frictional pressure losses were greater on helium/oxygen than on air, which resulted in a smaller cross-sectional area on helium/oxygen; hence density dependence decreased.
S N Mink
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