We measured the serum IgG, IgA, IgM and IgE levels in 243 patients with pneumoconiosis, and found that some patients had increased levels of polyclonal immunoglobulins compared to the control group. These results led us to suspect that inhaled mineral dust, including silica, acts as an adjuvant in the production of IgE and other antibodies. We then confirmed the adjuvant effects of silica and MnO₂, and the production of polyclonal immunoglobulins in mice by both the PCA reaction for IgE and passive HA reaction for other antibodies.

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The present experiment was designed to study the pathogenesis of amniotic fluid embolism in 69 rabbits with near-term gestation. For the production of amniotic flluid embolism, the supracervically hysterectomied rabbits were divided into 3 groups, and received an intravenous infusion of either autologous amniotic fluid, autologous cell-free extracts of placenta or tissue thromboplastin. Fifteen hysterectomied rabbits were used as controls.
Autologous amniotic fluid induced numerous thrombi composed of platelets and fibrin in the pulmonary vessels of 33 rabbits. Furthermore, strands of fibrin were often adherent to the interendothelial gaps. Fibrin thrombi increased in number at 2 hours, but decreased at 10 hours. From day 5 on, the thrombi underwent organization characteristic of proliferation of smooth muscle cells and capillaries. Twenty days later, mild arteriosclerotic lesions characterized by proliferated smooth muscle cells, collagen fibers and elastic fibers occurred just beneath the new endothelial covering of thrombi. Fetal elements such as mucin and keratin were always observed in the vascular lumen in throughout the course of the experiment. Two hours after the intravenous infusion of amniotic fluid, leukostasis appeared in the pulmonary vessels and reached a peak at 10 hours.
In 14 rabbits receiving infusion of cell-free extracts of placenta, and 7 rabbits undergone to the infusion of tissue thromboplastin, however, only numerous fibrin thrombi were demonstrable. Five out of 15 control rabbits showed a few neutrophils in the small pulmonary arteries 3 hours after hysterectomy. In 10 control hysterectomied rabbits received saline infusion, however, only small aggregates of platelets appeared in the capillaries of inter alveolar septa at 30 minutes.
The pulmonary lesions in the present study may be interpreted to be no more than pulmonary thrombosis brought about by the intravenous infusion of tissue thromboplastin, and also by the increased vascular permeability due to fibrin in the thrombus, fibrin degradation products and neutrophils. On the other hand, mucin in the meconium, that is a fetal element in the amniotic fluid may activate the complement, and then induce leukostasis as well as thrombosis by activation of the factor X in the pulmonary vessels. It is suggested that “amniotic fluid-induced pulmonary thrombosis” is a more preferable term than “amniotic fluid embolism” in this experiment.

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The use of diesel engines has increased greatly in recent years and has led to concern about the contribution of diesel engine exhaust gas to air pollution. Although many of the pollutants emitted by diesel engines have been studied, the toxicological effects of exhaust gas have not yet been elucidated.
In the present investigation we tried to elucidate the chronic effect of diesel-engine exhaust gas on metabolic functions in rat lungs. Rats were exposed to diesel-engine exhaust gas for two years. Fifty percent effective doses of acetylcholine in isolated rat tracheal strips, conversion or inactivation of vasoactive substances through isolated perfused rat lung lobes were studied. Rats were classified into 3 groups, i. e. control group, filtered exhaust gas (F. E . G.) group and exhaust gas (E. G.) group
1) Fifty percent effective doses of acetylcholine in F. E. G. and E. G. rats tracheal strips showed a significant decrease compared with those in control rats.
2) Inactivation of serotonin through isolated perfused lung lobes in E. G. and F. E. G. groups showed a decrease compared with that in control group.
3) Inactivation of prostaglandin E₂ and F_2α through isolated perfused lung lobes in E. G. and F. E. G. groups showed a decrease compared with that in the control groups.
4) Conversion of angiotensin I to angiotensin II through isolated perfused lung lobes in E. G. and F.E.G. groups showed a significant decrease compared with that in control group.
The above results suggest that two years exposure to diesel engine exhaust gas may affect pulmonary metabolic functions and tracheal reactivity.

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Respiratory function of 217 healthy subjects and 42 patients undergoing thoracotomy were examined by exercise tolerance tests using a treadmill and stairs.
On blood gas analysis, healthy subjects showed an elevation of PaO₂ and a fall of PaCO₂ with exercise. On the other hand, postoperative patients who underwent lobectomy or more extensive pulmonary resection showed a significant elevation of PaCO₂ following exercise compared with the preoperative value. Furthermore, as following pneumonectomy PaO₂ decreased and PaCO₂ elevated with exercise, these phenomena showed an inverted response to healthy subjects.
Maximal oxygen uptake and maximal carbon dioxide gas output decreased in proportion to resected lung volume. Prediction of postoperative maximal oxygen uptake and maximal carbondioxide gas output was possible using the following formula.
Postoperative VO₂max=Preoperative VO₂max ×{(the number of whole segments-the number of resected segments)/the number of whole segments}×0.9.
Postoperative VCO₂max=Preoperative VCO₂max×{(the number of whole segments-the number of resected segments)/the number of whole segments}×0.9.
Maximal oxygen uptake can be obtained from the exercise test using stairs. In this simple test the pulse rate is counted before and after going up the stairs and the time required for going up the stairs. As a result, a formula was obtained as follows. Because of the reproductivity of the obtained value, this was named the Stairs index.
Stairs Index={height of stairs (km)×Body weight (kg)}×(fcmax-resting pulse rate at standing/min.)/time required for going up the stairs (min.)×the number of increased pulse rate (/min.)
There was a correlation between the Stairs index and the maximal oxygen uptake (r=0.78). The correlative formula was followed.
Maximal oxygen uptake=250×Stairs Index+902
The exercise tolerance test using stairs is very easy; can be done everywhere and by anybody. This research showed that the stairs test was so useful that it could be used as a routine exercise tolerance test.

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It is said that air pollution is a cause of the onset of bronchial asthma and an inducing factor in attacks and their aggravation.
In the present study, changes in the peripheral airways in patients with bronchial asthma who were living in the Kawasaki coastal industrial zone, a region with severe air pollution, were morphologically investigated, in order to determine the pathological conditions of such bronchial asthma, namely, ascertaining the effects of air pollution.
The present study included 24 patients with clinically reversible dyspneic attacks and dry rales found on chest auscultation in whom bronchial asthma was diagnosed on the basis of various clinical laboratory tests.
Morphological characteristics of the peripheral airways in bronchial asthma occurring in a region with severe air pollution have been elucidated. 1) Selective alvelobronchography revealed a high frequency of dilatation in the peripheral airway. 2) Endoscopic findings of the peripheral airway were divided into three groups, with distinct features. 3) Histopathological findings of this disease were different from those of conventional bronchial asthma.
The bronchial asthma in the present study was totally different in its morphological characteristics from conventional bronchial asthma.

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Pleural fluid concentrations of Cefotiam (CTM) after intravenous drip infusion of 2g were determined in 12 thoracotomized patients.
CTM concentration reached a peak level 21.261μg/ml at 2 hour after the dosage and remained at more than 10μg/ml for 4 hours. The concentration in the pleural fluid, at 2 hours, after the dosage, read from 16.40μg/ml to 19.786μg/ml for 4 days postoperatively except the 3rd day.
The pleural fluid concentrations had mutual correlations with age and serum creatinin but not with sex, BUN, %VC and the dose of CRM/body weight.

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With recent advancements in the flexible bronchoscope and cell sampling technique, the preoperative diagnostic rate for peripheral lung cancer is improving. Recently transbronchial lung biopsy-stamp cytology (TBLB-SC) and transbronchial aspiration cytology (TBAC) were employed in our institute and a good preoperative diagnostic rate was obtained, in combination with percutaneous fine needle biopsy (PCNB). We report the preoperative cytodiagnostic rate for peripheral lung cancer in our institute during the past 2 years.
A total of 68 resected peripheral lung cancer were examined. Histologic types of these cases were examined. Histologic types of these cases were 49 adenocarcinomas, 15 squamous cell carcinomas, 2 large cell carcinomas, 1 small cell carcinomas and 1 carcinoid.
Bronchofiberscopy was performed in 67 cases and transbronchial cell sampling was perfomed under bi-plane fluoroscopy. Positive rates for each cell sampling method were as follows. Brushing: 32/47 (68%), TBLB-SC: 48/57 (84%), TBAC: 42/53 (79%). The total transbronchial diagnostic rate was 60/67 (90%). For the negative cases, PCNB was also performed and positive results were obtained in 4 cases. The total preoperative diagnostic rate was 96%.
Transbronchial cell sampling technique combining with TBLB-SC and TBAC was effective for the diagnosis of peripherally originating lung cancer and PCNB was indicated only for transbronchial negative cases. These procedures under transbronchial or percutaneous approaches could not only improve the preoperative diagnostic rate but also accelerate the decision concerning therapy including surgery.

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It has been suggested that airway hyperresponsiveness correlates well with the existence of airway inflammation. In the present study, the relationship between the airway responsiveness to inhaled methacholine and the number of white blood cells in bronchoalveolar lavage fluid was investigated before and after inhalation of endotoxin. Ten cases of guinea pigs with bacterial α-amylase (BA) sensitization and 9 cases without sensitization were studied. Pulmonary resistance and dynamic compliance were employed to record the dose-response curves and provocation concentration was determined.
In group I (4 sensitized and 4 unsensitized), dose-response curves were recorded before and three hours after saline inhalation, and in group II (6 sensitized and 5 unsensitized) dose-response curves were obtained before and three hours after endotoxin inhalation. Bronchoalveolar lavage was performed at the end of the experiment and numbers of white blood cells were counted.
In group I, PC did not change before and after saline inhalation and white blood cell counts in BALF were normal. On the other hand, PC was significantly reduced following endotoxin inhalation and white blood cell counts in BALF were increased after endotoxin especially in sensitized cases.
These results may indicate that airway hyperresponsiveness is closely related to the migration of white blood cells to the airway wall.

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A previously healthy 21 year-old woman who suddenly developed fever on November 20, 1984. In spite of treatment with various antibiotics, she complained of high fever, productive cough and dyspnea. On November 29, she was admitted to the National Minami Fukuoka Chest Hospital. On admission, her chest X-ray showed diffuse infiltrates in the bilateral lungs and arterial blood gases on ambient air breathing revealed PaO₂ of 27.7torr. She was mechanically ventilated with CPPV, and received various antibiotics, γ-globulin and Methylpredonisolone pulse therapy. Her chest X-ray finding and pulmonary function, thereafter, gradually improved. Mycoplasma pneumoniae was found from the culture of a throat washing taken on the day of admission. The passive hemagglutination titer for Mycoplasma rised from 1:20 on November 24, to 1:2560 on admission, then rose further to 1:10240 on the twelfth hospital day. The complement fixiation titer for Mycoplasma rose similarly. Therefore the case was diagnosed as acute respiratory failure due to mycoplasma pneumoniae infection. The histological diagnosis of the specimen taken from TBLB was interstitial pneumonia associated with lung edema.
Pneumonia due to Mycoplasma pneumoniae is usually a benign self-limited illness. Mycoplasma pneumoniae, however, must be considered as one of causes of acute respiratory failure. In such cases, appropriate diagnotic and therapeutic measures with pulse therapy should be initiated promptly.

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Paraquat, a widely used weed-killer, is well known to cause severe organ-toxicity, especially pulmonary injury in man. We experienced 40 autopsy cases of paraquat poisoning in the past 10 years in our institute. The histopathological findings of paraquat lung and pathogenesis of fibrosis are described in this paper. The initial stage with a clinical duration of up to 60 hours was found in 20 cases in which shock was the cause of death. The early organizing stage, up to 2 weeks, was found in 13 cases and the terminal fibrotic stage, past the 20th day, in 7 cases. These 20 cases died of respiratory failure. The initial histologic findings were alveolar capillary congestion, interstitial edema and inflammation with subsequent focal hemorrhage and intra-alveolar exudation. Twenty hours following paraquat ingestion, hyaline membrane was observed along alveolar walls and ducts associated with mild collapse of the surrounding alveoli. Massive hemorrhage was seen from the 4th day on. Immature mesenchymal cells appeared in the intra-alveolar exudate without absorption after the 6th day and thickening of alveolar walls with interstitial fibrosis and organization of hyaline membrane developed simultaneously. Injury of type II epithelium results in subpleural collapse and fibrosis with fine collagen fibers. Fibrosis in paraquat lung is different from idiopathic interstitial pneumonia in that the alteration occurs mainly in the form of intra-alveolar organization and fibrosis. After the 20th day, pulmonary fibrosis is completed with formation of cystic air-spaces resulting from emphysematous dilatation of non-collapsed alveoli.

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The tendencies and pathogenesis of occupational asthma due to timber dust in forestry workers was studied by a community survey and allergic examinations using basophil reactivity. The number of bronchial asthmatics in wood-workers (4.9%) was significantly higher than that in sawing-workers (1.1%). This difference seems to depend on the allergic tendency of workers, or size of inhaled timber dust and the circumustances of the work space. Other respiratory diseases such as rhinitis and chronic bronchitis were also shown in wood-workers rather than in sawing-workers. The mechanism of bronchoconstriction in a case of bronchial asthma induced by inhalation of Zelkova tree timber dust was based on the IgE mediated reaction as well as the airway hyperresponsiveness for methacholine.

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A 70 year-old male was admitted to Kanazawa Medical University Hospital, because of bloody sputum, general malaise and fever. He had a history of tuberculous pleurisy at age 33. Physical examination revealed dullness or absence of respiratory sounds over the right lung field. The chest X-ray film (Fig. 1) showed opacity and thickening of the pleura with calcification of the right side. Mucoid and non-mucoid type Salmonella enteritidis were isolated from sputum, transtracheal aspirate, bronchoalveolar lavage, duodenal juice and stool. He was treated with chloramphenicol, however, the organism was still isolated from sputum and stool. Right pneumonectomy was performed, because S. enteritidis was not eradicated and a bronchopleural fistula was shown by bronchography (Fig. 5). Pathological findings revealed a pseudocapsule surrounded the pleura with thickening and calcification (Fig. 6). There were coagula and leucocytes collected with bacteria in the pseudocapsule (Fig. 7). Mucoid type S. enteritidis was isolated from the resected materials. After pneumonectomy, S. enteritidis was not isolated from all clinical specimens such as sputum, blood, duodenal juice, stool and urine.

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A 50 year-old woman with rheumatoid arthritis had pneumonitis in the form of PIE (pulmonary infiltration with eosinophilia) syndrome. She had previously received a course of sodium aurothiomalate therapy for three months (total 305mg), until she developed dry couth, skin rash, slight eosinophilia and unilateral diffuse patchy shadows on chest roentgenogram. Gold salt was considered to be the cause of pneumonitis. Despite cessation of gold salt, the shadows on roentgenograms spread throughout the bilateral lung fields.
Bronchoalveolar lavage fluid revealed marked eosinophilia (21.6%), neutrophilia (14.6%) and lymphocytosis (17.2%) with a OKT4⁺/OKT8⁺ratio of 0.35. Lung tissue specimens obtained by open lung biopsy contained numerous Masson's bodies and some granulomas accompanied by alveolitis. The gold concentrations in two different lung biopsy specimens were 324 and 644μg/100g wet weight, and that in serum was 12μg/dl. The difference in the gold concentration did not appear to be related to the localization of the disease in the lung. It was suggested that immunological mechanisms play an important role in this disease and that eosinophils might have cytotoxic effects against lung tissue.
Prednisolone treatment was started, resulting in the rapid disappearance of pulmonary manifestations, improvement of pulmonary function and clearing of shadows on chest roentgenograms.
This case of gold-salt-induced pneumonitis was very interesting in terms of the pathogenesis of this disease, which presented marked eosinophilia in bronchoalveolar lavage fluid and significant development of Masson's bodies.

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A 65 year-old female case of chronic pulmonary emphysema presented with severe liver dysfunction complicated with respiratory failure. She developed CO₂ narcosis as a result of administration of too high a concentration of oxygen, showed signs of congestive heart failure, i. e., jugular vein dilatation, pretibial edema, high a hepatomegaly. Systemic hypotension, and severe hypoxemia also appeared. She had suddenly manifested marked elevation of serum transaminases (GOT 4010 I. U. 3rd day on admission and GPT 940 I. U. 5th day on admission), which were difficult to distinguish clinically from viral hepatitis. However this hypertransaminasemia quite rapidly returned to normal as she recovered from heart and respiratory failure. The clinical course and the negativityy of both hepatitis B surface antigen and IgM hepatitis A antibody in her serum suggested a relationship between the acute exacerbation of respiratory failure and liver dysfunction. Rapid normalization of serum transaminases with recovery from respiratory and circulatory failure suggest that decreased oxygen delivery to the liver was one of the main pathogenetic causes.

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