Abstract
The pathologic physiology of bronchial asthma has mainly been evaluated by the pulmonary ventilation function tests.
However, it is considered that these tests alone may be unable to demonstrate the real physiologic change of respiration because they are impossible to indicate exact alveolar function which takes up oxygen and eliminates carbon dioxide.
To clarify the pathologic physiology of bronchial asthma, the parameters of pulmonary gas exchange were measured by modified oxygen saturation method of Briscoes and compared with the data of other pulmonary function tests, such as spirogram, FRC, DLCO, and so forth, before and after administration of bronchodilator using I. P. P. B..
At the calculation of alveolar ventilation volume, the existence of physiologic dead space was taken into consideration.
The results were as follows:
1) Normal space increased from 28 to 34 per cent whereas slow space decreased from 64 to 57 per cent, making no change in fast space.
2) Alveolar ventilation increased from 4.44 to 4.82 1., especially its distribution to slow space increased from 14 to 16 per cent.
3) Turn over rate of slow space elevated from 0.27 to 0.41. There was tendency to approach towards that of normal space.
4) The percentage of perfusion of fast-normal space increased from 52 to 57 whereas that of slow space decreased from 45 to 40. These results indicated that fast-normal space was over-perfused and slow space was underperfused. Besides, these uneven distributions of perfusion were also observed by syncigram using I131 M. A. A..
5) Ventilation-perfusion ratio of fast-normal space decreased from 1.35 to 1.18 whereas that of slow space increased 0.25 to 0.34, therefore, the improvement of gas exchange in the whole lung was observed.
6) Shunt like effect due to ventilation-perfusion unevenness, calculated A-aDO2, and a-ADCO2, were much reduced from 23.0 to 14.1 per cent, from 32.4 to 22.6mmHg, from 6.2 to 3.4mmHg, respectively.
7) The existence of about 1 to 4 per cent of perfusion passed through unventilated space was presumed from an anatomical shunt. Consequently, these observations apparently indicate that the rate of venous admixture in the whole lung is the most superior indicator to demonstrate unevenness of ventilation-perfusion relationships.
8) The fact that the rate of venous admixture maintained within 17 per cent even after administration of bronchodilators shows that some cases of bronchial asthma should be improved gas exchange following the elevation of oxygen tension in the arterial and mixed venous blood by inspiration of high concentrated oxygen with the aid of bronchodilators.
9) It is clear that these analyses of alveolar function used the present study are accurate because correlative relation was observed between calculated A-aDO2, a-ADCO2, and observed values of the same cases.
Based on these findings, it is evident that not only uneven distributions of alveolar ventilation but those of perfusion also exist in the patient with bronchial asthma even while mild attack or remission. In addition, it is reasonable to presume that when severe attack occurs, the perfusion of slow space may increase inspite of the decrease of its ventilation, so that the regulation mechanisms of ventilation-perfusion might be disturbed.
