Abstract

Pulmonary physiologically, diffusing capacity (DL) is described as the product of diffusing coefficient (K) and alveolar diffusing area (A), not as physical diffusing coefficient, because of treating the gas exchange through the alveolar membrane. The purpose of measurements of diffusing capacity as a pulmonary function test is the possibility to decide the efficiency of gas transfer from the atmosphere to pulmonary circulation through lungs. When this gas transfer is disturbed, several factors are considered which are the hypertrophy of alveolar membrane, the reduction of pulmonary capillary bed, shortening of the contact time, and ventilation-perfusion, its ratio and its uneven distribution. We considered the uneven distribution of ventilation-perfusion as the most important factor to reduce DLCO, then substituted the results of uneven distribution of ventilation-perfusion in chronic pulmonary emphysema and bronchial asthma for the ideal formula of pulmonary diffusing capacity induced from two compartments lung model constructed by ENGELBERG and COHN, and we studied theoretically and practically. Methods : Pulmonary function tests, pulmonary carbon monoxide diffusing capacity (by the single breath method), and uneven distribution of ventilation-perfusion etc. were tested in ten cases of bronchial asthma same as in chronic pulmonary emphysema. The predicted value for DLCO was refered to KANAGAMI et al. DLCO obtained from two compartments lung model is explained as, [numerical formula] where A1 indicates diffusing area (=pulmonary blood flow) of the first compartment, and Mo1 indicates alveolar carbon monoxide volume (=ventilation) just before the beginning of diffusion. Substituting for A1 and Mo1, the observed value of blood flow (Qi/QT) and ventilation (VAi/VAT) for poorly ventilated alveoli and compensatory hyperventilated alveoli in chronic pulmonary emphysema and bronchial asthma, the relations between DL, A1, and Mo1 were obtained on four curves calculated by the digital computer, and from them, influences of L3 and L1 in both diseases, i.e., uneven distributions of ventilation-perfusion in the lungs upon DLCO of overall the lung, were compared.

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