A case of bronchial asthma caused by cat hair was presented. A 28-year-old female complaining of cough and wheezing was admitted to our hospital. The patient had had asthmatic attacks for five years. She has kept one cat in her parents' house for about ten years and the other one in her own house for six years. It was found that she had positive skin test, IgG-RAST score and bronchial provocation test to cat hair. Especially, a bronchial provocation test to cat hair was positive in both immediate and late responses. Thus, her asthma was thought to be caused by cat hair. This case is the sixth case report of cat induced asthma and the first one of cat induced dual asthmatic responses in literature in Japan.

View full abstract

Effects of vitamin E deficiency on bleomycin-induced pulmonary fibrosis were studied on pressure volume curve analysis and morphological examinations in hamsters. Golden hamsters were divided into four groups; a control diet (group C), vitamin E deficient diet (E), control diet and bleomycin treated (CB), and vitamine E deficient diet and bleomycin treated (EB). In group EB, the pressure volume curves shifted most towards the right and downward 10 days after the administration of bleomycin. In the later period (30, 60 days after bleomycin treatment), the curves of group EB shifted gradually upward and to the left more than in group CB. Histologically, group EB was characterized by relatively severe interstitial pneumonitis in the early stages. In the later stages of the experiment, emphysematous changes appeared in combination with a lesser degree of fibrosis in group EB. The mean thickness of alveolar wall of group CB was larger but that of group EB was smaller than group C at 30 days after bleomycin treatment. The results indicate that vitamin E deficient hamsters showed increased distensibility in pressure volume curve and emphysematous changes mixed with focal fibrosis in the morphological examination at later stages after bleomycin administration.

View full abstract

When rabbits reive intravenous administration of complete Freund's adjuvant, numerous epithelioid cell granulomas develop in the lung and serum angiotensin-converting enzyme (ACE) levels increase gradually after adjuvant injection, and the reason of the increasd serum ACE levels has ben thought owing of ACE production from epithelioid cell granulomas. However, in this experiment there was positive but no significant correlation between the developing epithelioid cell granuomas and serum ACE levels in the individual rabbits. Thus, we investigated the reason for the difference. It was clarified that numerous granulomas developed in the white pulp of the spleens and paracortical areas of the intrathoracic lymph nodes (hilar and mediastinal lymph nodes0 from 21 days after administration of complete Freund's adjuvant and that they had strong or moderate ACE activity evaluated by ACE substrate film method. Splenic sinusoidal lining cells of red pulp and histiocytes of lymph sinuses in the thoracic lymph nodes also had moderate ACE activity. On the other hand, epithelioid cell granulomas did not develop in the popliteal lymph nodes, but moderate ACE activity was seen in the histiocytes of the lymph sinuses and the activated macrophages infiltrated in the deep paracortical areas.
These results showed that the serum ACE levels might represent the sum total of ACE produced by several sources containing developing epithelioid granulomas, splenic sinusoidal lining cells and histiocytes and/or activated macrophages in the reticuloendothelial system.

View full abstract

Fifty-six bronchoscopic procedures were performed for the diagnosis of pulmonary diseases in 50 immunocompromised hosts with various underlying diseases. In 30 cases (60%) of these, diagnostic findings were obtained.
Transbronchial lung biopsy yielded a diagnostic sensitivity of 55.1% (27/49 procedures), bronchoalveolar lavage 29.4% (5/17), aspiration of intra-bronchial sputum 8.3% (2/24), brushing 0% (0/1). Especially, overall diagnostic sensitivities were high in diffusely infiltrating and non-infectious diseases. All 5 positive lavages were pneumocystis carinii pneumonia. In 2 lavages, cytomegalovirus was isolated but this was not significant clinically. Complications from procedures occurred in 9 cases (18%) but they were not serious; 3 were pneumothorax, and 6 were transient increase in body temperature. No prolonged morbidity was related to diagnostic bronchofiberscopy. We concluded that bronchofiberscopy is a safe and useful diagnostic procedure, and further studies should be done in the evaluation of the role of this procedure in immunocompromised hosts with pulmonary diseases.

View full abstract

Monocrotaline, a pyrrolizidine alkaloid, is well known as an inducer of pulmonary hypertension in rats. In order to investigate the mechanism of the development of pulmonary hypertension, we studied the reactivity of the great vessels excised from rats which had received to electrolytes and vasoactive agents.
Male Sprague-Dawley rats (130-145g) received saline 2ml/kg (C) or monocrotaline 40mg/kg (MC) by subcutaneous injection. After four or five weeks, the pulmonary artery systolic pressure (PASP) was measured. Following sacrifice, the heart weight and the lung weight were measured. Then each ring preparation (5mm long) excised from the left main pulmonary artery and the thoracic aorta was attached to L-shaped hooks in a glass chamber. The chamber was filled with Krebs-Henseleit solution saturated with 95% O₂+5% CO₂ at 37°C. The upper hook was connected to a force-displacement transducer for the measurement of isometric tension of the preparation. We evaluated the reactivity of the vessels to KCl, CaCl₂, noradrenaline, serotonine, histamine and isoproterenol.
PASP was more markedly elevated and the weight of the right ventricle was heavier in MC than those in C respectively. There was a close correlation between PASP and the degree of right ventricular hypertrophy (RV/LV+S). CaCl₂ induced the most potent and concentration-related contraction of the pulmonary artery in MC. The response was completely abolished by adding a calcium antagonistic agent, diltiazem (10^-6M). However, CaCl₂ did induce no contraction in C. The pulmonary artery in MC showed much more reactivity to KCl than that in C. These results suggest the abnormality of both the resting membrane potential and the calcium influx through the potential dependent calcium channels in the pulmonary arterial smooth muscler in MC. The pulmonary artery in MC showed also more marked reactivity to serotonine and histamine than that in C while the pulmonary artery in MC showed less reactivity to isoproternol. The aorta of each group showed the similar reactivity to the electrolytesand the vasoactive agents. The contraction due to CaCl₂ was not observed in the aorta. It is possible to state that these functional changes in the pulmonary artery lead to the increase in the pulmonary vascular resistance.
In conclusion, the present experiment suggests that the functional changes in the pulmonary artery is very closely related to the development of pulmonary hypertension.

View full abstract

Miliary tuberculosis is an unusual cause of adult respiratory distress syndrome (ARDS). In this report, we described a 28 year-old man with miliary tuberculosis who developed ARDS. A chest roentgenogram 3 days before admission showed a pattern of diffuse finely nodular lesions compatible with miliary tuberculosis, but on admission it had deteriorated to diffuse alveolar infiltration consistent with pulmonary edema. Arterial blood gas studies showed severe hypoxemia with hypocapnaemia. Miliary tuberculosis was suspected and highdose corticosteroid therapy with antituberculosis drugs was instituted.
During the following week, the PaO₂ rose rapidly to 74 Torr breathing room air and the alveolar infiltration on the chest roentgenogram disappeared. The experience with this case served to emphasize the importance of suspecting this condition because miliary tuberculosis is a potentially treatable cause of ARDS and also emphasizes the good effect of early treatment with high-dose corticosteroid.

View full abstract

A 56 year-old woman with primary alveolar hypoventilation syndrome associated with mild proximal myopathy was reported. Examination on admission revealed cyanosis, somnolence, cardiomegaly, moderate diaphragmatic elevation, signs of right-sided heart failure, pulmonary hypertension and polycythemia (RBC; 683×10⁴/mm³). Arterial blood gas analysis revealed a state of chronic respiratory acidosis, PaO₂ 46 Torr, PaCO₂ 65 Torr, and pH 7.40. After hyperventilation with room air, these values improved to PaO₂ 64 Torr, PaCO₂ 42 Torr, and pH 7.56 which indicated the presence of alveolar hypoventilation at rest, partially ameliorated by voluntary effort. Lung function tests showed a restrictive defect more likely to be caused by muscle weakness of the diaphragm than pulmonary disease. She showed blunted ventilatory responses to either carbon dioxide or simple hypoxia, but combined hypoxia and hypercapnia caused a powerful synergistic effect on ventilatory responses. The administration of 100% oxygen was followed by a paradoxical increase in minute ventilation as well as an improvement in blood gas pictures which were explained by, so called, “medullary depression” during room air breathing. The analysis of sleep stage showed that the amount of stage I was more than half of total sleep time (67%) and the amount of slow wave sleep and REM sleep were decreased. (SWS; 5%, REM; 2%) This fact was considered to be related to somnolence during the daytime. In this case sleep was associated with severe hypoxemia. Nocturnal administration of O₂ was an effective treatment of this case because the amount of stage I was decreased to 42 percent and the REM stage was slightly increased up to 5% and overall oxygen saturation level was elevated. Aminophylline was effective on the respiratory center during sleep because its administration decreased duration of periodic change in oxygen saturation with improvement of oxygen saturation.

View full abstract

A case of endobronchial lipoma in a 54 year-old man was reported. He had a history of recurrent pneumonia in right S¹⁰ four times during the last nine years and was admitted because of a tumor-like shadow in right S¹⁰. Bronchography disclosed a filling defect in right B¹⁰ and saccular ectatic change distal to the defect, medial to the tumor-like shadow. TBLB was performed and revealed severe lymphocytic infiltration and granulation, which was not diagnostic. Right lower lobectomy disclosed endobronchial lipoma with ectatic changes of right B¹⁰ and organizing pneumonia. This is the fifteenth reported case of endobronchial lipoma in Japan. Analysis of these fifteen cases yielded the following results.
Of the total, 67% of endobronchial lipomas (ED) were located in the right airway, and 60% of ED occurred in lobar or main bronchi. Transbronchial biopsy was of no use in making an accurate diagnosis. Futhermore, in 93% of the cases thoracotomy was performed, and lobectomy or pneumonectomy was performed in 79% of the ED. The importance of diagnosis in the early phase of the disease was also emphasized.

View full abstract

This report describes a 57 year-old female case of lymphoid interstitial pneumonia (LIP) associated with polyclonal gammopathy and generalized lymphadenopathy. Her primary complaints were cough, exertion dyspnea and loss of weight. Chest X-ray film showed bilateral diffuse patchy and nodular shadow and decreased lung volume. Transbronchial lung biopsy revealed marked infiltration of mature plasma cells and lymphocytes into the interstitium. Remarkable plasma cell proliferation was noticed in swollen lymph nodes histologically, but follicular structures were not destroyed.
In vitro IgG and IgM synthesis by peripheral blood lymphocytes were assessed by means of mixed culture of T and B lymphocytes. Patient B cells were suggested to be polyclonally activated. The polyclonal B cell activation might be the consequence of the augmented helper function of patient T cells. We believe LIP in the present case is a pulmonary manifestation of systemic lymphoplasmacytic proliferative disorder.

View full abstract