Satisfactory methods, utilizing measurements of transthoracic or transpulmonary pressure and airflow, are now available for determining "nonelastic" pulmonary resistance. However, the nonelastic pulmonary resistance has two components, tissue resistance and airway resistance, and no valid direct method is available for measuring either of these components separately in man. Since airway resistance is the ratio of alveolar pressure during flow to airflow, airway resistance alone could be measured if there were a method for determining alveolar pressure during flow. This report presents a new method for accomplishing this measurement, and gives data for airway resistance obtained in normal subjects and in patients with respiratory disease.Of previous attempts to measure airway resistance, one of the earliest was the painstaking study by Rohrer (1) who made anatomical measurements on the tracheobronchial tree of a human lung post mortem and calculated the cumulative resistance to airflow of the entire system using Poiseuille's law and turbulence theory. The first important experimental study of pulmonary resistance in the living animal was made by von Neergaard and Wirz who, in 1927 (2), analyzed intrapleural pressure into two major components, "dynamic" (which is essentially resistive) and "static" (which is predominantly elastic in nature). This approach made it possible to obtain values for total pulmonary resistance, though not for airway resistance alone. Bayliss and Robertson (3), reasoning that airway resistance, but not tissue resistance, would vary with the viscosity of the gases breathed, ventilated isolated animal lungs with gases of different density and viscosity; 1 These studies were aided (in part) by a contract between the Office of Naval Research, Department of the Navy, and the University of Pennsylvania, NR 112-323. from the changes in pressure and volume during artificial ventilation with different gases, they calculated the fraction of non-elastic pulmonary resistance attributable to airway resistance. Studies based upon the revised principle of utilizing several different gas mixtures of different density and viscosity have been carried out more recently in man by Fry, Ebert, Stead, and Brown (4) and McIlroy, Mead, Selverstone, and Radford (5) who made the point that gas combinations which have equal kinematic viscosities should be selected. The results using this technique have been at variance to date, possibly owing to other factors affecting airway resistance (5).

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The uptake of gases such as oxygen, carbon monoxide, or nitric oxide by the erythrocyte involves: (a) diffusion across the cellular membrane, (b) intraerythrocytic diffusion, and (c) chemical combination with hemoglobin. The aim of this investigation was to obtain data which would permit an analysis of each of these factors in limiting the rate of gas uptake.The initial over-aU rate of uptake of gases which combine chemically with hemoglobin to produce a color change can be measured by a modified version of the Hartridge-Roughton-Millikan constant flow, rapid reaction apparatus. If nitric oxide is the reactant gas, only (a) and (b) are measured since the chemical combination of this gas with hemoglobin is extremely rapid. Our studies have shown that human biconcave discoidal erythrocytes at 38 and 48°C., have the same initial rate of carbon monoxide and nitric oxide uptake as the same cells converted into spherocytes of equal volume. Similarly there was no difference between discs and cells sphered with a 30 per cent increase in volume. Shrunken erythrocytes showed a marked decrease in rate of gas uptake. This suggests that surface area and maximum linear distance for intracellular diffusion of this magnitude do not measurably retard gas uptake. In the shrunken cells, a change in the orientation and concentration of intraerythrocytic hemoglobin and/or of the membrane components may have impeded gas diffusion.Oxygenation of pulmonary capillary blood involves several processes. Oxygen molecules present within the alveoli must first traverse the alveolar-

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We used the body plethysmograph to measure the ratio of airway conductance (reciprocal of airway resistance) to thoracic gas volume (TGV) in a group of healthy subjects, including 23 noncigarette smokers and 25 cigarette smokers. There was no significant difference between male and female smokers and male nonsmokers. Airway conductance/TGV was significantly higher in female nonsmokers. We studied the acute effect of inhalation of cigarette smoke on airway conductance/TGV in 36 healthy subjects (21 smokers and 15 “nonsmokers”) and 22 patients with cardiopulmonary disease (all smokers). The ratio decreased after the inhalation of cigarette smoke in both groups. The effects were almost immediate; the mean duration of effect was 35 min. Inhalation of 0.5% isoproterenol aerosol reversed or prevented the effect of inhalation of cigarette smoke. The decrease in conductance/TGV caused by inhalation of cigarette smoke did not appear to be related to inhalation of nicotine or of other volatile substances. Submitted on January 23, 1961

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