The delineation of normal bronchi was evaluated by high resolution CT. Under the usual conditions for lung survey, with window width of 1500, window level -650, and slice thickness 10mm, using high spatial frequency algorithm, the subsegmental bronchi were delineated in 77% of total branches. Sub-subsegmental bronchi were delineated in 8% of bronches. Under thin slice high resolution CT, with slice thickness of 1.5mm and slice interval 10mm, subsegmental bronchi were delineated in 89% of branches, and sub-subsegmental bronchi were delineated in 35% of branches. In two of the cases in which almost the whole lungs were studied on continuous slice images with thin slice high resolution CT, sub-sub-subsegmental bronchi could be easily delineated, except in for the lingular segment. High resolution CT is very useful for the interpretation of normal pulmonary structures and for diagnosis of bronchial lesions.

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The decrease of pulmonary vascular resistance with increase of pulmonary blood flow has been attributed to the function of the pulmonary vascular bed, consisting of capillary recruitment or dilatation. However, experimental evidence of a decrease of capillary resistance is lacking. To clarify this phenomenon, we perfused isolated cat lungs with diluted autologous blood and measured pulmonary microvascular pressure while changing pulmonary blood flow rate.
We set the initial flow rate to achieve Ppa of 20cmH₂O and changed the flow rate while keeping left atrial pressure (Pla) and alveolar pressure (Palv) constant at 10cmH₂O and 9cmH₂O, respectively. Thereafter, pulmonary flow rate was increased 2 to 3 fold, and pulmonary arterial pressure (Ppa) and venular pressure (Pvo) were measured by venous occlusion method. The initial flow rate was 150 to 270ml/min and the achieved maximum flow rate was from 300 to 543ml/min. There was a linear correlation between Ppa, Pvo, and flow rate, in which the slope (rate of increase of pressure with flow) of Ppa was slightly steeper than that of Pvo. We calculated total and segmental pulmonary vascular resistance from the mean pressure-flow relationship. The total and upstream resistance involving arterial and capillary segments decreased hyperbolically with increase in flow rate. The mean upstream resistance decreased about 54%, from 35.20×10^-3 (cmH₂O/ml/min) at a flow rate of 150ml/min to 16.27×10^-3 (cmH₂O/ml/min) at a flow rate of 450ml/min. The degree of this decrease was similar to the result observed by micropuncture method (Nagasaka, 1990). Downstream resistance, which represents venous resistance, did not change significantly with the flow rate.
We calculated pulmonary capillary resistance from the mathematical model of the pulmonary capillary bed by applying observed microvascular pressures. This enables estimation of the degree of capillary dilatation required to cause a decrease of capillary resistance where pulmonary blood flow rate is increased (Overholser, 1982). The calculated decrease of capillary resistance due to capillary dilatation was about 33%.
We conclude that the decrease of pulmonary vascular resistance during high pulmonary blood flow is attributable to the decrease of capillary resistance. This decrease is partially attributable to capillary dilatation.

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Pulmonary changes induced in a murine model by intraperitoneal injections of bleomycin were morphologically studied by light and electron microscopy. The number of pulmonary macrophages and the distribution of fibronectin in these cells were evaluated by acid phosphatase and affinity staining using anti-fibronectin horseradish peroxidase conjugates.
The onset of acute inflammation occurred 4 days after intraperitoneal injection of bleomycin and reached its peak on the 14th day post-injection. The inflammatory reaction then gradually decreased. Areas of subpleural fibrosis was observed on day 42.
On day 14, the ratio of the macrophage in bleomycin-treated mice to that in control mice was 5:1. Many activated and foamy macrophages were observed at that time. These findings indicate that macrophage turnover activity is remarkably increased during the acute inflammatory phase. Fibronectin was detected in the cytoplasm of macrophages on day 14, 21, and 28. It was also detected in both alveolar capillary and epithelial basal lamina as well as in interstital collagen fibers. On day 42, fibronectin staining was strongly positive in areas of subpleural fibrosis.
These results suggest that fibronectin released from pulmonary macrophages plays a role in the process of pulmonary fibrosis.

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Clinical and pathological investigations were performed in 58 cases of opportunistic pulmonary mycoses diagnosed at autopsy during the 10 years between 1979 and 1988 at Sasebo General City Hospital. The following findings were obtained.
1) The incidence of opportunistic pulmonary mycoses during the 10 years was 7.7%, with a significant increase in the incidence of fungal infections during the last 5 years of the study.
The incidence of pulmonary mycoses was higher in patients with blood dyscrasia than in those with solid tumor or benign disease (p<0.001).
2) Administration of steroid hormone and anticancer drugs were suspected to be causative factors in the development of pulmonary aspergillosis and cryptococcosis, but not in candidiasis.
3) Characteristic radiographic patterns and clinical symptoms were absent in cases of pulmonary candidiasis due to the small size of the lesions and the high incidence of other complicating pulmonary infections and edema.
4) The most common initial roentgenographic pattern in opportunistic pulmonary aspergillosis was localized infiltrate, subsequently progressing to either multifocal infiltrates or cavitation.
5) The initial symptom in opportunistic pulmonary aspergillosis was usually high fever, and the radiographic abnormalities appeared later. The median duration between onset and death in 19 patients with pulmonary aspergillosis was 23.1 days.
6) Pulmonary aspergillosis should be suspected in the compromised host with high fever refractory to antibiotics and pulmonary infiltrates. Empiric antifungal therapy should be initiated at an early stage for the best chance for survival.

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Cell-adhesive proteins such as laminin and fibronectin and their specific receptors play an important role in the processes of cancer proliferation, invasion, and metastasis. In the present study, we cloned the cDNA of 67kDa-laminin receptor both from human lung cultured cell line (IMR90) and from human small cell lung cancer (SBC3), and determined the nucleotide sequences. In addition, the expression of mRNA in 11 lung cancer cell lines with various cell types was estimated by the method of Northern blot hybridization. As a result, 1.2kb-message was detected in all cancer cell lines examined. It was also demonstrated that the mRNA level of 67kDa-laminin receptor was inversely proportional to the population doubling time of the cell line (r=-0.80).

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We examined the usefulness of 3 carbohydrate antigens, CA19-9, CA125, and SLX, as tumor markers in adenoid cystic carcinoma of the trachea and bronchus, immunohistochemically and clinically. CA19-9 and SLX were detected immunohistochemically in normal tracheal and bronchial glands, but CA125 was not detected. Bronchial secretions obtained from 7 patients without cancer contained high levels of these 3 carbohydrate antigens. There was positive immunohistochemical staining for CA19-9, CA125, and SLX in 5 of 9, 1 of 9, and 3 of 8 patients with tracheal or bronchial adenoid cystic carcinoma, respectively. In a case of bronchial adenoid cystic carcinoma in whom pretreatment serum CA19-9 showed a very high level, this marker changed in parallel with the clinical course. These results suggest the possibility that CA19-9 and SLX could be used as useful markers in patients with tracheal and bronchial adenoid cystic carcinoma.

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The supernatants from cultures of alveolar macrophages from 12 patients with sarcoidosis and 7 control subjects were assayed for interleukin-6 (IL-6) using an ELISA system. IL-6 was detectable without a stimulant in supernatants from all subjects with sarcoidosis and controls. However, the supernatants from 4 of 12 untreated patients with sarcoidosis contained significantly greater amounts of IL-6. When macrophages were stimulated by Propionibacterium acnes (P. acnes), the mean level of IL-6 in the supernatant of patients with sarcoidosis was 5.18±1.46ng/ml, which was significantly higher than in controls (3.34±0.39) (p<0.05). Furthermore, in patients with sarcoidosis, the mean level of IL-6 in the supernatant was significantly correlated with the percentage of lymphocytes in bronchoalveolar lavage fluid (p<0.05), the level of interleukin-1 released by alveolar macrophages stimulated by P. acnes (p<0.05), and the phagocytic index of alveolar macrophages (p<0.05). The large amount of IL-6 in the supernatant after stimulation by LPS was measured in patients with sarcoidosis (24.49±13.36) and in controls (12.4±8.53), and there was no significant difference between patients with sarcoidosis and controls. Small amounts of IL-6 were detectable in bronchoalveolar fluid from only 2 of 26 patients with sarcoidosis; however, it was detected in none of 15 controls. It is suggested that the enhancement of IL-6 release by alveolar macrophages has a role in the activation of immune effector cells at sites of sarcoidosis.

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Leukotoxin, a cytochrome P450-dependent metabolite of linoleate synthesized by neutrophils, caused dose dependent vasodilation (10^-5-5×10^-4M) of isolated rat pulmonary arterial rings preconstricted with endothelin 1 (10^-8M), although similar doses of linoleate had no effect. The relaxing effect of leukotoxin was largely ablated by mechanical denudation of the endothelium and by treatment with L-NMMA (1mM) and methylene blue (5×10^-6M), but not indomethacin (10^-5M). Endothelium-independent relaxation of leukotoxin was not inhibited by pretreatment with nicardipine (10^-6M) in both pulmonary arterial rings and aortic rings. In A7r5 cultured rat aortic smooth muscle cells, leukotoxin markedly inhibited Ca²⁺ uptake in the basal nonstimulated state, and in the stimulated state with endothelin 1. We conclude that leukotoxin causes vascular tone-dependent vasodilation via augmentation of EDRF production, and causes decrease of intracellular calcium concentration that is not related to the dihydropyridine-sensitive calcium channel, which may be a mechanism of the endothelium-independent relaxation caused by leukotoxin.

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We measured the right ventricular ejection fraction (RVEF) before and during unilateral pulmonary artery occlusion test (UPAO) by thermodilution method. We also measured the right ventricular end-diastolic volume index (RVEDVI), right ventricular end-systolic volume index (RVESVI), and right ventricular stroke volume index (RVSVI). RVEF and RVSVI were significantly decreased by UPAO (p<0.05), but there were no obvious changes in RVEDVI and RVESVI.
Some cases showed only a small decrease in RVEF by UPAO, even though their total pulmonary vascular resistance indices were over 700 dyne·sec·cm^-5/m² during UPAO. On the other hand, some cases had a decreased in RVEF of more than 10% by UPAO, even though their total pulmonary vascular resistence indices were under 400dyne·sec·cm^-5/m² during UPAO. We consider that it is important to measure right ventricular functions such as RVEF together with pulmonary vascular hemodynamics in the pre-operative evaluation of cases of lung resection.

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We studied the standard values and normal limits for arterial blood gases in healthy elderly Japanese subjects. The criteria for inclusion were; 1) older than 60 years and able to walk independently, 2) non-smoker, 3) no respiratory symptoms, 4) no thoracic deformity, 5) no clinical signs of chest disease, 6) no abnormal findings in chest X ray, and 7) no cardiac disease or obesity. The number of subjects was 78. The oldest subject was a 96-year-old female. Arterial punctures were performed with the subjects in a recumbent position. Pa_O2 ranged from 79 to 106 Torr, with a mean value of 89.8 Torr. Pa_CO2 ranged from 32 to 48 Torr with a mean value of 39.6 Torr. Maximum values of alveolar-arterial O₂ tension difference and arterial-alveolar N₂ tension difference were 20.2 Torr and 11.6 Torr, respectively.
The regression equation for Pa_O2 with respect to age was; Pa_O2=99.32-0.126×(age), and its residual standard deviation was 6.06 Torr. These values were not different from those obtained in healthy young Japanese subjects.

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To evaluate whether one can predict the course and prognosis of interstitial lung diseases from lung gallium-67 (⁶⁷Ga) uptake, we studied 31 subjects with sarcoidosis and 28 with idiopathic pulmonary fibrosis (IPF) retrospectively. We quantified the lung ⁶⁷Ga uptake using posterior scans by Line's method, and calculated a visual index (VI). The normal range of ⁶⁷Ga uptake was defined as less than 65 VI values, obtained from the 95 percent confidence interval of the control subjects. All subjects with stage I sarcoidosis, having only bilateral hilar lymphadenopathy (BHL) on chest X-ray, revealed normal lung ⁶⁷Ga uptake. Fifty percent of patients with stage II sarcoidosis, with both BHL and pulmonary involvement on chest X-ray, showed increased lung ⁶⁷Ga uptake. The patients with increased lung ⁶⁷Ga uptake showed decreased percent vital capacity and increased alveolar-arterial oxygen tension difference, but none of them showed clinical deterioration during the follow-up period of more than 6 months. Fifty-four percent of subjects with IPF showed increased lung ⁶⁷Ga uptake. But there was no difference between the subgroups with normal and increased lung ⁶⁷Ga uptake with respect to the severity of dyspnea, percent vital capacity, arterial oxygen tension, or alveolar-arterial oxygen tension difference. There was also no difference between the two subgroups of IPF in the cumulative percent survival after either the onset of symptoms or the ⁶⁷Ga scintigram. We conclude that lung ⁶⁷Ga uptake was not able to predict the clinical course or the prognosis of patients with sarcoidosis and IPF.

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A 57-year-old woman with bronchial actinomycosis associated with broncholith is presented. She had suffered from fever and productive cough for 7 years. Her chest roentogenograms showed atelectasis of the middle lobe and calcification in the middle lobe bronchus.
Bronchoscopic examination revealed a broncholith covered with pus and granulomatous tissue. The biopsy specimen revealed sulfur granules containing a partially calcified lesion, and it was diagnosed as actinomycosis. After treatment with antibiotics, the broncholith became movable, and it was removed Bronchoscopically. Its shape was like a molding of the right middle lobe bronchus. We speculate that the growth of this broncholith partially resulted from chronic inflammation associated with actinomycelial infection.

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A 47-year-old male was referred to our hospital with persistent high fever. He had received antibiotics (ASPC) for the diagnosis of acute infectious disease, which failed to respond, and subsequently developed marked lymphocytopenia and thrombocytopenia. During his hospitalization, hypoxic respiratory failure rapidly developed. A bone marrow aspiration revealed marked hemophagocytosis, leading to the tentative diagnosis of opportunistic respiratory infection associated with malignant histiocytosis. Treatment for suspected malignancy and Pneumocystis carinii pneumonia was commenced. However, because of the initial lack of response to ASPC, generalized skin rashes without an ordinary stick wound which had diminished before the hospitalization, and a history of working outdoors in a nearby mountain area, the possibility of new type tsutsugamushi disease was strongly suggested. Intravenous administration of minocycline promptly improved his symptoms and laboratory data. The diagnosis was confirmed by a significant increase in the titer of antibody to Rickettsia tsutsugamushi. The thrombocytopenia was considered to have been caused by co-existent hemophagocytic syndrome.

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A 27-year-old nonsmoking woman complained of cough and chest oppression for two years since an episode of pneumonia. Clinical tests showed decrease in FEV_1.0 during attacks of coughing and evidence of bronchial hypersensitivity. While these events fitted the picture of bronchial asthma, the nonwheezing cough suggested cough variant asthma. Antinuclear antibody and anti-ds DNA antibody were increased and leukopenia was recognized, suggesting the diagnosis of systemic lupus erythmatosus (SLE). Bronchoalveolar lavage showed lymphocytic alveolitis and decreased T₄/T₈. These results were suggestive of collagen lung induced by SLE. Inhalation challenge with capsaicin and rapid intravenous injection of lobelin and alinamin indicated that peripheral c-fiber receptors were involved in the induction of coughing. We conclude that the peripheral lesion of collagen lung stimulates the peripheral c-fiber receptors, leading to cough variant asthma.

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A 68-year-old male developed dry cough and exertional dyspnea after handling paint spray containing isocyanates (TDI, MDI) for three months. Initially, the symptoms fluctuated according to whether he was at work or not. He was admitted to our hospital on February 7, 1990, because of progressive worsening of symptoms.
In spite of admission to hospital and cessation of exposure to isocyanates, there was no improvement of symptoms. His chest X-ray film showed diffuse small nodular and reticular shadows. Transbronchial lung biopsy revealed thickening of the alveolar walls and formation of Masson's bodies associated with mononuclear cell infiltration in alveolar spaces. High titers of TDI-HSA and MDI-HSA specific IgG antibodies were detected by ELISA, and a high level of serum soluble IL2 receptor was also detected. From these results, we diagnosed hypersensitivity pneumonitis due to exposure to isocyanates. One week administration of prednisolone caused dramatic improvement of his symptoms, chest X-ray findings, and laboratory data.
His clinical course and response to prednisolone therapy indicated that long-term steroid administration could not be avoided. The prolonged symptoms and the necessity for long-term steroid therapy are disscussed.

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A case of posterior upper mediastinal angiomyolipoma is reported. The patient was an asymptomatic 63-year-old female, in whom an abnormal shadow was detected on chest x-ray at medical examination. On computed tomogram, the mass was located in the right paravertebral upper mediastinum, and its density had a CT-number of 12. It had high MRI intensity. Since there remained a possibility of malignancy, thoracotomy was carried out. The resected tumor was soft in consistency and the size was 20×23×37mm. Histological examination showed that the mass was composed of fatty tissue, smooth muscle, and vascular tissue. Therefore, the tumor was diagnosed as angiomyolipoma. Although angiomyolipomas are often found in the kidney, those in the mediastinum are very rare and there have been only 2 cases reported in the literature. We consider that angiomyolipoma is rare, but important in the differential diagnosis of mediastinal tumors.

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We present a 65-year-old female with myelodysplastic syndrome (MDS) who has attended our O. P. D. since 1983. In early December, 1990, dyspnea on effort developed which then progressed to dyspnea at rest at the end of December. She was admitted on January 8 with orthopnea. Chest X-ray films revealed loss of vascular shadows of the right lung. Blood gas analysis showed hypoxemia and hypocapnemia. Abnormalities in the coagulation-fibrinolytic system (increased TAT (thrombin-anti-thrombin III complex) and α₂-PIC (plasmin inhibitor complex)), possibly due to MDS, were detected. The diagnosis of pulmonary thromboembolism was made by pulmonary perfusion scintigram and pulmonary arteriography. After commercement of anticoagulation therapy on January 15, the subjective symptoms, blood gas analysis, pulmonary scintigram, and disorders of the coagulation-fibrinolytic system improved. The patient was discharged on March 5, 1991. The present case of myelodysplastic syndrome was associated with abnormalities of the coagulation-fibrinolytic system and was complicated by pulmonary thromboembolism.

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Gold lung, a gold-induced pneumonitis, is considered to be caused by hypersensitivity reaction to gold. We performed lymphocyte stimulation test (LST) to determine the response to gold, using lymphocytes obtained by bronchoalveolar lavage (BAL) from a patient with gold lung.
A 57-year-old man was admitted with progressive shortness of breath following a skin eruption. He had been receiving weekly sodium gold thiomalate (Shiosol^®) for rheumatoid arthritis, with a cumulative dose of 485mg. Chest roentgenogram showed diffuse interstitial infiltrates. LST for the response to gold, using peripheral lymphocytes, was positive. T cell lymphocytosis was observed in BAL, and transbronchial lung biopsy showed lymphocytic alveolitis and granulation tissue in alveolar ducts. From these findings, we diagnosed gold lung. Prednisolone (PSL) was started with an initial dose of 30mg/day and resulted in a rapid improvement. As the dose of PSL was tapered, the patient's condition deteriorated and he was treated with a maintenance dose of 10mg PSL. The second BAL revealed persistent lymphocytosis, and LST using bronchoalveolar lymphocytes for response to gold was positive. LST using peripheral lymphocytes was also positive, but was weaker than that using bronchoalveolar lymphocytes. This is the first report in Japan of a positive LST for response to gold, using bronchoalveolar lymphocytes from a patient with gold lung. This case suggests that the presence of activated lymphocytes against gold in the lung is cumulative, and that cell-mediated hypersensitivity is related to gold lung.

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A 64-year-old male was admitted to our hospital with complaints of the development of high fever, cough and dyspnea 5-6 hours after painting automobiles. His chest X-ray film showed interstitial shadows in both lungs. Pulmonary function test demonstrated reduction of diffusion capacity; and blood gas analysis demonstrated hypoxemia and an increase in alveolar-arterial oxygen tension difference. Marked lymphocytosis and a striking decrease in CD4/CD8 ratio were observed in the bronchoalveolar lavage fluid. Transbronchial lung biopsy specimens showed alveolitis and Masson's bodies. We suspected that the patient was suffering from hypersensitivity pneumonitis induced by isocyanates contained in the urethane paint he used. Immunological studies were performed using chemical compounds of three species of isocyanate molecules (TDI, MDI, HDI) and human serum albumin (HSA). The results were as follows: skin tests were positive for TDI-HSA and MDI-HSA; lymphocytestimulation tests on peripheral blood were positive for TDI-HSA; precipitation reaction was negative for all the isocyanates studies; enzyme-linked immunosorbent assay (ELISA) demonstrated the existence of specific IgG antibodies for TDI, MDI and HDI; inhalation challenge test by TDI-HSA was negative, but environmental provocation was considered to be positive. We diagnosed his pulmonary disorder as hypersensitivity pneumonitis due to isocyanates. Type III and Type IV allergic reactions of Gell-Coombs were suggested to be involved in the pathogenesis, however, there remains the possibility that the instability of isocyanate compounds as antigen modified the results of our immunological studies.

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A 45-year-old man was admitted to our hospital with chief complaint of fever. The chest X-ray examination showed 2-3mm fine nodular shadows throughout the entire lung fields. Eosinophilia was present in the peripheral blood. Spike-like high fever (39°C) appeared every 48 hours. All bacteriologic cultures from blood, bone marrow aspirate, sputum, gastric juice, and bronchoalveolar lavage fluid were negative. Furthermore, the antibody titer of malaria was negative. No antibiotics were effective in this case. Histological examination of the transbronchial lung biopsy showed non-specfic inflammation, but the open lung biopsy specimen showed scattering of tiny granulomatous lesions. These granulomas were composed of histiocytes with indented nuclei, fibroblasts, varying amounts of collagen fibers, and eosinophils. The histiocytes were positive for S-100 protein staining and identified as Langerhans' cells. Therefore, this patient was diagnosed as having pulmonary eosinophilic granuloma.
Two months later, the abnormal shadows on the chest X-ray and high fever spontaneously resolved without steroid therapy.
This case was considered to be unique with respect to the peripheral blood eosinophilia, the three-day fever, and spontaneous improvement, compared with the former reported case.

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Two cases of broncholithiasis, removed bronchoscopically, are reported.
Case 1 was a 38-year-old female who was admitted with hemoptysis. The chest tomogram showed calcification near the right middle lobe bronchus. Bronchoscopy revealed a broncholith in B⁴. Component analysis showed that more than 98% of this stone consisted of calcium carbonate.
Case 2 was a 75-year-old male who was hospitalized because of continuous cough. The chest radiograph showed calcification and atelectasis in the right upper lobe. Bronchoscopically, right B³ was obstructed by a broncholith. After removal of the stone, the distal part of B³ was noted to be filled with pus. Analysis of the stone's composition revealed calcium phosphate (77%) and calcium carbonate (230).

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A 16-year-old female was admitted for the treatment of bronchial asthma. She had a history of measles pneumonia at four years of age. Her chest radiograph revealed right unilateral hyperlucency. She was diagnosed as having Swyer James syndrome from the results of computed tomography, pulmonary angiography, bronchoscopy, and perfusion-ventilation scintigrams, which revealed unsuspected bilateral involvement, and irregularity of severity and distribution. In addition, she had a hypoplastic right upper bronchus, pulmonary hypertension, pneumothorax, and bronchial asthma. The findings of bilateral involvement, irregular distribution, and bronchial lesions strongly suggest that the etiology in this case was damage to the airways caused by measles infection in childhood.

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A 37-year-old man was admitted because of miliary tuberculosis. However, his fever and general condition did not improve with chemotherapy. Six months later, paraplegia occurred following sudden radicular back pain without any alteration of segmental sensation. There were no abnormal findings on X-ray films of the thoracic and lumbar vertebrae. Examination by magnetic resonance imaging revealed that the contents of a cold tuberulous abscess in the right chest wall had drained into the epidural space through the intervertebral foramen. Drainage of the chest wall abscess and laminectomy were performed. Further investigation showed that this case did not belong to the usual type of atypical spinal tuberculosis reported previously.

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Congenital aneurysms of the inferior vena cava (IVC) are very rare, and to our knowledge, only 4 cases have been previously reported. We describe the fifth case of fusiform aneurysm and briefly review the literature.
A 62-year-old woman was admitted to our hospital for investigation of a mass shadow on the right hemidiaphragm on a chest roentgenogram. CT, MRI, and DSA examinations revealed an aneurysmal dilatation of the IVC measuring 51×50×38mm inferior to the right atrium, and the diagnosis of fusiform aneurysm of the IVC was made. The newer imaging techniques of CT, MRI, and DSA have facilitated the diagnosis of this abnormality.

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