Although the location and mechanism of increased lung vascular permeability in pulmonary microembolism are still controversial, it has been suggested that vascular permeability could increase in open perfused portions of the microvascular bed by physical injuries. To test this hypothesis, unilateral microembolization was induced in anesthetized dogs by injected glass beads (80-120μm in diam., 0.1g/kg) into the right pulmonary artery and the filtration coefficient of the nonebolized left lower lobe was measured according to weight transient method of Drake and his associates. The filtration coefficient of the left lower lobe was doubled 30 minutes after microembolization, and the calculated vasculated resistance of left lower lobe did not change significantly. To further investigate the contribution of microvascular endothelial cell injury to a sequence leading to the heightened pulmonary vascular permeability, the concentration of 6-keto PGF_1α in the arterial blood was measured by radioimmunoassay and found to increase progerssively following microembolization. Pretreatment by indomethacin (10mg/kg) resulted in an increase in the filtration coefficient not only 30min but also 60min after embolization. The calculated arterial resistance increased significantly immediately after microembolization. Coutinuous infusion of PGI₂ methyl ester (20ng/kg/min) prevented an increase in the filtration coefficient observed at 30min following microembolization. By administration of mepyramine maleate, histamine H₁-blocker, (3.0mg/kg bolus+1.5mg/kg/hour) neither the filtration coefficient nor the concentration of 6-keto PGF_1α increased following microembolization.
Based on these results, the author concluded that:
(1) The lung vascular permeability increased in the nonembolized portion after microembolization. (2) Endogenous PGI₂ could be responsible for protection against increased lung vascular permeability induced by microembolization. (3) The release of endogenous PGI₂ could be mediated by histamine through H₁-receptor action. (4) Although glass beads activate Hageman factor resulting in activation of kinin system, histamine could play an important role in increased lung vascular permeability following microembolization in the present experiment.

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Slow-reacting substance (SRS) is released from lung and other tissues. It was thought that SRS might play an important role as a mediator of immediate hypersensitivity reactions in asthma and other symptoms. Immunologically generated SRS was named as a slow reacting substance of anaphylaxis (SRS-A). Recently, SRS-A was identified as the mixture of substances derived from arachidonic acid and named leukotrienes C₄ and D₄ (LTC₄ and LTD₄). The present investigation was conducted to explore the various physiological actions of synthetic LTC₄, D₄ and E₄ using anesthetized mongrel dogs.
Fifteen mongrel dogs, weighing 10-15kg were anesthetized with sodium pentobarbital (25mg/kg), the respiratory muscles were paralyzed with succinyl choline chloride, and the lungs were ventilated through a tracheal tube with a volume type respirator at a constant tidal volume (16-20ml/kg). The tracheal pressure (Ptr) was measured at the orifice of the tracheal cannula. Catheters were inserted into the left femoral artery and vein, measurement of systemic arterial blood pressure (Psyst) and drop infusion or injection of drugs were conducted, respectively. The left hemithorax was opened. The catheter was inserted into the pulmonary artery trunk and pulmonary artery pressure (Ppa) was measured using pressure transducer. A non-cannulating electromagnetic flow probe was placed around the ascending aorta and cardiac output (Qaorta) was measured
1) Ptr showed a marked increase by intravenous injection of LTC₄, LTD₄ and LTE₄, and their degree of increase was as follows: LTD₄>LTC₄>LTE₄.
2) Psyst showed a significant decrease by intravenous injection of LTC₄, LTD₄ and histamine, on the other hand it showed a slight increase by intravenous injection of LTE₄ and PGF₂α.
3) Ppa showed a significant decrease by intravenous injection of LTC₄ and LTD₄, while it showed an increase by PGF₂α, histamine and LTE₄.
4) Qaorta ahowed a dcrease by intravenous injection of LTC₄, LTD₄ and LTE₄, and their degree of decrease was as follows: LTD₄>LTC₄>LTE₄.
The above results suggest that leukotrienes may play very important roles in pathological conditions such as bronchial asthma or anaphylactic shock.

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Eosinophilic granuloma, Hand-Schüller-Christian disease and Letterer-Siwe disease have generally been included in the disease entity of histocytosis X. This concept, however, is not necessarily acceptable. As we have had no experience of a case whose histology and clinical features changed from one to another, we have separately observed these 3 diseases.
This report investigates eosinophilic granuloma, a relatively rare disease in Japan, in regard to its natural history, disease activity and effect of treatment. The cases were collected from all over the country in the cooperation with doctors who experienced these cases. The subjects of this study included 49 cases with histological evidence and the period of observation covered one year to 17 years.
This study was intended to reveal disease characteristics in this country. The sex ratios, ages and clinical features were similar to those in world literature. Points to be further investigated are as follows.
1) The description of shadows varies with reports. A unified description may be desirable.
2) Many cases were treated with corticosteroids with varying doses and duration. Deaths were found only in the treated group. Indications of corticosteroids should be investigated.
3) As mentioned before, the features of the 3 diseases should be investigated separately in clinically and pathologically diagnosed cases. Inclusive incorporation as an entity of histiocytosis X is not appropriate at present.

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A total of 76 chest X-ray films of 31 cases with eosinophilic granuloma were reviewed.
The main features of the disseminated shadows in lungs were ill-defined nodular shadows and ring shadows including those larger than 10mm in diameter. The ring shadows were not always round and many of them were distorted in configuration. In 75% of cases disseminated shadows were recognized throughout entire lung fields, but the remainder showed predominant distribution in upper and middle lung fields. The changes in the lungs were associated with exacerbation in some cases but improvement in others. Pneumothorax was found in 6 cases including one case of bilateral occurence.

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Histopathological observations were carried out on 42 collected cases of eosinohilic granuloma of the lung, from the standpoint of histogenesis of the granulomas. The chief components of the eosinophilic granulomas are Langerhans' cells which have markedly indented nuclei and Birbeck's granules in the cytoplasm. Fine reticulin fibers are produced surrounding the cells, which will turn later to collangenous fibers. Various numbers of eosinophils and a few lymphocytes are accompanied.
The granulomas are often formed in the peribronchiolar walls where Langerhans' cells were reported to be found in the normal lung. The lesions frequently develop along the respiratory bronchiolar walls and alveolar ducts, destructing and replacing the wall constituents, with consequent dilatation of the airway lumens partly due to desquamation of lining granulation tissue. Cystic change with granulomatous wall which are the peculiar histological feature to the disease, are thus formed. In late stage, Langerhans' cells become atrophic or desquamated, remaining fibrous cystic changes with a few eosinophils in the walls.
The other type is nodular lesion, the initial site of which is not sure but may be in the bronchiolar wall. The alveolar walls are infiltrated and thickened accompaneid by filling of involved alveolar spaces by histiocytic cells and eosinophils, finally forming nodular lesion as a whole. They transform into massive scars with surrounding emphysema in late stage.
In the initial stage of the disease, it will progress but soon turn to regressive phase remaining fibrous change. Two autopsy cases who died of concommitnat bacterial pneumonia or heart failure, revealed only fibrous change throughout the lung without active change anywhere.

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The electronmicroscopic structure of bronchial cilia was studied in patients with various diseases of the respiratory tract and normal subjects.
Ciliary abnormalities, including compound cilia, disorganized cilia, cilia beating in abnormal directions and cilia with abnormal cytoplasmic matrix, were statistically assessed. Incidence of compound cilia and cilia beating in abnormal directions in patients with respiratory tract disease was higher than in normal subjects. In patients with chronic respiratory infection with a history of over 2 years, incidence of compound cilia was significantly higher (p<0.05) in smokers compared with nonsmokers. In patients with immotile cilia syndrome lack of dynein arms and high incidence of cilia moving in abnormally directions were characteristic features. In patients with rubulla, 25% of cilia showed absence of ciliary membrane.
Thus, such findings suggests that respiratory infection produces significant changes in the axoneme, which are increased by smoking in patients with chronic infection, while ciliary abnormality observed in patients with immotile cilia syndrome reflects congenital defect in ciliary growth or genesis, and that rebella virus destroys bronchial cilia.

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A case of diffuse normolipemic plane xanthoma associated with multiple myeloma and pulmonary fibrosis was reported. The patient was a 61-year-old male complaining of general fatigue and yellow-colored skin.
The erythrocyte sedimentation rate was 158mm/hr. The serum protein was 8.4g/dl and a monoclonal pattern was observed in γ-globulin area. The serum lipid level was normal. The bone marrow examination showed typical myeloma cells. Diagnosis of IgG kappa type multiple myeloma was made by immunoelectrophoretic examination of the serum and urine. The skin biopsy specimen showed typical foam cells. His chest roentgenogram revealed diffuse micronodular shadows in the bilateral lower lung fields.
Pulmonary function studies showed normal total lung capacity, residual volume, vital capacity and FEV_1.0. Airway resistance and static compliance were normal, too. But diffusing capacity was markedly decreased. Lung specimens obtained by transbronchial lung biopsy revealed interstitial fibrosis. There were no amyloid deposits. Serum HDL-Paraprotein and VLDL-Paraprotein immunocomplexes were demonstrated by passive haemagglutination test.
In our case, this interaction may have resulted in autoimmune dyslipidemia, diffuse plane xanthoma and pulmonary fibrosis. The pulmonary involvement of diffuse plane xanthoma associated with myeloma is rare. In the literature, our case is the first report in Japan.

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A case of allergic bronchial asthma and contact dermatitis due to metallic cobalt is reported. This case report is the first in Japan.
A 38 year-old man was employed as a powder handler in a factory manufacturing hard metal tools. Two weeks after starting this work, he developed persistent contact dermatitis of the neck, arms and face. And two years and two months after its onset he developed bronchial asthma. The asthma attack appeared at night, and cleared up by halting work and drug treatment, and recurred on returning to work. His serum IgE-RIST during attack was high and the patch test was positive for cobalt. This case was diagnosed as occupational allergic bronchial asthma due to metallic cobalt. Non-specific irritative bronchial asthma due to hard metal dusts in the literature is discussed.

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A rare case of primary hemangioma of the diaphragm is reported. A 67 year-old female was admitted to the hospital because of right hypochondriac pain and general fatigue in February, 1980. A chest X-ray film showed deformity of the right diaphragm. A liver cyst was suspected, but the symptoms subsided and she was discharged. She was readmitted with a recurrence of right hypochondriac pain in April, 1982. No additional change in the chest X-ray film was noticed. Pneumothorax and pneumoperitoneum disclosed a tumor of the diaphragm. A round, smooth-surfaced tumor was resected.
The tumor was 6×4.5×4cm in size and 60g in weight. Macroscopically, it was encapsulated and conisted of a coagulated and necrotic mass. Microscopically, vascular structures were found in the peripheral area of the tumor. A diagnosis of hemangioma was made.

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53歳, 男性, 25年間, トンネル工事に従事. 高度の呼吸困難を主訴として入院. 胸部レ線で肺門部より両側中下肺野に拡がるびまん性微細粒状陰影を認める. 経気管支肺生検により肺胞腔内に充満したエオジン好性でPAS染色陽性の顆粒状物質を認め, 肺胞蛋白症と診断した. 体外循環を併用して全身麻酔下に気管支肺胞洗浄を行い, 軽快せしめた.

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