A follow-up study of 130 cases of emphysema over a period of 20 years (1959-1978) revealed that the 10-year survival was 52.3%. Ten functional parameters were compared between short survivors (average survival 6.5 years) and long survivors (average survival 15.4 years) on the basis of initial values. Factors determining the prognosis were identified as: Pa_O2, %VC, and FEV_1.0.
The mean annual changes were decreases of 40ml/yr for FEV_1.0, 2.1Torr/yr for PaO₂ and increases of 2.5Torr/yr for Pa_CO2. Data are compatible with the concept that emphysema is a slowly progressive disorder. The major cause of acute exacerbations was respiratory infection (61.4%). Blood gases showing Pa_O2 below 40 Torr and Pa_CO2 over 55 Torr in acute exacerbations were a bad prognostic sign. It is therefore very important for to control respiratory infections in emphysema cases.

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Prostacyclin (PGI₂) is an unstable prostaglandin which is made by blood vessel walls, and is a vasodilator and a potent inhibitor of platelet aggregation. Thromboxane A₂ (TxA₂) is also a derivative of arachidonic acid and is even more unstable, and is a vasoconstrictor and a potent accelerator of platelet aggregation.
In the present investigation the effect of hypoxemia and pulmonary thromboembolism on plasma levels of 6-keto PGF_1α (a stable derivative of PGI₂), TxB₂ (a stable derivative of TxA₂), histamine and serotonin was studied in anesthetized dogs.
1) In pulmonary thromboembolism induced by an intravenous injection of thrombin, the plasma level of TxB₂ reached a maximum 3min. after the injection of thrombin and decreased gradually thereafter. The plasma level of 6-keto PGF_1α decreased gradually for 20min. after the injection of thrombin.
2) In the same way the plasma level of histamine increased significantly 5min. after the injection of thrombin, while the plasma level of serotonin decreased significantly 1min. after the injection of thrombin.
3) In hypoxemia induced by ventilation of 10% O₂ (balanced with 90% N₂), the plasma levels of 6-keto PGF_1α and TxB₂ did not show any significant change.
4) In the same way the plasma level of histamine showed a tendency to increase gradually, while the plasma level of serotonin showed a tendency to increase initially.
5) The above results may suggest that TxA₂ and histamine play an important role in the pathophysiology of pulmonary thromboembolism, while PGI₂ dose not play an important role in the pathophysiology of hypoxemic change in bronchopulmonary system.

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Cellular and protein components in the bronchoalveolar lavage (BAL) fluid were analyzed in patients with hypersensitivity pneumonitis (10 cases), sarcoidosis (19 cases), and idiopathic pulmonary fibrosis (8 cases) and in controls (14 cases).
BAL fluid obtained in the control contained 33.3±18.3×10⁴cells/ml. A differential cell count of these cells showed 85±10% of alveolar macrophages, 13±10% of lymphocytes and less than 3% of neutrophils or eosinophils by Giemsastain.
BAL fluid in cases of hypersensitivity pneumonitis showed a markedly increased number of lymphocytes, particularly T cells, and elevation of both IgG and IgA and elevation of the IgG/albumin ratio. The number of lymphocytes in BAL fluid of hypersensitivity pneumonitis cases decreased following the improvements of clinical symptoms and laboratory findings. However a proportional increase of lymphocytes in BAL fluid remained even after improvement of chest X-ray findings. There was no correlation between BAL fluid and peripheral blood in terms of the number of lymphocytes and the levels of IgG and IgA.
BAL fluid in the patients with sarcoidosis revealed a wide variety of lymphocyte population and elevated IgG/albumin ratio. However, positive correlation was observed between the number of lymphocytes in BAL fluid and serum angiotensin converting enzyme (p<0.01). The phenomenon of macrophage-lymphocyte adherence was observed in sarcoidosis and hypersensitivity pneumonitis.
Cell population in BAL fluid of the patients with idiopathic pulmonary fibrosis showed an increased number of lymphocytes, neutrophils and eosinophils when compared with that of the controls.
From these results, the bronchoalveolar lavage appeared to be a useful diagnostic method for the diagnosis of hypersensitivity pneumonitis, sarcoidosis and idiopathic pulmonary fibrosis.

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We studied the effect of acute hemorrhagic shock and resuscitation on pulmonary vascular permeability in anesthetized dogs. We used lung lymph flow and the lymph-to-plasma protein ratio as sensitive indices of transvascular fluid filtration rate and protein permeability. We measured pulmonary vascular pressures, lymph flow, and lymph and plasma proteins before and during a 2 hour period of shock, and a 2 hour period of resuscitation. In addition, the levels of serotonin in plasma were measured to clarify the mechanism of the change in pulmonary microcirculation during shock and resuscitation.
1) Lung lymph flow decreased during early shock as animals were bled into bags until the aortic pressure was approximately 50mmHg. However, the lymph flow gradually increased to baseline during late shock as pulmonary vascular pressure returned to control level.
2) During the resuscitation period, lymph flow increased by 72%, as pulmonary artery pressure and pulmonary artery wedge pressure increased by 42% and 25% respectively. This increase of lung lymph flow with the lymph-to-plasma protein ratio being significantly decreased indicates that a change in pulmonary vascular permeability to protein does not occur.
3) Regarding the lung water content and histological findings, we could not demonstrate remarkable changes during the hemorrhagic shock and resuscitation periods. However 24 hours after recovery, the lung water content increased by 33% and we observed atelectasis and apparent thickening of alveolar septums, together with intra-alveolar edema.
4) We found a slight increase of plasma serotonin levels in four of five animals during hemorrhagic shock and resuscitation periods.
5) Furthermore, we demonstrated that the changes of pulmonary vascular pressure and lung lymph flow could be prevented by serotonin antagonist during hemorrhagic shock and resuscitation periods. Consequently, we considered that serotonin might be related to the pathophysiology of the lung in hemorrhagic shock.

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A total of 290 pleural biopsies were performed in 253 patients with exudative pleuritis using the Cope needle biopsy technique.
Specimens were obtained in 95 cases (94.1%) out of 101 patients with a subsequently proved diagnosis of tuberculous pleurisy, and a pathological diagnosis as tuberculosis was made in 69.5%. Culture of the pleural effusion from these patients was positive for tubercle bacilli in only 10.9 per cent. In these cases, the probability of diagnosis by pleural biopsy was higher in patients in which the procedure was performed earlier after onset, with profuse or non-bloody effusion, or with tuberculous lesions in the lung field.
Specimens were obtained in 147 cases (96.7%) out of 152 patients with carcinomatous pleurisy (121 cases were primary lung cancer). A pathological diagnosis was made in 65.3 per cent. In particular a diagnosis was made in 26 out of 50 patients in whom the effusion cytology was negative by this method.
This procedure is simple, safe and approximately 70 per cent accurate in the diagnosis of subsequently proved carcinomatous or tuberculous pleuritis. The Cope needle biopsy of the parietal pleura is a valuable procedure commonly used in evaluation of patients with exudative pleuritis.

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A 46-year-old female office worker was admitted to Seirei Hamamatsu Hospital on February 8, 1979 because of nonproductive cough and exertional dyspnea for a period of one month. She had had no symptoms suggesting collagen disease except occasional sausage digit since last February. The patient was febrile (38.4°C) without muscle weakness and bibasilar Velcro rales were audible. Chest roentgenogram showed coarse linear opacities just above the elevated diaphragm and ground glass appearance in the mid and lower fields of the lungs. Clinical features were compatible with those of interstitial pneumonia (IP), so prednisolone 40mg was administered daily. The next day she became afebrile and dyspnea was alleviated within a week.
Open lung biopsy was performed on the eighth hospital day. Microscopic examination revealed thickening of the alveolar septa with predominant lymphocytic infiltration and fibrosis partially accompanied with honeycombing. There was mucinous type intimal fibrous thickening of the vessels and fibrous thickening of the pleura. These findings suggested the pulmonary complication of collagen disease, especially polymyositis (PM) because of high levels of creatine phosphokinase (CPK). However, biopsy of the right rectus femoris muscle performed on February 23 revealed no appreciable pathological changes.
She was discharged on July 1, but readmitted on January 21, 1980 because of general fatigue with alternating diarrhea and constipation for two months. PM was strongly suspected from her slow movement and the further increase of CPK, but she showed no marked muscle weakness on physical examination. Biopsy of the left deltoid muscle carried out on February 8 revealed lymphocytic and histiocytic infiltrations in perivascular regions of perimysium, floccular degeneration of muscle fibers, phagocytosis of degenerated muscle fibers, and focal proliferation of sarcolemmal nuclei, which were compatible with those seen in PM.
The increasing dosage of prednisolone improved general fatigue and slow movement, but gastrointestinal symptoms were aggravated. The gastrointestinal examination showed barium stagnation in the esophagus, dilatation of the duodenum (loop sign) and hypoperistalsis of the intestine. These findings suggested the overlap of progressive systemic sclerosis (PSS) though there were no skin lesions. There was no evidence of PSS in skin biopsy performed on June 5, and biopsy of the left extensor carpi ulnaris muscle revealed features which were considered to be the repair process of PM. The patient has been suffering from so-called intestinal pseudo-obstruction without worsening of respiratory and muscular symptoms.
This case is characterized by the fact that the IP preceded symptoms of PM, and that an increase of CPK preceded development of muscle weakness and appearance of histopathological findings in serial muscle biopsies.
In our review of the literature, sixty-one cases of PM with IP were reported since 1956 (Table 2). There were twelve cases (19.7%) in which the specific muscular symptoms were not seen within at least a month after initial diagnosis of IP. Thus, examination for occult muscle disease is thought to be important in patients with chronic IP, as well as examination for pulmonary disease in patients with overt PM as emphasized by Webb.

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A 31 year-old electrician was admitted because of mild dyspnea. His occupational history was negative for exposure to Beryllium and/or Asbestos. The chest roentgenogram on admission revealed bilateral diffuse fine nodules, especially in both upper lung fields, which was suggestive of eosinophilic granuloma of the lung. The physical examination results were all within normal limits. Lymph node biopsy from the chest wall as well as the Kveim test showed no granulomatous lesions. There was no elevation of serum ACE.
Open lung biopsy revealed many confluent noncaseating granulomas with giant cells in the centers of the lesions. They were usually confined to the subpleural tissue and interlobular septum as well as lung parenchyma on occasion. Elastic stain clearly demonstrated the destructed blood vessels in the lesions, suggesting the presence of vasculitis. Prednisolone was given with prompt improvement of symptoms and chest X-ray findings.
The constellation of findings; namely mild symptoms, diffuse nodular shadows, sarcoid like granuloma with necrotizing vasculitis, and good response to the corticosteroid therapy was consistent with the characteristics of NSG previously reported.
This case is the first example of NSG reported in Japan.

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The patient, a 60 year old man was shot in the neck on the right side, in 1944, (in World War II). He has had recurring fevers, chills and coughs several times each year since 1949. These symptoms went untreated.
In July, 1979, he was transferred to our hospital from an other hospital because of recurring pneumonia. At admission, the chest X-ray showed atelectasis in the upper lung field, where the bullet was found. Then bronchofiberscopy was performed. It showed a white coated bullet at the orifice of the left upper lobe bronchus.
Attempts to remove it by using various foreign body forceps failed. Because of this and recurring pneumonia, left upper lobectomy was performed.
We think this case is quite interesting for the following reasons: First of all, this bronchial foreign body was a bullet. Second, it is relatively rare for a foreign body to be found in the left upper lobe. Third, the patient had lived 35 years without serious symptoms. Fourth, it is not clear how and when the bullet had reached the orifice of the left upper lobe bronchus from the right side of the neck. Because detailed records of the gun shot incident were not available, this case appeared to be complicated.

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