To evaluate the validity of the scoring method of small airway function tests, selective alveolo-bronchography (SAB) was performed on 13 patients with bronchial asthma, 7 patients with chronic pulmonary emphysema and 4 patients with other lung diseases. The small airway lesion observed on the SAB film was compared with the pulmonary function data including closing volume (CV), ΔN₂/L, volume of isoflow (Visov) ΔV₅₀ and the SAO score. The functional scores of small airway were given, based on the abnormality of each parameter, CV, ΔN₂/L, Visov and ΔV₅₀. These scores were totaled and named the SAO score. Additionally, to evaluate the influence of the elastic recoil on the small airway lesion, the mean diameter of ring shadows observed on SAB film were compared with the elastic properties and small airway parameters.
The severity of small airway lesions in SAB was expressed as the mean of maximum diameter/minimum diameter ratios (ratio of bronchial diameter; RBD) in each 1cm-long segment on magnified film (3 to 4 fold).
1. Loose but significant correlation was found between FEV_1.0% and RBD although no significant correlation was found between respiratory resistance and RBD.
2. Significant correlation was found between SAO score and RBD.
3. Significant correlation was found between elastic recoil and the mean diameter of ring shadow.
4. The correlation between the SAO score and the mean diameter of ring shadow was significant in all patients with chronic pulmonary emphysema but was not significant in patients with bronchial asthma.
We conclude that the scoring method of small airway function test is useful for evaluating small airway obstruction. The small airway obstruction in bronchial asthma is related to the lesion of airway wall, and that in chronic pulmonary emphysema is related to loss of elastic recoil.

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The pulmonary function was evaluated in 122 cases with sarcoidosis, particularly with regard to peripheral airway dysfunction. The 122 cases with sarcoidosis in Toranomon Hospital over the past 17 years consisted of 71 males and 51 females; one stage 0 case, 63 stage I cases and 58 stage II cases. The data were compared between stage I and II.
There were no significant differences in mean values of FEV_1.0%, %MMF, RV/TLC, PMI, Cst, Cdyn60/Cst, R_L, %D_LCO/V_A and Pa_O2 between stage I and II groups. However, significant decreases in mean values of %VC, %D_LCO and Pa_CO2 were observed in the stage II group. There were no significant differences in the prevalence of pulmonary function impairment between stage I and II groups. Frequency dependence of dynamic compliance was present in 6 of 12 stage I patients (50%) and in 11 of 18 stage II patients (61%) with normal pulmonary resistance (R_L), regardless of their smoking habits. There was a close correlation (r=0.538, p<0.01) between Pa_O2 and Cdyn60/Cst, but no correlation between Pa_O2 and %D_LCO/V_A.
The data of frequency-dependent dynamic compliance and normal pulmonary resistence (R_L) observed in stage I and II patients suggest that there might be peripheral airway dysfunction in sarcoidosis.

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We have chosen the excised canine lung lobe preparation perfused with pulsatile flow to study the response of the pulmonary vascular bed to vasoactive agents. This preparation enabled us to detect the predominant site of action of the vasoactive agents on the pulmonary vascular bed by observing changes in flow amplitude at the inflow site of the lobe.
The present study was undertaken to prove the validity of this procedure by means of pulmonary vascular input impedance analysis. The excised lung lobe was perfused either via the pulmonary artery (antegrade perfusion) or pulmonary vein (retrograde perfusion) with autologous blood employing a pulsatile pump. Moduli of pulmonary vascular input impedance were calculated from a pair of pressure and flow waves at the inflow site of the lobe. Serotonin, nor-adrenaline, prostaglandin F_2α and histamine increased the impedance modulus at O-frequency to the same degree in either antegrade or retrograde perfusion. The impedance pattern was markedly changed by serotonin and noradrenaline in the antegrade perfusion, while it was changed by prostaglandin F_2α and histamine in the retrograde perfusion. In the model circuit which was composed of a series of compliance (air chamber) and resistance (rubber tube) resembling the lung lobe preparation, an increase in the impedance modulus at O-frequency occurred in the situation of an increase of resistance corresponding to that in the lobe, and a change in the impedance pattern occurred only in the situation of a decrease of compliance corresponding to that of the proximal vessels in the lobe. Therefore we can conclude that serotonin and noradrenaline mainly constrict the arterial side of the pulmonary vascular bed, and prostaglandin F_2α and histamine mainly constricts the venous side.
In conclusion, the present study using the analysis of the pulmonary vascular input impedance confirmed that the excised canine lung lobe preparation perfused with pulsatile flow is useful to determine the predominant site of action of the vasoactive agents on the pulmonary vascular bed.

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Clinical, roentgenological, and pathological findings of 6 cases of primary small lymphoid tumors of the lung were reviewed. All cases were resected, by penumonectomy, lobectomy, or wedge resection, except for 1 open lung biopsy. Later metastasis to the other organs, invasion to the parietal pleuras, metastasis to the hilar or mediastinal lymph nodes, or immunohistochemical confirmation of monoclonality of tumor cells, were considered to be evidence of malignant lymphoma.
Three cases were diagnosed as lymphomas and the other 3 not, and these 2 groups were compared. Each group showed similar features. Typical features were as follows: 1. Relatively asymptomatic persons. 2. Scanty inflammatory reaction in laboratory data. 3. Rather fair prognosis. 4. Roentogenologically non-segmental infiltrative or mass shadows with rather hazy margin and clear air-bronchogram. 5. Macroscopically, whitish, ill-defined tumor without necrosis. 6. Microscopically, monotonous infiltration of small lymphoid cells to the lung parenchyma with extension along lymphatics at the periphery. Invasion to the vascular walls, bronchial walls and mucosal layer, bronchiolar walls and mucosal layer, and visceral pleuras. No. qualitative differences between the 2 groups were found.
It is thought that these 2 groups are actually same disease (malignant lymphoma).

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Transbronchial lung biopsy (TBLB) was performed 112 times in 108 patients suspected of sarcoidosis. TBLB revealed noncaseating granulomas in 92 of the 112 examinations (82%).
The analysis of the ratio of positive biopsies between the upper lobe and the lower lobe was made in terms of the roentgenographic stage of sarcoidosis. Positive biopsies were obtained in 15 of 43 (34.9%) specimens from the upper lobe, and in 3 of 45 (6.7%) from the lower lobe with roentgenographic stage O disease, in 37 of 90 (41.1%) from the upper lobe, and 29 of 120 (24.2%) from the lower lobe with stage I disease, in 69 of 93 (74.2%) from the upper lobe, and in 43 of 88 (48.9%) from the lower lobe with stage II disease, and in 11 of 16 (68.8%) from the upper lobe and in 11 of 18 (61.1%) from the lower lobe with stage III disease. The proportion of positive biopsies from the upper lobe was significantly higher than that from the lower lobe except for stage III disease. From these results, it may be concluded that noncaseating granulomas of sarcoidosis appear preferentially in the upper lobe. For this reason, it may be necessary to obtain more biopsy specimens from the upper lobe by TBLB in cases of sarcoidosis. This might increase the ratio of positive biopsies by TBLB in this disease.

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Porcine pancreatic elastacse was intraperitoneally injected into SD male rats. On days 1 and 3 after injection rats were killed and the surface appearance in central and peripheral airways was examined by means of a scanning electron microscope. Central airways in elastase-treated rats showed morphological abnormalities, such as shortened and thickened cilia and non-ciliated cells with prominent bulging. In contrast, there were no morphological changes in peripheral airways.
These results suggest that there are considerable differences between central and peripheral airways in the response to acute injury with porcine pancreatic elastase.

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Pulmonary involvement was studied by respiratory manifestations, chest roentgenograms and pulmonary function tests in sixteen patients with progressive systemic sclerosis (PSS).
Respiratory symptoms were found in 13 patients (81.3%), and non-productive cough, with or without breathlessness, was most common. Objective manifestations, namely fine crackling rales, roentgenographic fine reticular markings, or certain abnormalities of pulmonary function tests, were found in 15 of 16 patients (93.8%). On serial chest roentgenograms, slow but obvious progression was observed in 9 of 15 patients. The most common abnormalities of pulmonary functions in the early stage of PSS were reductions in the vital capacity as a percentage of predicted value and the carbon monoxide diffusion capacity (D_LCO), and a fall in the static compliance of the lung. Serial measurements of pulmonary functions were also studied. The mean rate of loss of the vital capacity for the 8 patients was 0.16 liters per year, and that was remarkably more than the expected rate of loss for a normal population. However, that of the one-second % FEV (0.33 percent per year) and that of the carbon monoxide diffusion capacity (0.1ml/min/mmHg per year) were similar to those for a normal population.
Corticosteroid was administered in 15 patients but it failed to show any obvious effectiveness as regards the pulmonary involvement of every patient. Three out of 16 patients died. The cause of death for one patient was lung cancer and that for the others was reapiratory failure, and the mean survival period was 14.7 years.
In conclusion, pulmonary fibrosis develops at a very high rate during the course of progressive systemic sclerosis, and progresses slowly but steadily thereafter, resulting in restrictive ventilatory insufficiency.

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A 76 year-old female suffered from exertional dyspnea and productive cough which had been gradually increasingly aggravated over three years. Her chest roentgenogram showed bilateral diffuse reticulonodular shadows. Results of her pulmonary function tests revealed restrictive impairment and decrease of V₂₅ and hypoxemia. Furthermore, her could hemagglutinin titer was elevated. Rhonchi and crackle sounds were audible over both lungs by auscultation. Expectorants were used by oral administration and nebulizer inhalation, and her symptoms improved. Eight months later, exertional dyspnea and productive cough became markedly worse with intractable diarrhea and general malaise. She died due to hypovolemic shock caused by severe diarrhea and respiratory failure.
Autopsy revealed systemic amyloidosis in the walls of microvessels from the staining property of Congo red stain. This amyloid protein was recognized as AA protein. Principal changes in the lungs were chronic inflammatory cell infiltration, and goblet cell metaplasia both in bronchi and particularly in bronchioles. These findings were compatible with chronic bronchiolitis, thus, this case was diagnosed as diffuse chronic bronchiolitis associated with secondary amyloidosis.
In this paper, we reported a rare case of diffuse chronic bronchiolitis with secondary amyloidosis and discussed previous reports.

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A 37 year-old man was admitted because of a coin lesion on chest x-ray film. He exhibited no respiratory symptoms. The nodular shadow lay in the right lower lung field (S⁶) and showed indentation. Laboratory data suggested no obvious abnormality. Sputum cultures for cryptococcus, bacteria and tubercle bacillus were negative and sputum cytology was class I. A transbronchial biopsy was performed but failed to reveal any sign of disease. PPD skin test was markedly positive. Various examinations failed to diagnosis. Tuberculoma or cancer of the lung was suspected. Open-lung biopsy was performed and the indented tumor lay in S⁶. Tubercle bacillus smear of the specimen was negative. Stamp cytology of the specimen showed giant cells with multiple sherical bodies surrounded by a clear halo. A diagnosis of pulmonary cryptococcosis was confirmed and right S⁶ segmentectomy was performed. Histological findings of the resected specimen showed granuloma on Cryptococcus neoformans. This case showed the usefulness of open-lung stamp cytology procedures for diagnosis.

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A 48 year-old male was admitted with cough, abnormal shadow on chest X-ray film and continuous fever which showed no response to antibiotics.
On admission, peripheral blood examination revealed slight anemia (Hb 10.3g/dl), slight increase of percentage of monocytes (16%) without leukocytosis and increase of ESR. Other laboratory data revealed slight hyperbilirubinemia and elevation of serum transaminase. Concerning tumor marker, marked elevation of ferritin and IAP were detected.
Chest X-ray film on admission, showed a reticulo-nodular pattern of bilateral lower lung fields, suggesting interstitial pulmonary disease. Fever did not respond to antibiotics, so 60mg/day prednisolone was administered. Shortly after, fever decreased but only transiently.
We performed several diagnostic technique, TBLB, bone marrow biopsy, and lymph node biopsy. Anemia and jaundice increased gradually, and the general condition worsened. Histological examination of the biopsy specimen revealed large mononuclear atypical cell proliferation. This was recognized as atypical histiocytic proliferation by electromicroscopical, immunohistochemical, and chromosomal analysis.
Finally, the patient was treated with ACNU (100mg). Then the general condition of the patient rapidly improved. At 15 months from onset, the general condition of the patient continues to be good.
Malignant histiocytosis is characterized by systemic, progressive, fatal disease. Pulmonary involvement is not a rare complication of the disease. Previous reports described a 30-40% incidence of pulmonary involvement. We reviewed the Japanese cases reported in the last 10 years (1975-1985), there were 28 reported cases, 11 of which had pulmonary involvement confirmed by autopsy.
In this case, we performed chromosomal analysis of the bone marrow biopsy specimen. An abnormal clone was identified (chromosome number: 75, mainly near tetraploid karyotype, and a couple of marker chromosomes).
For the histopathological study of this case, we used immunohistochemical techniques employing lysozyme, alpha-1-antitrypsin, S-100 protein. Specimens of both the pulmonary lesion and bone marrow were positive for lysozyme and alpha-1-antitrypsin but negative for S-100. There are many different ideas about the reactivity of immunohistochemical markers. Some investigators suggest that malignant histiocytosis is derived from a “monocyte-histiocyte lineage”, white other claim that it is derived from a “T-zone histiocyte lineage” Therefore there is a difference between the two concerning the reactivity of immunohistochemical staining. Up to the present, there is no commonly accepted assessment of the reactivity of immunohistochemical markers.
This case was treated with ACNU only, which was very effective for this patient. In the Japanese literature there is another report of malignant histiocytosis effectively treated with ACNU. These results show that ACNU can be effective in the treatment of malignant histiocytosis.

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An autopsied case (55 year-old woman) of acquired tracheobronchomalacia is presented. The following histopathological findings were observed on autopsy. Macroscopically, the cartilages of trachea were short and thin, and the arch of the tracheal cartilages was flat. On the contrary, the membranous portion of trachea was elongated, which resulted in elongation of the total circumference of trachea. The cartilages of both main bronchi were short, but the membranous portion was not elongated, which resulted in reduced total circumference of main bronchi. Microscopically, thin tracheal cartilage had ossifying lesions with inflammatory cell infiltration. A thick collagenous layer, which is not observed normally, was observed outside the tracheal cartilage, and the longitudinal elastic fibers were preserved in the cartilagenous portion, but were missing at the membranous portion of the trachea. The smooth muscle bundles were missing in the membranous portion, and collagen fibers replaced them with inflammatory cell infiltration.
Very few autopsied cases of tracheobronchomalacia have been reported, emphasizing the value of this report.

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