Seven healthy males and 5 patients with COPD were studied with increasing dead space; 250, 500, and 750ml, respectively. The slope of the P_CO2-ventilation relationship and the slope of the metabolic hyperbola are defined as S and S_L, respectively. The product of S and S_L is defined as “gain”, which represents the ability of homeostatic control mechanism for blood gas levels. In fact, the magnitude of P_ACO2 change is assumed to be as great as (gain+1) times the actual change with the lack of chemical control of respiration.
In both normal subjects and patients, the values of gain were found to be between 10 to 20 which were well in accord with the value calculated from actual P_ACO2 change and S_L. The agreement was best in the experiments with VD increment of 500ml. The reason why no differences in the gain were seen between the normals and patients was assumed to be due to a slight depression in pulmonary functions in the latter.
The degree of scatter in S was far greater than that in SL, thus the values of gain were mostly determined by individual differences in S values. Therefore, when S_L was calculated by using allometric coefficients, the value of gain can be estimated only by measuring P_ACO2 respiratory frequency and body weight. This calculation was conducted by the following equation:
Estimated gain=-ΔV_D×(P_ACO2)²/0.863×V_CO2×ΔP_ACO2-1
Reasonable agreements were seen between actual gain and this simplified estimations. This approach is intended to be used in routine examination for evaluating the ability of homeostatic control mechanism for blood gas levels.

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There has been a drastic increase in the incidence of lung cancer, to three times that of ten years ago. Not with standing efforts for early detection of lung cancer and for extended applications of surgery, the resection rate of lung cancer is still as low as 30% with the results of surgery poorer than in other carcinoma cases. Aged patients with lung cancer will increase and there will be more cases of lung complications caused by the deterioration of lung function after surgery. When the functional limit of operation is broadened, there arises the problem of post-operative management. This problem can be coped with by establishing an RCU to facilitate the post-operative respiratory care. Post-operative death is actually caused by adventitious pulmonary complications. The post-operative lung complication is liable to develop especially in patients with lowered pulmonary function. The importance of the best possible preservation of lung function is clear. A preservation of lung function without impairment of surgical curability is attempted by performing sleeve lobectomy in cases for which a pneumonectomy is normally indicated and further by giving serious consideration to a limited operation.
The high incidence of metastasis means management of patients with a combination of chemotherapy, radiation therapy and immunotherapy. Much efforts have, therefore, been exerted to develop long term post-operative intermittent therapeutic modalities. Respiratory cripples in the RCU cannot be weaned from the respirator and are confronted by death. Experiments have been carried out by the authors and others for lung transplantation and total cardio-pulmonary transplantation. The operative technique has almost been established, and the problems related to the function of the transplanted lung and the regulation of respiration have almost been overcome. However, there are still problems in lung preservation and rejection.

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The mechanical interdependence between bronchi and lung was studied by obstructing the bronchi with beads. The bronchi was narrowed with smooth muscle tone and with negative bronchial pressure as that during forced expiration. We found that the smooth muscle mechanics and local peribronchial lung compliance were the determinants of maximum expiratory flow.

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In order to examine the diagnostic value of broncho-alveolar lavage (BAL) for diffuse interstitial pulmonary diseases, we performed BAL in young healthy normal volunteers (17 cases), control patients with an average age of 58 (37 cases), patients with diffuse interstitial fibrosing pneumonia (DIFP) (16 cases), patients with hypersensitivity pneumonitis (6 cases) and patients with sarcoidosis (5 cases), and analyzed the cellular and protein contents in the lavage fluids.
A segment or subsegment of the right middle lobe/or lingula was lavaged with 50ml of saline with 3 times. In control patients, the lavage was done at the site free from lesion. A site related to the pulmonary disease should be lavaged in order to obtain broncho-alveolar components with constantly high yield. Age-matched controls are necessary for evaluation of the nature and extent of diffuse interstitial pulmonary diseases. Various components in the broncho-alveolar lavage fluid (BALF) must be expressed not only as concentration in BALF but also as ratios to other components, in order to evaluate the nature and extent of diffuse interstitial disease accurately.
Cellular and protein components of BALF in the 5 groups were analysed. It was concluded that analysis of cells in BALF obtained from patients with hypersensitivity pneumonitis (HP) was highly diagnostic. The increased number of lymphocytes in HP may be related to the etiology of HP. BALF from patients with chronic DIFP showed an increased number of polymorphic nuclear neutrophils compared to controls.

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In 58 patients with pulmonary emphysema and/or chronic bronchitis (mean age=60.5±SD 10.6 years, EEVl/FVC=49.8±15.2%, and VC=72.4±21.2% of predicted), mixed venous and arterial blood gases obtained during cardiac catheterization were used to calculate an efficiency index (EI) of the pulmonary gas exchange, a newly defined word. The patients were classified into 9 groups according to the severity of arterial hypoxemia. PaO₂ ranged from 90.0 to 35.3mmHg (mean=60.5mmHg) and PaCO₂ from 25.3 to 60.5mmHg (mean=42.2mmHg).
The EI was calculated by the equation: EI=avD_O2/AvD_O2, where, avD_O2: arterial to mixed venous difference in P_O2 (mmHg) and AvD_O2: alveolar to mixed venous difference in P_O2 (mmHg). Alveolar P_O2 (P_AO2) was calculated from the standard alveolar air equation.
The El correlated with PaO₂ (r=0.83), AaD_O2 (r=-0.726), and PaO₂ (predicted-observed values, r=-0.704). The EI did not correlate with D_LCO/VA which was measured in separate occasions. Right to left shunt correlated weakly with EI.
avD_O2 and AvD_O2 decreased and AaD_O2 increased as PaO₂ decreased. The EI decreased progressively as PaO₂ decreased and it was 0.5 at PaO₂ 70mmHg indicating that inefficient part for the pulmonary gas exchange overcame the efficient part at this critical point.
These results indicate that the efficiency of pulmonary gas exchange is best reflected by PaO₂, AaD_O2, and PaO₂. Patients with PaO₂ less than 70mmHg may be defined as pulmonary failure.

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It has been established that accumulation of fluid in any compartment within the thorax will reduce transthoracic electrical impedance (Zo). Previously we reported that electrical currents applied simultaneously on bilateral thoracic walls will flux relatively indifferently through respective thorax spaces through studies of the impedance changes during unilateral obstruction of the airway, unilateral induction of experimental lung edema. Based on these results we further studied the ratio of Zo on FRC level between the right and left hemithorax (Left side/Right side) in normal subjects and patients who were suffering from chest disease localized within a hemithorax.
52 and 48kHz alternative currents were simultaneously applied through four electrode configurations on bilateral chest walls. The electrodes attached on the frontal chest surface at the bilateral midclavicular lines and on the back at the level of the xyphoid process and the bilateral midscapular lines.
The ratio of the right and left Zo in normal subjects (N=97, male=56, female=41, age 14-79 year-old) was 1.04±0.08 (mean±one S.D.). The unilateral Zo decreased in cases of pleurisy, lung collapse and with lobectomy and pneumonectomy, and increased in patients of pneumothorax at the disease site of the thoracic wall. Therefore the ratio of the right and left Zo was greater than 1.0 or less than 1.0 in accordance with disease processes within the unilateral hemithorax. The ratio returned to normal valves as a normal condition was regained.
These results again confirm our previous results which suggested that electrical currents applied simultaneously on bilateral thoraces will flux relatively indifferently through the respective hemithorax and suggest that the measurement of the ratio is valuable in clinical evaluation of dynamics of these disease processes in respective hemithorax.

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In 94 coal miners whose chest X-ray classification indicated type P1 to Type C pneumoconiosis, comparative studies on selective alveolo-bronchography (SAB) findings and pulmonary function tests were carried out. Controls consisted of 26 individuals without symptomatic pulmonary disease. Results were as follows.
1. Of 94 pneumoconiosis cases 41 had pulmonary emphysema as a complication (43.6%). This percentage was definitely higher than that of the control group which had pulmonary emphysema in 15.4 per cent. The emphysema which was seen in coal miners pneumoconiosis was centrilobular type in 51.2%, panacinar type in 34.1% and mixed type in 14.6%.
2. Findings of chronic inflammation in the bronchi, recognized on SAB, were seen in 83.7 per cent of pneumoconiosis cases.
3. Even in early stage pneumoconiosis by X-ray classification, emphysematous changes were proved to be present.
4. Emphysematous changes were observed in 50.0% of cases with severely damaged bronchi, in 43.2% of cases with mildly damaged bronchi and in 33.3% of cases with normal bronchi. These findings suggested that bronchial damage was an important factor in the development of emphysema in coal miners.
5. The degree of damage in bronchi and alveoli as shown on SAB showed a tendency to correlate with that of incompetency on the pulmonary function test. Statistical studies by multiple regression analysis showed that stenosis at bifurcations, irregularity of the bronchial wall and spastic narrowing of bronchi and emphysematous changes of the alveoli were related to lowering of the values of FEV_1.0/pred. VC and V₂₅/Ht.
6. SAB was useful for the early diagnosis of bronchial damage and emphysematous changes in alveoli which affect the pulmonary function in pneumoconiosis.

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Scanning electron microscopic study of bronchial glands was carried out. Bronchial tissues from resected lung lobes without bronchial diseases and those with bronchiectatic materials were used. Bronchial glands of cats were also studied. In cases of cats and humans without bronchial diseases, the openings of the glands on the bronchial mucous membrane were usually oval in shape and several ten microus in diameter. The distance between each of them was several hundred microus to 1mm. Diverticula about several hundred microus to 1mm in diameter were found in some bronchial mucous membranes and some openings of the glands were observed at their walls or lower portions.
Ciliated ducts, collecting ducts, mucous tubules, and serous tubules were observed on the fracture surface of bronchial tissues. The luminal surface of ciliated ducts was covered with abundant cilia. On the surface of collecting ducts, short microvilli and polygonal partitions of epithelial cells could be observed. Round openings of secretory tubules with secretory products were scattered on the surface.
Profuse granules were found in the cytoplasm of secretory cells. The granules of serous cells were well demarcated and those of mucous cells had a tendency to be confluent. Scanty microvilli and a few small openings through which secretory substances might have been discharged were observed on the surface of secretory cells.
In the case of bronchiectasis, nonciliated areas were observed around the openings of bronchial glands. In ciliated ducts, hyperplasia of goblet cells was observed. Marked alterations were found in the collecting ducts, and secretory tubules. The top of each of the epithelial cells lining these ducts and tubules showed prominent protrusions toward the lumen. The cells of collecting ducts contained abundant granules about 0.8 micra in diameter in their cytoplasm. These findings might suggest these cells to be accelerated functionally.

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A 54 year old male with stiff-man syndrome was examined in terms of respiratory function. A restrictive pattern on spirograms without marked abnormalities in small airways function (V₅₀, V₂₅, and dynamic compliance) was attributed to respiratory muscle stiffness, because Pes max and static compliance were quite normal. Hypercapnic ventilatory response was markedly blunted, whereas hypoxic ventilatory response was normal. These changes were in accord with findings in arterial blood gases (normal PaO₂ and high PaCO₂). Hypercapnia was probably a product of either excessive CO₂ production or blunted respiratory chemosensitivity to CO₂.
Intravenous administration of diazepam (20mg) induced an increase in VC and MVV and a decrease in V_E, V_T, V_O2, V_CO2, and R. Ventilation and hypercapnic ventilatory response decreased and PaCO₂ increased after the administration of diazepam.
The postmortem examination disclosed diffuse proliferation of glia cells in the anterior columns of the spinal cord. Histology of the medulla oblongata was not available due to so-called “respirator brain.”
These abnormalities in respiratory functions might be a precursor of clinically manifest respiratory failure. Treatment of this disabling disease by diazepam must be performed with great care because of its depressant effect on respiratory chemosensitivity to CO₂.

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An eight-year old boy admitted to our hospital for further examination of left unilateral hyperlucency revealed by chest X-ray. As a result of bronchography, pulmonary arteriogram and pulmonary scincigram, he was diagnosed as Swyer-James syndrome.
At the age of four he was hospitalized for treatment of severe pneumonia. Since that time a chest X-ray had been taken every month for one year. We could observe the course of pathologic formation on the film. The narrowing of the left pulmonary artery began five months after recovery from pneumonia and this was followed by the formation of the distinctive of this syndrome for months later. This case suggests that this syndrome may well be caused by broncho-pulmonary infection.

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