Impulsive sounds have been widely used to investigate the acoustic transmission in the elastic bodies. We have recently reported that reverse dispersion was found in the wave forms of discontinuous adventitious lung sounds, i.e., crackles, rales and crepitations.
In this study impulsive sounds were generated by electrical spark discharge at the needle-gap inserted into the canine air way, and the wave forms on the chest wall were analysed. The level of voltage on spark discharge was 7.5kV, and the peak level of sound pressure was about 110dB at 1cm distance from the electrode in the free air field. The duration of the wave on the chest wall was 10msec or more and it consisted of three different phases.
The first phase, which was synchronic with the timing of discharge, was considered to be caused by mixing of the electric wave on spark discharge.
The second phase was the maximum wave in terms not only of amplitude but duration. Reverse dispersion was shown as well as in discontinuous adventitious lung sounds. This phase was regarded basically as a surface wave and not as a body wave directly derived from the source. It was also estimated that discontinuous adventitious lung sounds had characteristics of a surface wave.
The physical meaning of the third phase, which showed dumped oscillation in many cases, is uncertain.

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In order to examine the diagnostic value of broncho-alveolar lavage fluid for lung diseases, we performed broncho-alveolar lavage by two methods in 11 normal volunteers (aged 23.9±0.8 years), 30 patients without diffuse interstitial fibrosing pneumonitis (non-DIFP patients, aged 59.6±11.3 years), and 12 patients with diffuse interstitial fibrosing pneumonitis (DIFP, aged 59.8±5.8 years), and analyzed the cellular and biochemical components of the lavage fluids. In Method I, we infused 25ml of saline into the basal brounchus through a bronchofiberscope which was inserted without wedging the tip, and recovered the infused fluid by aspiration with an aspirator. In Method II, after the bronchofiberscope was wedged into a segmental bronchus, 50ml of saline was infused into the segment. The infused fluid was gently aspirated by a syringe. In both methods, the lavage procedures were repeated 3 times.
1) Recovery of the infused fluid from the non-DIFP patients in Method I and II was 15.1±5.9% (mean±SD) and 44.2±11.6%, respectively.
In Method II, the percentage recovery from normal volunteers was fairly constant (65.7±8.9), and significantly higher than those from the non-DIFP patients and patients with DIFP (p<0.001). The low value in the latter two groups may be due to anatomical and physical changes in the lung tissues due to various causes, such as aging and pathological changes.
2) The mean numbers of cells recovered from the non-DIFP patients by Methods I and II were 3.1±3.2×10⁶ and 21.4±11.8×10⁶, respectively. The increase of cells by Method II was mainly represented pulmonary alveolar macrophages (PAM).
Increases in both number and percentage of neutrophils, lymphocytes, and eosinophils were seen in patients with DIFP, while the number of PAM did not significantly increase. This suggests that an inflammatory process exists in DIFP.
3) Lecithin content of the lavage fluid by Method II was 2.5 times that by Method I. In Method II, total lecithin and disaturated lecithin contents of lavage fluid from normal volunteers were about 2 and 1mg, respectively.
There was no significant effect of smoking on the lecithin content of the lavage fluid. The lecithin contents of lavage fluids from the non-DIFP patients and patients with DIFP were about 40 and 30% of that from normal volunteers.
These results indicate that bronchial and alveolar components are predominant in the lavage fluid obtained by Method I and II, respectively. However, it is postulated that only about 20 to 30% of alveolar components could be obtained even by Method II.

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We experienced 66 cases of pulmonary complication postoperatively in 463 surgical cases. The relations between complications and some factors of patients were studied clinically. The incidence of complications was 7.4% in patients under 50, however in patients over 60 it was 30.6%. Atelectasis and pneumonia were most commonly observed. 6 cases of ARDS which showed edematous shadow roentgenologically were encountered, in 5 of those esophageal surgery had been performed. Bacteremia due to the insufficiency of the anastomosis in digestive organ was considered to be the main contributory factor to ARDS. Cytological investigation in ARDS was necessary to estimate the extent of concomitant bacterial infection in lung.

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Lung lavage fluid was obtained from normal rabbit lungs by transbronchial washings with saline. After elimination of cellular components by centrifugation, it was concentrated and sterilized with a millipore filter. The fluid was used as alveolar lining material. IgG-rich fraction was separated from the alveolar lining materials by column chromatography with Sepharose 4B. Alveolar macrophages from normal rabbit lungs were incubated with Staphylococcus aureus in RPMI 1640 and 10% heat-inactivated fetal calf serum without antibiotics. The ratio of the cells and the bacteria was 1:10. After 45 minutes, nonphagocytized bacteria were lysed by lysostaphin, which does not enter phagocytes. The alveolar macrophages which phagocytized bacteria were stimulated with alveolar lining materials, IgG-rich fraction or normal rabbit serum. Intracellular killing was determined by comparing the number of viable bacteria remaining in the cells 2 hours after stimulation.
Normal alveolar macrophages killed 25% of the bacteria during the incubation time. On the other hand, when the cells were stimulated with these three stimulants, the intracellular killing was enhanced further and about 65% of the bacteria were killed (P<0.015). However, there were no differences among the effects of three stimulants. The enhanced intracellular killing was correlated with the intensity of NBT reduction by the cells.
These results and our previous results suggest that alveolar lining materials enhance the activity of the intracellular killing of alveolar macrophages, that the factor in the materials is IgG, and that the mechanism of the killing is correlated with superoxide production by the cells.

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Serum angiotensin-converting enzyme (ACE) level was measured in various diseases to evaluate its diagnostic value in sarcoidosis.
The measurement of the enzyme activity was performed after Cushman's spectrophotometric assay, but borate buffer was used instead of phosphate buffer, because the buffering action of phosphate buffer is insufficient at pH 8.3, the optimal pH of the reaction.
Diseases examined were sarcoidosis (64 active and 21 inactive), pulmonary tuberculosis(25), chronic obstructive lung diseases(20), silicosis(29), liver cirrhosis(24), leprosy(50) and hyperthyroidism(21). The Mean±SD of the S-ACE level for 63 normal control subjects was 31±9U, and the enzyme activity was markedly elevated in active sarcoidosis (53±14U). However, it was also elevated in liver cirrhosis(48±11U), silicosis(45±10U) and hyperthyroidism(38±12U).
In active sarcoidosis, elevated ACE level decreased during corticosteroid therapy with improvement of chest radiological findings, and this decrease also occurred in patients who had normal ACE levels before therapy.
It was concluded that measurement of S-ACE level is a simple and useful diagnostic tool for sarcoidosis, although elevation of the S-ACE level is not specific for sarcoidosis. Futhermore, the decrease of the enzyme activity during corticosteroid therapy seemed to be characteristic of sarcoidosis and confirm the diagnosis of this disease.

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A 49 year-old female was admitted on March 20, 1979 with a chief complaint of loud cough, purulent sputum and a constant “rattle in the throat”. Chest roentgenogram showed prominent dilatation of trachea and main bronchi. The width of the trachea was larger than that of the vertebral column. The bronchogram showed unusually wide trachea and left main bronchus and outlines of sac-like recesses. The largest widths of the trachea, right and left bronchi were 50, 15 and 30mm. The bronchoscopic examination showed an enormous tracheal lumen and sacular dilatation of the wall.
Generally, tracheobronchiomegaly has been ascribed to a congenital defect of elastic and muscle fibers of the trachoeobrnchial tree by most authors. But in our case, in addition to this, chronic airway infection was thought to be another important etiologic cause.

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A case of Behçet's syndrome associated with pulmonary artery obstruction and aneurysm was reported.
A 30 year-old man began to have ulcers in the mouth and the scrotum three years prior to admission. On April 17, 1978 he was admitted with complaining of cough, bloody sputumm and high fever. Chest roentgenogram showed abnormal shadows in the middle and lower fields of both lungs. Pulmonary angiography demonstrated the obstruction and aneurysm of the pulmonary arteries. These findings were consistent with a diagnosis of vasculo-Behçet.
Predonisolone was administered, and the symptoms and the pulmonary manifestations improved for a while. Three months after starting treatment, aneurysm in pulmonary artery began to reappear and become larger in spite of continuation of the steroid treatment.

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