Although respiratory regulation has been extensively studied so far, the relation between the vagal nerves and respiratory reflex in man is still open to controversy. This paper describes the effect of bilateral vagal blockade on respiration.
1) Dyspnea due to unilateral bronchial occlusion.
This type of dyspnea is caused by extreme depression of the intrabronchial pressure on the occluded side and is accompanied by a rapid increase in respiratory rate and a rapid decrease in tidal volume. This type of dyspnea is relieved by blockade of the ipsilateral cervical vagal nerve.
2) Animal experiments on bilateral lung transplantation, heart-lung transplantation and bilateral cervical vagal blockade.
The respiratory changes induced by CO₂ inhalation, low O₂ inhalation, respiratory stimulant. Loss of blood or fever stimulation in the manipulated dogs were compared with those in normal controls. CO₂ inhalation alone produced differences in the respiratory rates and tidal volumes between the two groups.
The tidal volume increase under CO₂ inhalation was suppressed by the inflation reflex but other afferent vagal nerves seemed to be closely associated with the increased respiratory rate.
3) Vagal nerve reflex in humans.
Blockade of the bilateral cervical vagal nerves in an awake state resulted in irregular P_ETCO2 in cases that had been stable and sometimes produced a pattern of Cheyne-Stokes respiration. Inhalation of 5% CO₂ restored the regular rhythm of respiration and enhanced the response to CO₂. When subjected to bilateral vagal blockade in an awake state, the patient expressed an unbearably uneasy dyspneic sensation as if he were pulled into a bottomless abyss. This was demonstrated by the unstable FRC level.

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We studied community acquired pulmonary infections in general hospital. Forty-seven outpatients (group I) and 107 inpatients (group II) were analyzed respectively.
The mean age of group I was 43.4 years old and that of group II was 57.4 years old. Significant underlying diseases were present in 45% of group I and 62% of group II. In group I, the underlying diseases were chronic respiratory diseases, and in group II, chronic respiratory diseases and other significant diseases such as diabetes mellitus, cardiovascular diseases, malnutrition or malignancy.
All of group I and 81 cases of group II were pneumonia. Pleuritis with pneumonia (11), lung abscess or cavitary infection (11), and pyothorax (4) were included in group II.
Etiologic organisms were determined in 48.6% of the cases in group I, and 44.0% in group II. Invasive methods such as transtracheal aspiraiton and percutaneous lung puncture aspiration were very useful for isolation of the pathogen. The pathogens isolated included H. influenzae (17), S. pneumoniae (10), M. pneumoniae (4), C. psittaci (4) in total cases. In group I, H. influenzae was mostly isolated and in group II, S. pneumoniae was mostly isolated and opportunistic pathogens were also isolated. The form of pneumococcal pneumonia was almost always focal pneumonia in this study. There were 8 fatalities (5.2%), all of which were very old or had other serious diseases.

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Various bacteria with pili are able to agglutinate human and aminal red blood cells. Hemagglutinating activity of 131 strains of Escherichia coli isolated from respiratory tract (24 strains), urine (64 strains), feces (36 strains) and blood (7 strains) were tested using human type A, guinea pig, bovine and chicken erythrocytes.
Concerning the hemagglutination activity for erythrocytes from at least one of four species (human, guinea pig, bovine, chicken), the strains isolated from respiratory tract showed a higher level than those isolated from feces (p<0.01) or those isolated from blood (p<0.1).
Agglutination of human erythrocytes: Of 131 strains, mannose-sensitive agglutination was observed in 31 strains, mannose-resistant agglutination in 40 strains and non-agglutination in 60 strains. More agglutinated strains were isolated from the respiratory tract than those isolated from blood but not with statistical significance (p<0.1).
Agglutination of guinea pig erythrocytes: Of 131 strains, mannose-sensitive agglutination was observed in 56 strains, mannose-resistant agglutination in 10 strains and non-agglutination in 65 strains. More agglutinated strains were isolated from the respiratory tract than from urine, feces and blood (p<0.01), and of those, 89% were manose-sensitive agglutination.
Agglutination of bovine erythrocytes: Of the 131 strains, mannose-sensitive agglutination was observed in 4 strains, mannose-resistant agglutination in 6 strains and non-agglutination in 121 strains. Therefore, only a few agglutinated strains were seen.
Agglutination of chicken erythrocytes: Of 131 strains, mannose-sensitive agglutination was observed in 39 strains, mannose-resistant agglutination in 27 strains and non-agglutination in 65 strains. There were no difference between the agglutination of strains isolated from the respiratory tract and those isolated from other.
These results indicate that pili, especially type 1 pill, play an important role in the pathogenesis of respiratory tract infection.

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To elucidate the pathogenesis of adult respiratory distress syndrome (ARDS), bleomycin is often used to induce lung injury because of is acute inflammatory and late fibrogenic effects on the lung. This study was undertaken to determine if fibroblast growth factors or suppressive factors might exist in bronchoalveolar Lavage fluid (BALF) when acute lung injury is induced by bleomycin in rats. In the experimental group, 1.5 U of bleomycin was administered intratracheally, whereas in the control group, saline solution was given. In both groups, rats were sacrificed serially up to 4wks. In each rat, bronchoalveolar Lavage was done three times using an aliquot of 5ml saline solution. BALF was centrifuged to obtain cells and supernatants which were further fractionated by gelfiltration. Fibroblast stimulatory and inhibitory activities were evaluated by [³H]-thymidine incorporation by fibroblasts. In the experimental group, the recovered cell count increased threefold compared with the control group and most of the increase was attributed to the increase of neutrophil. The fraction whose molecular weight is about 20, 000 potentiated the [³H]-thymidine incorporation by fibroblast and its peak activity was found on the 5th day after BLM administration. On the other hand, the fraction of small molecular weight (<1, 000) showed inhibitory activity which did not change throughout the study period. These results suggest that the imbalance between the fibroblast stimulatory and inhibitory activities after the acute lung injury may have a key role to develop pulmonary fibrosis.

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Three cases of relapsing polychondritis are reported. They all complained of dyspnea, which derived from tracheal involvement. Other clinical manifestations were saddle nose (3 cases), painful swelling of ear (2 cases), arthralgia (1 case) opthalmodynia (1 case).
The pathological examination of biopsied cartilage of the pinnae showed loss of basophils with cellular infiltration, fibrosis and breakdown of the matrix.
We also performed PAP (Peroxidase-Anti-Peroxidase) staining of biopsied cartilage, which showed the deposition of IgG, C₃, C₄ and fibrinogen. The results suggested that the pathogenesis of RP might be related to the autoimmune mechanism.

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Among 64 sarcoidosis cases, 6 cases with autoantibodies or autoimmune disorders are discribed. All 6 cases were females over 40 years old, and made up 24% of the original 25 patients over 40 years old. Rheumatoid factor was observed in 2 cases, anti-DNA antibody in 4 cases and anti-microsomal antibody in 2 cases. Four cases of sarcoidosis were associated with ITP or Hashimoto's disease or rheumatoid arthritis. The presence of these autoantibodies or autoimmune diseases seemed to correlate with continued disease activity of sarcoidosis. The analysis of the clinical features of sarcoidosis with coexistent autoimmune diseases may clarify immunologic processes involved in the pathogenesis of both disorders and also provide clues to understanding the relatively poor clinical outcome of longstanding sarcoidosis.

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To evaluate the role of the neutrophil in the pathophysiology of bronchial asthma, we examined the luminol dependent chemiluminescence of peripheral neutrophils (CL) in steroid-dependent asthmatic patients during an acute attack (n=18), during stable period (n=10), and in normal controls (n=21). When stimulated with formyl-methionyl-leucyl-phenylalanine (fMLP 0.1μM), the CL of patients in acute attack was lower than that of normal controls. (5.29±1.25vs. 9.29±0.84 relative light units p<0.01) Among 18 patients, we could examine 10 patients during the stable period after receiving steroids. The CL of those 10 patients during the stable period was significantly higher than their CL during acute attacks, when evaluated by the paired t-test (p<0.05), and was not very different than in normal controls. When stimulated with opsonized zymosan (5 mg/ml), CL was similar in the three groups. We also examined the CL of peripheral neutrophils of normal persons after the preincubation with serum of patients during acute attack and stable period. When stimulated with fMLP, CL after preincubation with serum of patients during acute attack was lower than CL after preincubation with the serum of patients during the stable period. It was suggested that the respiratory-burst activity of peripheral neutrophils in acute asthmatic attack was reduced to the chemotactic stimulus of fMLP.

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Trehalose dimycolate (TDM) is a glycolipid contained in the cell walls of Mycobacteria, Nocardia and Corynebacteria. An intraperitoneal injection of TDM into mice has been known to produce hemorrhagic pneumonia without affecting any other organs. Thus, it provides a unique experimental model for studies of the mechanisms of alveolar hemorrhagic syndrome, including idiopathic pulmonary hemosiderosis. It has been reported that T lymphocytes are essential for the production of TDM-induced hemorrhagic pneumonia, however, the overall cellular mechanism is not yet clear. The purpose of this study is to re-examine and clarify the role of T lymphocytes in the pathogenesis of TDM-induced hemorrhagic pneumonia. To achieve it we considered 1) the dynamics of infiltrating lymphocytes to find out if there is a certain T lymphocyte subpobulation infiltrating predominantly into the lung, 2) the effect of in vivo depletion of T lymphocyte subpopulation by monoclonal antibodies, and 3) the effect of transfer of T lymphocytes into nude mice. The analysis of the dynamic change of the number of lymphocytes showed that the number of L3T4⁺ cells as well as Lyt2⁺ cells decreased on day 2 or 3 after TDM injection, thereafter increased, however, neither subpopulation infiltrated predominantly into the lung. Alveolar hemorrhages occurred in L3T4⁺ cell-depleted and/or Lyt2⁺ cell-depleted mice, and hemorrhages were enhanced in Lyt2⁺ cell-deplete mice. Alveolar hemorrhages occurred even in nude mice, and the intensity of hemorrhages or the cell numbers in the lung did not differ from those in T lymphocyte-reconstituted nude mice, however, hemorrhages were enhanced in L3T4⁺ cell-reconstituted nude mice. These results suggested that T lymphocytes are not primarily involved in the cellular mechanisms of the pathogenesis of TDM-induced hemorrhagic pneumonia, however, L3T4⁺ cells modify the process of the production of hemorrhagic pneumonia secondarily and enhance it.

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We report a case of chronic obstructive pulmonary disease associated with central alveolar hypoventilation diagnosed by exercise test. A 61-year-old man with chronic obstrucitve pulmonary disease was admitted to our hospital because of respiratory failure caused by bacterial pneumonia. After recovery from pneumonia, we examined his functional ventilatory response to incremental exercise. Exercise was discontinued because of his maximal target heart rate, and there was no complaint of dyspnea throughout the exercise test. Although the patient had enough ventilatory reserve during exercise (V_Emax/MVV=50%), there was a marked progressive retention of carbon dioxide disproportionate to the extent of his air flow obstruction. Moreover the patient was able to reduce the carbon dioxide tension to a subnormal level by voluntary hyperventilation, and his ventilatory response to carbon dioxide and mouth occlusion pressure at rest was significantly diminished as compared with normal subjects. These findings suggest that this patient has several features compatible with central alveolar hypoventilation. Exercise test was useful for the diagnosis as well as exercise prescription because the patient could develop dangerous hypoxemia without alarming symptoms like dyspnea.

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We report the first case of primary pulmonary sporotrichosis in Japan. A 53-year-old man was admitted to our hospital for further examination of the abnormal shadows on chest X-ray film. Six months before admission, he was admitted to another hospital because of alcoholic liver disease and diabetes mellitus. Since the initial chest film showed cavities with infiltration in the left upper lung field, he was treated with antituberculous drugs despite negative sputum cultures for mycobacterium. In spite of the medication, his chest X-ray film revealed another cavitary lesion, so he was referred to our hospital. He had been asymptomatic during this period.
Chest X-ray on admission disclosed multiple cavities in the left upper lobe and a cavity in the right lower lobe. Repeated sputum speciemens, bronchial washings and brushings for cytology and cultures were all negative. In an attempt to clarify the pathogen, percutaneous lung aspiration (PLA) was performed. The PLA smaple yielded a positive culture of Sporothrix shenckii. After the diagnosis, S. schenckii was also cultured from sputa. A sporothrix skin test and yeast agglutination test for S. schenckii were positive. In the absence of a history for skin lesion, the patient was diagnosed as a primary pulmonary sporotrichosis. As iodide therapy was ineffective, he was started on a regimen of intravenous amphotericine B. However his renal function progressively deteriorated, so amphotericine B was discontinued. Now he receives miconazole intravenously and is still under careful observation.
As far as we know, this is the first report of primary pulmonary sporotrichosis in Japan. The possibility of sporotrichosis should be considered in any cases of undiagnosed cavitary lung diseases.

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We reported a case of spontaneous pneumothorax associated with pulmonary metastasis of urinary bladder carcinoma. A 73-year-old male patient complaining of chest pain and dyspnea was admitted, who had undergone transurethral resection of the urinary bladder carcinoma and diagnosis of inactive pulmonary tuberculosis based on the chest X-ray film finding one year previously. On admission, chest X-ray film showed right pneumothorax, and the re-expanded chest X-ray film revealed a cystic lesion in the right upper lung field adjacent to the anterior chest wall, corresponding to the previous pulmonary lesion. Three months later, right thoracotomy was performed because of relapse accompaning by profuse air-leakage. There was a pleural fistula on the surface of the cystic lesion and necrotic tissue in it. Drainage bronchi were involved by surrounding tumorous tissue. Histological examination of the specimen from the cyst wall disclosed metastasis of transitional cell carcinoma of the bladder. The probable mechanism of the spontaneous pneumothorax probable consisted of stenosis of the right B³ bronchus caused by the metastatic tumor produced a check valve mechanism leading to cystic lesion, the rupture of which caused the spontaneous pneumothorax.

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A 39-year-old woman complained of an oppressive feeling in her chest and abnormal shadows were detected in the left lower lobe. On a preoperative diagnosis of primary or metastatic lung cancer, left lower lobectomy was performed. There were 3 nodular tumors in the left S⁶, S¹⁰ but no metastasis to regional lymph nodes was found.
Histological examination confirmed “so-called” sclerosing hemangioma. She has remained well for 4 years after surgery. A review of the literatures on sclerosing hemangioma in Japan showed that 12 (5%) of 225 cases of sclerosing hemangiomas had multiple tumors.

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This report describes a rare case of bronchial mucosal injury caused by aspiration of a delayed-iron tablet.
A 44-year-old woman had been taking delayed-iron tablets (Fern-Gradumet^®) regularly because of iron deficiency anemia, and accidentally aspirated a tablet into her bronchus. After this accident, she had complained of wheezing and short ness of breath. On bronchoscopy, the bronchial mucosa of left lower lobe initially showed remarkable swelling and redness, and became corroded and narrowed gradually by iron toxicity over several months, although we tried to remove some fragments of tablet as completely as possible. While we had examined her bronchi repeatedly by bronchoscopy, the bronchial mucosa gradually normalized during 15 months, but moderate Stenosis of the left basal bronchus remained.
The pathological findings showed infiltration of inflammatory cells, edema and granuloma formation in the submucosal region.
This report suggests that the bronchial injury was due to the toxicity of persistent ferrous sulfate eluted from the iron tablet which had adhered firmly to the wet bronchial wall for a long time.

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