To investigate the correlation of diameters of airways with lung volume and flow rate during forced expiration, serial bronchography and simultaneous spirography with records of exposure were performed.
Expiratory flow rate was calculated from spirogram analyzed by computor. Three groups; normal (9 cases), chronic bronchitis (12 cases) and emphysema (6 cases) were selected as subjects for this study.
The results obtained were as follows:
1) Reducing rate (%/sec) of airway diameters in the early phase of forced expiration:
In the normal group, the rates in the lower lobe were higher than those in the upper lobe and those of small airways were larger than those of large airways.
In the chronic bronchitis group, the rates were generally lower than in the normal and emphysema groups. Such regular relations between different parts of airways, as seen in the normal group, were not observed.
In the emphysema group, the rates were markedly higher than those in the chronic bronchitis and the normal group. The rates for segmental bronchi in the emphysema group were highest. In some cases with emphysema, the phenomenon of expiratory obstruction appeared in spirograms in the early phase of forced expiration, and at that time all the diameters of airways were reducing markedly. Therefore it was suspected that the airways which contribute to the phenomenon were smaller airways than those measured.
2) Time from the beginning of forced expiration to peak flow (T) and the value of peak flow (PF):
Mean value of T in the emphysema group was smallest. Mean value of PF was largest in the normal group and smallest in the chronic bronchitis group. To elucidate the relations between changes in airway diameters and Vmax at low lung volume (V50, V25) further investigations should be made.
The results of this study and our previous report suggest that each of the three groups has a characteristic pattern of airway diameter changes during forced expiration.
In the normal group, most airway diameters reduce almost linearly in the first one second, and those in lower lobe reduce faster than those in upper lobe. On the other hand, small airways reduce faster than large airways.
In the chronic bronchitis group, all parts of airways reduce slowly with various reducing ratios.
In the emphysema group, most of the airways reduce markedly and maximally in the early phase of forced expiration (within 1/3 second), and are in such condition till the end of forced expiration.

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Respiratory and circulatory effects and other side effects of buffer solution, prostaglandin (PG)E₁ and metaproterenol aerosol were compared in the same patients with bronchial asthma.
The effects of infused PGE₁ were also compared with those of inhaled PGE₁ aerosols. Aerosols were inhaled through IPPB (Bennett PR-2) for about ten minutes with dosages of 50μg for PGE₁ and 10mg for metaproterenol. 50μg PGE₁ in a saline solution was infused intravenously for about five minutes.
Airway resistance (R_A), functional residual capacity (FRC) and specific airway conductance (SG_A) were measured by whole body-plethysmograph before and after administration. Systemic blood pressure and heart rate were also examined by sphygmomanometer and electrocardiogram respectively. The conclusions derived are as follows
In eleven subjects, control aerosol (sucrose-menthol-saline without PGE₁) did not show any bronchodilating effects, irritation of throat, or circulatory changes, whereas in the same subjects, sucrose-menthol-saline aerosol with PGE₁ showed bronchodilating effects for ten to thirty minutes. Inhalation of PGE₁ aerosol also showed a slight hypotensive effect, and a productive cough was also seen in most of the subjects.
Therefore, the bronchodilating, hypotensive and other side effects are thought to be due to PGE₁ itself, not due to control aerosol. The bronchodilating effects of PGE₁ aerosol were significantly evident in patients with marked bronchoconstriction.
In some subjects, bronchoconstriction also occurred due to PGE₁ aerosol. However, no correlation was found between such bronchoconstriction by PGE₁ and the cough seen during inhalation.
Intravcnous infusion of 50μg PGE₁ rcvcaled a slight bronchodilating effect of short duration in only six out of twenty subjects. A marked fall of blood pressure, especially in hypertensive patients, and atrial tachycardia of short duration also occurred.
Intravenous infusion of PGE₁ also produced cough in two out of twenty subjects, palpitation in four, and headache in one, respectively.
Inhalation of 10mg metaproterenol revealed marked bronchodilating effect, without circulatory or other side effects.
The bronchodilating potency of 10mg metaproterenol aerosol was thought to be slightly stronger than that of 50μg PGE₁ aerosol in the same 13 subjects. But no significant difference was seen between the percent changes of SG_A after PGE₁ and metaproterenol aerosol. Therefore, the bronchodilating potency of PGE₁ aerosol is about two hundred times stronger than that of metaproterenol aerosol.
Considering about the side effects and ronchodilating potency, metaproterenol aerosol is better suited for clinical application than PGE₁ aerosol.

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The fraction of acid glycosaminoglycans was isolated from the tissue of a benign localized pleural mesothelioma and was analyzed by histological and biochemical means. The weakly PAS-positive substances in the interstitium was digested almost completely with hyaluronidase “Amano”. Disappearance of alcianophilia of the specimen after methylation and the results of staining with alcian blue in graded concentrations of MgCl² indicated the presence of a large amount of hyaluronic acid in the tissue. In the next experiment the tissue from the above pleural mesothelioma was digested exhaustively with pronase. The crude glycosaminoglycan was isolated from the resulting digest by means of fractionation with ethanol and precipitated with cetylpyridinium chloride. The crude glycosaminoglycan was analyzed by column chromatography using Dowex-1. Elution was effected with graded concentratons of NaCl. The 0.5 M-NaCl eluate from the column showed the same mobility as the hyaluronic acid from the human umbilical cord on the membrane of cellulose acetate. Only glucosamine was found in the acid hydrolysate of the 0.5 M-NaCl eluate. It was digested with hyaluronidase “Amano” just as the hyaluronic acid from human umbilical cord. In addition the hyaluronic acid from meothelioma (0.5 M-NaCl eluate) and that from the human umbilical cord had the same infrared spectrum pattern. However the former migrated more slowly than the latter in electrophoresis on paper. The mobility of the former remained unchanged even after repeated digestion with pronase. In gel filtration chromatography using Sepharose 4B it was found that the hyaluronic acid from mesothelioma was eluted prior to the hyaluronic acid from human umbilical cord.
Thus it was suggested that hyaluronic acid from pleural mesothelioma had a larger molecular size than that from the human umbilical cord.

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A 42-year-old house wife was admitted with superior vena caval syndrome. The chest X-ray disclosed tumor masses in the right upper lobe associated with hilar and mediastinal lymphadenopathy.
Investigations revealed persistent hyponatremia, serum sodium level ranging between 112.3MEq/L-130MEq/L.
The patient was suspected to have pulmonary carcinoma associated with a syndrome of inappropriate secretion of ADH.
⁶⁰Co theray on the mediastinum resulted in the disappearance of the superior vena caval syndrome. After superior vena caval syndrome disappeared, ⁶⁰Co therapy on the primary tumor was started. ⁶⁰Co therapy resulted in the improvement of hyponatremia, serum sodium increasing from 113MEq/L to 135MEq/L.
Plasma ADH activity, 5 hours after the water-load, was 8.0μU/ml.
These laboratory data and clinical course suggested the ectopic production of ADH by the pulmonary carcinoma.
Histological findings of the lungs at autopsy were interpreted as oat cell carcinoma. Ectopic ADH production was confirmed by the presence of ADH activity and electron microscopic findings of neurosecretory-like granules in the tumor tissue.

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24才の男子. 喀血を主訴に来院, 胸部レ線で中央陰影の右方への偏位, 右肺野の網状結節状陰影と右肺門部より右方にブラ様の陰影を認めた. ¹³¹I-MAA肺血流シンチ及び肺動脈造影で右肺動脈欠損症を疑い, 大動脈造影で先天性右肺動脈欠損症と確診した. また, ブラ様の変化は左上葉の右胸腔内への嵌頓であつた.

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