A single dose of 50mg/kg Monocrotaline was injected i.p. in male S-D rats aged 5-6 weeks. Pulmonary hypertension manifested in almost all rats 4 weeks after injection of monocrotaline. The systolic and mean pressures of the pulmonary artery were 57mmHg and 38mmHg respectively. The weights of right ventricles and the wall thickness of the pulmonary trunk in monocrotaline-treated rats were significantly greater than those of normal rats.
Morphological changes due to this agent were seen in the pulmonary alveoli and pulmonary vascular system. Pulmonary vascular changes: The changes in pulmonary vasculature of monocrotaline-treated rats included medial thickness and perivascular edema of pulmonary artery, vasoconstriction, muscularisation of arteriole, vascular obstruction and arteritis. Ultrastructurally, changes in endothelial cells of the artery were particularly noticeable. Vesicles and mitochondria increased in the cytoplasm of endothelial cells. Cell nuclei were sometimes significantly enlarged with scanty chromatin which was suggestive of loss of endothelial function. Other than these findings, these cells had various patterns, they were almost normal, showed apparent cyst formation in the cytoplasm which compressed the nuclei, had vacuolation, contained intensely heterotypic nuclei, revealed a tendency to cell destruction, or contained abundantly Weibel-Palade bodies. All of these findings seemed to be directly related with the increased vascular permeability.
Alveolar changes: Histological examination of the alveoli revealed the pulmonary edema, intra-alveolar haemorrhage, proliferation of alveolar cells and multiplication of mast cells. Ultrastructurally the proliferation of type B alveolar epithelial cells increased in monocrotaline-treated rats compared to those in normal rats, suggesting slightly larger size of individual cells with abundant lamellar inclusion bodies. Vacuoles were also seen in the cytoplasm of these cells, in addition to frequent evidence of marked mitochondrial development. Ultrastructurally vacuoles and micropinocytotic vesicles increased in general in the endothelial cells of the capillary. Mast cells were rarely seen in the alveolar septa of normal rats, but proliferation of mast cells rich in granules having strong affinity for osmium was remarkable in the alveolar septa in monocrotaline-treated rats.
These findings were also believed to be involved greatly in the increased capillary permeability and occurrence of alveolar interstitial edema.

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SRS-A (Slow Reacting Substance of Anaphylaxis) is an important mediator in bronchial asthma and in anaphylactic shock. The structure of SRS-A was recently shown to be leukotriene (LT) C₄ and/or LT D₄. In present investigation the effect of synthetic LTC₄ and LTD₄ on isolated perfused rabbit aorta and pulmonary artery strips was studied.
Male rabbits, weighing 2.7-3.9kg, were killed. The pulmonary artery and descending aorta were removed, cut spirally, suspended in a bioassay glass chamber and superfused with Krebs-Henseleit solution at 37°C saturated with oxygen and carbon dioxide (95:5, v/v).
1) LTC₄ and LTD₄ elicited contractile responses in rabbit aorta and the pulmonary artery strips dose-dependently.
2) LTD₄-induced contractile responses in rabbit aorta and pulmonary artery were 5 to 10 times longer than those induced by LTC₄.
3) Prostaglandin F_2α-, angiotensin II-, epinephrine- and norepinephrine-induced contractile responses in rabbit aorta and pulmonary artery were markedly potentiated with continuous infusion of LTC₄ and LTD₄. The above results suggest that LTC₄ and LTD₄ may play an important role in pathological conditions such as bronchial asthma and anaphylactic shock.

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Cytophotometric Fulgen-DNA measurement was carried out on mesothelial cells from the pleural surface and effusion in 27 autopsy cases (malignant pleuritis: 9, non-malignant: 18). By evaluating nuclear DNA amounts with a cellular activity index, the cell kinetics of mesothelial cells in pleuritis was studied.
In non-malignant pleuritis, mesothelial cells in effusion always showed higher activity than on the pleural surface and both showed a significant decrease of activity with progression of the inflammatory stage of pleuritis. In malignant pleuritis, however, the activity of the latter was often significantly higher than in the former and this reversal increased as the pleural inflammatory stage develops. This difference is probably due to various factors such as pleural metastasis, tumor invasion, or continuous and intensive pleural reactions caused by neoplastic proliferation.

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We have invented a quantitative inhalation apparatus for small animals. Experimental ^99mTc-albumin inhalation in anesthetized guinea pigs revealed that the drug can be delivered efficiently by ultrasonic nebulizer to the lung with the aid of a volume-type respirator. Using this apparatus it was easy to monitor the airway pressure concomitantly with various hemodynamic parameters. It is now apparent that our new apparatus could be an inexpensive and effective tool for both physiological and pharmacological studies on experimental asthma in small animals.

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In a previous investigation we reported the usefulness of the measurement of adenosine deaminase (ADA) activity in patients with pleural effusion, and demonstrated that ADA activity in pleural effusion from patients with tuberculous pleuritis was significantly higher than that of patients with carcinomatous pleuritis.
In the present investigation we measured ADA activity in pleural effusion and peripheral serum from 30 male Japanese albino rabbits with experimentally-induced pleuritis.
1) Pleural effusion was obtained from rabbits injected with complete Freund's adjuvant(CFA), acetic acid or λ-carrageenin to the pleural cavities, while no effusion obtained from rabbits in saline was injected pleural cavities.
2) The mean value and standard deviations of ADA activity in pleural effusion induced by CFA was 78.85±39.01U/L, while that induced by 2% acetic acid and λ-carrageenin was 18.03±3.17U/L and 11.06±4.81U/L, respectively. There were significant differences between the former group (CFA) and the latter two groups (2% acetic acid and λ-carrageenin).
3) Serum ADA activity in these three groups did not show any significant changes before and after drug injection into the pleural cavity during 1 week observation period.

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Two cases of granulomatous mediastinitis and two cases of fibrosing mediastinitis were reported.
Both cases of granulomatous mediastinitis were admitted to our hospital complaining of chest pain and dyspnea. Their roentgenograms revealed pleural effusion and a tumor-like shadow in the mediastinum. One was diagnosed by mediastinal biopsy through right parasternal incision, and the other was diagnosed after the removal of the mediastinal mass. Both were diagnosed as granulomatous mediastinitis due to tuberculosis, and they were treated and cured by anti-tuberculosis drugs.
Two cases of fibrosing mediastinitis were admitted with symptoms of superior vena caval obstruction. The chest roentgenograms showed widening of the upper mediastinum. The definitive diagnosis was established by mediastinal biopsy through parasternal incisions. One of them was treated with corticosteroids. The other underwent reconstruction of the superior vena cava. Superior vena caval obstruction symptoms subsided in both cases, and they were discharged.
Mediastinal biopsy through right parasternal incision is a useful method to establish the diagnosis in cases of indeterminate upper mediastinal lesions.

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Sarcoidosis has been recognized as a systemic disease that may involve the lung, lymph nodes and some other organs, and death is frequently caused by cardiac involvement. There have been only a few cases of cardiac sarcoidosis diagnosed by transvenous endomyocardial biopsy.
We experienced a case with secondary cardiomyopathy of sarcoidosis diagnosed by this method and which responded well to treatment with corticosteroids.
The case was a 68 year-old male suffering from iritis. The chest roentgenogram demonstrated slight enlargement of hilar lymph nodes, but no abnormal findings in the lung field or in the cardiac shilhouette. ECG showed first degree A-V block, complete RBBB and left axis deviation. The specimen was obtained by transvenous right ventricular endomyocardial biopsy and showed noncaseating granuloma with giant cells.
He responded well to corticosteroid and first degree A-V block and complete RBBB disappeared.

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A 72-year-old case diagnosed as esophageal cancer was admitted because of non-productive cough and exertional dyspnea after receiving a total dose of 150mg of Bleomycin. He had a history of asbestos exposure for seven months nineteen years previously. The physical examination showed fine crackles at the base of the chest and clubbed fingers. A chest X-ray film revealed irregular opacities and honeycombing in the lower lung fields and bilateral pleural thickening. A diagnosis of Bleomycin pneumonitis was made and Predonisolone, 30mg daily, was begun, with some improvement. However, he suffered from influenza A and died of progressive respiratory insufficiency.
The autopsy revealed squamous cell carcinoma of the esophagus, fibrosis of the lung, which was thought to be mainly due to asbestosis, and remarkable bilateral pleural plaques. The inhaled asbestos fibers were demonstrated to be amosite by X-ray analysis. The histological examination of the pleural plaques revealed a developmental process from the early to mature stage; i.e. each step of fibrinous exudation, organization and hyalinization. These steps suggest a mechanical irritation of the parietal pleura by asbestos fibers within the lung. This theory of mechanical irritation was also supported by another result of our own study that the number of asbestos fibers found in the pleural plaques obtained at autopsy from the subjects with asbestos exposure is quite small.

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A 67 year-old female complained of biliptysis. Her chest X-ray film showed collapse of the righ middle lobe, infiltrates of the left lower lung field, and right subphrenic calcified opacities. ^99mTc-E-HIDA liver-biliary system scintigraphy revealed communication between the right middle lobe bronchus and the biliary system. This case was diagnosed as bronchobiliary fistula with biliptysis. Closure and drainage of the fistula were performed but effects were temporary. She died of cachexia. Autopsy revealed congenital hepatic lobulation anomaly, the abnormally situated bile duct system, and inflammatory stenosis of the common hepatic duct with stones. The stenotic common hepatic duct penetrated through the diaphragm into the right middle bronchi.

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A 25-year-old female was admitted in April, 1981 because of two abnormal shadows on a chest film. Under a preoperative diagnosis of benign tumors of the chest wall and upper mediastinum, right thoracotomy was carried out. An encapsulated tumor arising from the right vagal nerve and another tumor arising from the third intercostal nerve were found and the vagal nerve and the third intercostal nerve were transected to remove the tumors. Postoperative clinical course was uneventful. The pathological diagnosis of both tumors was neurofibroma.
Based on the literature previously reported, mediastinal neurofibroma arising from the vagal nerve is extremely rare and this case is only the second one reported in Japan.

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A 41 year-old male was admitted to our hospital, complaining of slight fever, dry cough and general fatigue. On auscultation, bubbling rales were audible at the mid to lower portion of left posterior chest. Plain chest roentgenogram showed multiple cystic shadows with an air-fluid level in the left lower lobe. An abnormal finger-like shadow, which extended from the left hemidiaphragm to the multiple cysts, was found on lateral chest tomogram. Bronchogram revealed cystic dilatation of left B6 and B10. Computed tomogram with contrast enhancement demonstrated multiple cysts and an abnormal round-shaped structure, consisted of high density material, in the left lower lung. At the level of 12mm below the round-shaped structure, an abnormal finger-like structure contiguous to the thoracic descending aorta was demonstrated.
The density of these abnormal structures was 80 Hounsfield units, which was the same as that of the descending aorta. Thoracic aortogram disclosed an abnormal artery arising from the thoracic descending aorta, just above the left hemidiaphragm, which proceeded to the left lower lung horizontally, and extended to superior direction and divided into multiple branches. These vessels drained into the left atrium via left lower pulmonary vein.
Diagnosis of intralobar pulmonary sequestration was confirmed by operation and consequently, the sequestered lung and the abnormal artery were successfully removed. It is emphasized that computed tomography with contrast enhancement is useful to detect the abnormal artery of pulmonary sequestration and that this method should be used to evaluate the vascular relationship of lung lesions.

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A case of pulmonary tuberculosis with characteristic roentgenographic findings was reported. A 29 year-old woman was found to have a gloved finger shadow in the left lower lung field on chest roentgenogram. On tomogram, the density was homogenous and there were a few cavities. PPD test was strongly positive and there was mild leukocytosis. Left lower lobectomy was perfomed, because various examinations including bronchograph, bronchoscopy, brushing cytology, and computed tomography could not rule out the possibility of malignancy.
Histological examination revealed three typical tuberculomas which were connected to each other, and which appeared as an irregular shape on chest roentgenogram.

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