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Bronchodilatation was produced in normal subjects by the inhalation of atropine, a parasympatholytic agent, and isoproterenol, a beta adrenergic stimulator. Density dependence of maximal expiratory flow (Vmax), expressed as a ratio of Vmax with an 80% helium-20% oxygen gas mixture to Vmax with air at isolung volumes, indicated that the predominant flow regimes across upstream airways changed differently after each agent was given separately. After atropine Vmax increased, elastic recoil pressure did not change, and density dependence decreased. Utilizing the equal pressure points analysis which defines upstream and downstream segments of the intrathoracic airways at flow limitation, these results suggest a greater relative dilatation of the larger upstream airways such that more of the driving pressure is dissipated across the smaller airways in which flow is less  dependent upon gas density. After isoproterenol Vmax increased, elastic recoil pressure did not change, and density dependence increased. This suggests a preferential dilatation of the smaller and more peripheral airways with less density-dependent flow regimes such that more of the driving pressure would be dissipated in the larger airways in which flow is more dependent upon gas density. Systematic decreases after isoproterenol lead independently to the same conclusion. After both agents together, Vmax increased and density dependence and critical alveolar pressures did not change from control, suggesting a relatively uniform dilatation of all the airways comprising the upstream segment.

Relative contributions of large and small airways to flow limitation in normal subjects before and after atropine and isoproterenol.