Thromboxane A₂ (TxA₂) and prostacycline (PGI₂) are two novel prostaglandin (PG)-like substances which are derived from arachidonic acid via PG endoperoxides (PGG₂ and PGH₂). TxA₂ is a potent labile platelet aggregator and vascular constrictor, whereas PGI₂ is a potent labile antithrombotic compound and vasodilator.
In the present work we investigated the effect of thromboxane synthetase inhibitors, OKY-046 and OKY-1580, on the action of bronchoactive agents in guinea pig tracheal strips, and on arachidonic acid metabolism through isolated perfused guinea pig lung lobes.
1) OKY-046 and OKY-1580 attenuated histamine-, serotonin-, acetylcholine-, bradykinin- and PGF_2α-induced contractile responses in guinea tracheal strips dose-dependently.
2) OKY-046 and OKY-1580 potentiated isoproterenol, salbutamol and PGE₂-induced relaxation responses in guinea pig tracheal strips dose-dependently.
3) OKY-046 and OKY-1580 inhibited the biosynthesis of TxA₂ and accelerated the production of 6-keto PGF_1α from arachidonic acid through isolated perfused guinea pig lung lobes.
The above results suggest that OKY-046 and OKY-1580 might become useful therapeutic agents for the treatment of pulmonary thromboembolism and chronic obstructive lung diseases.

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To elucidate the hemodynamic characteristics of acute pulmonary hypertension due to miliary embolism, pulmonary vascular input impedance was computed by means of Fourier analysis of individual pressure and flow wave in dogs.
Seven healthy dogs weighting 8.5-17.5 (mean 11.8) kg were anesthetized with sodium pentobarbital (25mg/kg), and thoracotomy was performed at the left 5th intercostal space under artificial ventilation. A properly fitted electromagnetic flow transducer was placed around the pulmonary trunk and a micro-tip pressure transducer (pc-350) was set in the pulmonary artery near the flow transducer. A femoral vein was exposed, and doses of 0.3-0.6ml (50mg/ml) of lycopodium spore suspension was given repeatedly as needed. The degree of pulmonary circulatory disturbance was graded on the basis of the ratio of peak pulmonary arterial to peak aortic pressure. This ratio was used to assess relative pressure overload of the right ventricle, that is, in the control group less than 0.25, mild group 0.25-0.40, and moderate group greater than 0.40.
A four component lumped analog model for the pulmonary vascular bed, R₁-L-C-R₂, was employed, which consisted of a resistance R₁ equal to the characteristic impedance in the proximal pulmonary artery, a fluid inertia L combined in series, parallel combination of a peripheral resistance R₂ and a lumped compliance C. These parameters of an analog model were calculated by the computer by the method of least squares from the pattern in pulmonary vascular impedance.
In the mild and moderate group, pulmonary vascular input impedance as changed with an elevation of pulmonary areterial pressure compared with the control group. From the above-mentioned model simulation, R₂ increased while C decreased markedly, according to the grade of pulmonary hypertension. The characteristic impedance, as estimated by averaging impedance spectrum at 7-11Hz, was unchanged. In this state, however, frequency at which the first input impedance showed minimum value shifted to a higher frequency.
Considering this hemodynamic mechanism, in acute pulmonary hypertension due to miliary embolism, the peripheral resistance increased remarkably and the compliance of the proximal pulmonary artery decreased. It appeared that the proximal pulmonary artery responded to induced pulmonary hypertension with an increase of its radius and cross-sectional area.
In conclusion, it is possible to estimate local alterations in the pulmonary vascular bed by means of pulmonary vascular impedance analysis in pulmonary hypertension and it is very reasonable that the energy output of the right heart is more precisely expressed in terms of pulmonary vascular input impedance than pulmonary vascular resistance.

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1. In our series of 14 cases of farmer's lung, it was shown that serum gammaglobulin, especially IgG and IgA, as well as serum complement activity were increased in more than half of the cases.
Serum precipitating antibodies to thermoactinomycetes were positive in all cases, mainly to Micropolyspora faeni. Some patients showed precipitating antibodies to other antigens associated with other types of hypersensitivity pneumonitis in addition to Micropolyspora faeni and Thermoactinomyces vulgaris. Almost all cases were nonsmokers.
2. Effects of smoking habits on serum antibody prevalence in farmers and on lymphocytosis in bronchoalveolar lavage fluid in cases of sarcoidosis were analysed. Our epidemiological study of farmer's lung showed that serum antibody prevalence was significantly increased in nonsmokers. There was significant difference in the findings of lymphocytosis in lung lavage fluid between nonsmoking and smoking sarcoidosis patients, that of smokers being decreased.
On the basis of these facts, the effects of smoking on the pathogenesis of hypersensitivity pneumonitis were discussed with a review of the literature.

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Differential diagnosis of alphafetoprotein (AFP)-producing chest tumors was investigated using combined characterization of serum lactate dehydrogenase (LDH) isozyme pattern and binding capacity of AFP to Concanavalin A (Con-A). Studied cases included mediastinal yolk sac tumors and AFP-producing lung cancers, as well as hepatoma as a control.
Mediastinal yolk sac tumor showed marked increase of LDH-1, and Con-A nonbinding AFP was about half of the total AFP. AFP-producing lung cancers showed normal LDH isozyme patterns with high LDH-2, 3, 4, and Con-A nonbinding AFP was also about half. In hepatoma there was characteristic increase of LDH-5 and 0-10% of AFP was found to be Con-A nonbinding.
From these results, combined characterization of LDH isozyme pattern and binding capacity of AFP to Con-A appears useful in the differential diagnosis of AFP-producing chest tumors.

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Four out of 11 cases of Wegener's granulomatosis experienced during the past 15 years had tracheobronchial involvement. Six cases had lung lesions and four of those 6 had tracheobronchial lesions.
These lesions were demonstrated focally or widespread throughout the bronchial tract, from the trachea as far as the subsegmental bronchi. In the acute phase, mucosal redness, swelling, ulceration, granuloma formation and narrowing were observed, while in the chronic phase, cicatricial stenosis was seen bronchoscopically.
Most tracheobronchial lesions developed simultaneously with lung lesions in the acute phase, but in one patient, tracheal stenosis due to granuloma progressed insidiously and dyspnea occured abruptly, when systemic features of the disease suggested remission.
Tracheobronchial involvement has been regarded as a rare manifestation of Wegener's granulomatosis, but hereafter it will probably increase in frequency because the survival of cases of this disease will be extended due to progress of treatment.

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This study was conducted to clarify the acoustic features of adventitious sounds in patients with DPB (diffuse panbronchiolitis). We analysed the lung sounds by phonopneumography using a soundspectrograph.
Among fourteen patients, crackles were observed in all patients and wheezes in eleven patients. Crackles occurred on early inspiration but no fixed tendency was observed on expiration. Crackles were not affected by posture and were transmitted over a wide area. The average number of crackles per inspiratory phase was 11.6 and per expiratory phase was 9.1. The frequency of the sound was 200Hz to 1, 150Hz. The number and frequency of the crackles in DPB were less than in fibrosing alveolitis. Therefore, crackles in DPB were regarded as coarse crackles. This was confirmed by wave-form analysis using a zero-crossing method.
Wheezes were obtained throughout the respiratory cycle in both inspiratory and expiratory phases and had overtones which were integral multiples of the fundamental frequency. Acoustically, wheezes in DPB resembled those of asthma. Adventitious sounds in DPB may derive from the larger airways.

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A 67-year-old female was admitted because of abnormal chest X-ray findings, which had been found thirty years previously. She complained of cough and sputum about one and half year ago.
Lateral tomography showed three well-circumscribed elliptical masses of uniform density in left S⁶. Her bronchogram revealed that the abnormal shadows were independent of the branches of B⁶, and it was also suggestive of chronic bronchitis. Left S⁶ segmentectomy was carried out. The abnormal shadow on chest X-ray film turned out to be a dilated bronchial structure, “bronchial mucocele”. The exact connection between the cysts and the proximal part of left B⁶ broncus was not evident by gross examination. However microscopic examination of serial sectionings revealed a pinhole connection between the cysts and the proximal part of bronchus. We considered it was not a functional opening because of the size of the connection and the results of gross examination. Therefore we would like to diagnosis this case as “bronchial atresia”. The etiology of this case is difficult to explain. There was no remarkable cause of the stenosis around the tiny connection such as inflammation or neoplasm. As a possible cause for this atresia, we prefer developmental error to acquired factor.
Fourteen cases, including our case, have been reported in the Japanese literature. We discussed the clinical features of bronchial atresia and emphasized the characteristic aspects on chest X-ray examination.

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A 44-year-old housewife was admitted to Maebashi Red Cross Hospital complaining of cough, sputum and dyspnea. Her husband had similar symptoms about that time. On admittion she was orthopneic, and physical examination revealed dry rales in the chest. Laboratory data showed eosinophilia and elevated erythrocytes sedimentation rate, cold agglutinin titers and LDH levels in the peripheral blood.
Arterial blood gas studies and pulmonary function tests disclosed hypoxemia and decreased vital capacity. The chest X-ray film showed diffuse bilateral nodular and macular shadows with pleural changes. Immunological studies revealed elevation of serum IgM and IgA levels and negative conversion of skin reactivity to PPD.
Mycoplasma pneumoniae infection was confirmed by a change in the Mycoplasma hemagglutination titers from 1:1280 to 1:40 during the clinical course.
An open lung biopsy was done on the 48th hospital day. Microscopic examination of the lung tissue disclosed some findings as follows.:
1) Some bronchiolar walls were infiltrated by mononuclear cells and eosinophils.
2) Alveolar walls were slightly thickened with mononuclear cell infiltration.
3) Small epithelioid cell granulomas were scattered in the specimen.
4) Mason's bodies were seen along the alveolar ducts.
This patient with Mycoplasma pneumoniae infection is very interesting because it may be the first case, to our knowledge, to show granulomatous interstitial pneumonia with Masson's bodies resembling pulmonary lesions of hypersensitivity pneumonitis.

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A 78-year-old man was admitted to our hospital in October 1979 complaining of a tumor on his right leg with central ulceration. Except the skin lesion the results of his physical examination were normal and there was no peripheral lymphadenopathy. Routine laboratory examinations revealed normal differential leukocytic counts, urinalysis and blood chemistry. Biospy of the skin revealed non-Hodgkin's lymphoma. Subsquently radiation therapy was started and resulted in the regression of the skin lesion. In July 1980 multiple skin lesions developed, and VEMP therapy resulted in alternating regression and exacerbation. In June 1981 his chest roentgenogram showed multiple small nodular lesions. At the end of August 1981 he suffered cough, puta and fever. Fiberoptic bronchoscopy revealed a tumor occupying the bronchus (left B⁵). He died on September 7, 1981. At the autopsy his lung revealed multiple nodular lesions and a tumor obstructing left B⁴ and B⁵a. His autopsy diagnosis was extranodal non-Hodgkin's lymphoma.
Malignant lymphoma infiltrating the lung is not so rare but tumor formation in the bronchial lumen is extremely rare. On fiberoptic bronchoscopy this endobronchial mass was seen without invasion in the surrounding bronchus. The mass consisted of malignant lymphoma cells (pleomorphic type of diffuse lymphoma).

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Ultrastructural examination of bronchoalveolar lavage fluid confirmed the diagnosis of a 23-year old man with pulmonary eosinophilic granuloma. The diagnosis of Histiocytosis-X (H-X) had been previously established by open lung biopsy. A few H-X cells were identified by electron microscopy among alveolar macrophages and other inflammatory cells obtained by bronchoalveolar lavage. H-X cells contained characteristic cytoplasmic granules, pentlaminar structure of constant width scattered in the periphery of cytoplasm and lacked the pigment bodies that were often seen in the cytoplasm of macrophages.
These H-X cells are more active than Langerhans cells which are seen in normal epidermis or fibrotic lung tissue and migrate into air spaces and among bronchiolar epithelium, as shown by their occurence in bronchoalveolar lavage fluid.
Ultrastructural examination of bronchoalveolar lavage fluid is considered to be an important diagnostic procedure in the diagnosis of pulmonary eosinophilic granuloma, eliminating the need for an open lung biopsy.

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An abnormal chest X-ray shadow in a 54 year-old man was pointed out in 1977. Though the abnormal shadow increased gradually, he did nothing about it as he had no complaints. In June, 1980, he visited our outpatient clinic, and left intrapleural tumor was diagnosed after some examinations including chest CT. The tumor was resected in July 1980. Pathologically, the resected tumor was a localized malignant fibrous histiocytoma of the chest wall projecting into the thoracic cavity.
A second operation was performed in May, 1982 because of recurrence. Malignant fibrous histiocytoma was recognized pathologically, the resected tumor was located on the left diaphragma, but no other metastasis was found.
This is a rare case of malignant fibrous histiocytoma of the chest wall projecting into the thoracic cavity.

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