Pulmonary uptake of norepinerphrine (NE) was measured in patients with ARDS. The relationship between the clinical course, pulmonary uptake of NE and pathogenesis of hypertension frequently associated with ARDS was studied. Also the site for metabolism of NE was examined by histofluorescence and microspectrofluorometric techniques.
Pulmonary uptake of NE was 3.75±4.2% in ARDS. Each measurement was allocated one of three groups according to the date of measurement after admission to ICU. NE uptake was lowest 10-19 days after admission and improved after more than 19 days. The different NE uptake correlated with duration rather then the cause of ARDS. As compared to ARDS without hypertension, NE uptake in ARDS with hypertension decreased significantly (p<0.05). Intense amine fluorescence was seen within the endothelium of small vessels in canine lung and could be identified as NE by microspectrofluorometric technique.
These data indicate that endothelium within small vessels was identified as the major site of NE metabolism, NE uptake reflexted damage to pulmonary microvascular injury in ARDS and strongly contributed to the pathogenesis of hypertension associated with ARDS.

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The production mechanism of crackle is believed to be closely related to airway closing and opening phenomena. But there is no direct evidence which confirms this relationship and the possibility that crackles are produced by opening of alveoli remains. To clarify the production mechanism, we studied physiological conditions in which fine crackle is generated, using excised normal canine lung lobe ventilated in an air-tight box.
Respiratory flow (V), transpulmonary pressure (Ptp), transairway pressure (Pta) from alveoli to airway opening (Palv-Pao) and generated crackles were recorded simultaneously. Alveolar pressure (Palv) was measured by the pleural capsule method. In this method, the pleural surface was multipunctured by a small needle (0.6mm OD, 2mm long) and Palv was directly measured as the inside pressure of the capsule (15mm OD, 5mm depth) glued on the punctured surface. Crackles were picked up from the inside of the capsule by an electret condenser microphone (SONY ECM150). We measured all parameters in various inspiratory and expiratory Ptp, and the following investigations were made: 1) characters of crackles generated (using fast Fourier transformation and time expanded wave form analysis), 2) relationship between Pta and beginning of crackle generation, and 3) the condition of previous end expiratory and inspiratory Ptp in which crackles were generated.
Crackles were heard only on inspiration and had high frequency, and were considered to the fine crackles. At the initial phase of inspiration, Pta changed in a negative direction according to the changes of Ptp, then changed direction and returned to zero gradually. Crackles were produced from this turning point in Pta which may show the beginning of airway opening. When end inspiratory Ptp was kept constant (15-20cmH₂O), inspiratory crackles were produced at previous end expiratory Ptp under -1 to 1 cmH₂O and increased in number with the decrease of end expiratory Ptp. When end expiratory Ptp was kept constant (-10cmH₂O), crackles were produced at end inspiratory Ptp over 4 to 6cmH₂O and increased in number with the increase of end inspiratory Ptp. These Ptp were agreed with the previously known airway closing and opening pressures and were different from alveolar closing and opening pressures.
These results suggest that fine crackles are generated in the excised normal canine lobe and that they are produced during inspiration by opening of peripheral airways which close during expiration.

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We investigated the effect of AA-861 and Sch 1000 on the increase of histamine, serotonin and leukotriene levels in peripheral venous blood and on the change of tracheal pressure and systemic blood pressure induced by vagus nerve stimulation in anesthetized dogs.
We anesthetized 38 mongrel dogs, weighing 10 to 20kg, with sodium pentobarbital (25mg/kg), paralyzed the respiratory muscles with succenyl choline chloride, and ventilated the lungs through a tracheal cannula at a constant tidal volume (200ml/kg) and of a frequency of 16/min. Catheters were inserted into the left femoral artery and vein, and measurement of systemic blood pressure and infusion of drugs or blood sampling were conducted, respectively. The pressure transducer catheter was connected to the orifice of the tracheal cannula to monitor the tracheal pressure. Bilateral vagosympathetic nerve trunks were isolated at the level of thyroid cartilage. We stimulated the right neural trunk electrically with 30 volts from a square-wave stimulator, pulse duration was 1ms and the frequencies were 30shocks/s. We also measured histamine, serotonin and leukotriene levels in peripheral venous blood.
1) The increase of plasma levels of histamine induced by vagus nerve stimulation was markedly suppressed by pretreatment with AA-861 or Sch 1000.
2) The increase of plasma levels of serotonin induced by vagus nerve stimulation was moderately suppressed by pretreatment with AA-861 or Sch 1000.
3) The increase of blood level of leukotriene C₄ induced by vagus nerve stimulation was markedly suppressed by pretreatment with AA-861 or Sch. 1000.
4) The increase of tracheal pressure and the decrease of systemic blood pressure induced by vagus nerve stimulation were markedly suppressed by pretreatment with Sch 1000, while they were not suppressed by AA-861.
5) The percentage increase of tracheal pressure and the percentage change of systemic blood pressure induced by the intravenous infusion of PGF_2α histamine, serotonin, acetylcholine, leukotriene C₄ and D₄ were suppressed by vagotomy.
The above results may suggest that the vagus nerve play a very important role in the regulation of tracheobronchial smooth muscle tones.

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We measured regional ventilation-perfusion ratio (V/Q) by continuous inhalation of Kr-81m and also continuous injection of Kr-81m.
The V/Q distribution can be divided four types. Type I is the normal pattern and V/Q value is the highest at apex. Type II has the highest V/Q value not at the apex but one third lower from the apex and the V/Q value gradually decreases towards the base. In type III V/Q has no gradient from the apex to the base. In type IV V/Q of the base higher than that of the apex. Most pulmonary emphysema show type I, most chronic bronchitis show type II and many interstitial pneumonia denote type IV. The ratio between the area in which the V/Q value was lower than 0.75, and the area of total lung (%0.75) correlated with PaO₂ (r=-0.59 p<0.01).
Coefficiency of variation (COV) of V/Q was larger in pulmonary emphysema and in interstitial pneumonia than in normal lung and COY of V/Q was the largest in chronic bronchitis.

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A case of tracheobronchopathia osteochondroplastica was reported. The case was a 63 year-old male with manicdepressive psychosis who had been suffering from recurrent aspiration pneumonia caused by major tranquillizers. His chest X-ray film showed a tumor-like shadow on the right lower lung field even after the resolution of pneumonia. Fiberoptic bronchoscopy was performed and multiple small nodular lesions were detected by chance on the wall of trachea, right main bronchus and truncus intermedius, but not in the membraneous portions. The histological examination of the specimen obtained by punch biopsy revealed submucosal bony and cartilaginous deposits. There was no amyloid substance in this specimen. As for the tumor-like shadow, primary lung cancer was ruled out but a postinflammatory pleural lesion was suspected.
Thirty-four cases with tracheobronchopathia osteochondroplastica including this case have been reported in the Japanese literature. The clinicopathological characteristics of the disease were discussed.

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A 46 year-old male confectioner was admitted because of dyspnea on exertion and for further evaluation of abnormal shadows on chest X-ray.
Three months after he had began to deal with fine wheat flour for Japanese cookies, he became aware of dyspnea with a slight cough which was progressive and became aggravated in the afternoon. His chest X-ray on admission revealed granular shadows in the lower fields of both lungs. Fine crackle sounds were audible over the lower fields of both lungs by auscultation. There were no data suggesting an inflammatory process such as leucocytosis, elevation of ESR and positive reaction of CRP. Changes in the levels of complements, precipitating antibodies and immune complexes were also not detected. On the other hand, positive reaction to wheat flour and negative reaction to PPD were demonstrated by intradermal skin test. In addition to a high percentage of lymphocytes in bronchoalveolar lavage (BAL) fluid, the proliferative responses of these BAL lymphocytes were dependent on the concentration of fine wheat flour with a maximum stimulation index of 5.53 (1.0μg/ml).
Provocation was attempted by inhaling emulsified fine wheat flour in phosphate-buffered saline with ultrasonic nebulizer in the patient. As a result, dyspnea became progressively worse, and the crackle sounds became coarser 6-12 hours after inhalation. The decrease in V50 value and the increase in γ-globulin levels appeared 6-12 hours after.
In the specimen of transbronchial lung biopsy from the right lower lung, thickening of the alveolar walls with infiltration of mononuclear cells was revealed. Alveolitis in the interstitium and Masson bodies in the centrilobular regions were shown in the open lung biopsy specimens obtained from S8, S4 and S2, whereas no granuloma was observed.
His chest X-ray had showed no abnormalities 9 months before admission. His symptoms and abnormal shadows in chest X-ray on admission have improved without any therapy in the hospital.
The diagnosis was chronic hypersensitivity pneumonitis, with fine wheat flour as the causative agent, as suggested by the data described above.
Clinical features of this case closely resembled idiopathic interstitial pneumonia in several points such as slowly progressive dyspnea lacking in general symptoms, and the granular shadows and volume loss chiefly found in the lower lung fields of both lungs on chest X-ray.
There are two interesting points in this report;
1) This is probably the first case-report of hypersensitivity pneumonitis induced by wheat flour.
2) The clinical course can be regarded as chronic, and it is very probable that some of chronic hypersensitivity pneumonitis case have been included among idiopathic interstitial pneumonia.

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A 17 year-old male with congenital partial pericardial defect associated with left spontaneous pneumothorax and pneumopericardium was referred to our hospital for surgical treatment of the pneumothorax.
He complained of cough and dyspnea on excercise. Chest X-ray films showed left pneumothorax and pneumopericardium. Preoperatively it was strongly suspected that the origin of the pneumopericardium was left congenital partial pericardial defect.
At operation for spontaneous pneumothorax, a 5×4cm partial pericardial defect was found; the left atrial appendage and the lower edge of the aortic arch could be observed through the defect. A bulla was found adhering to the posterior chest wall on the left S¹⁺². Bullectomy and partial resection of the left S¹⁺² were carried out; no surgical repair of the pericardial defect was performed.

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The patient was a 21 year-old female in whom a diffuse infiltrative shadow on chest X-ray was pointed out for 10 years. Diagnosis of DIP with fibrosis was made by open lung biopsy. A moderate amount of steroid was used and improvement of chest X-ray findings and lung function were obtained. The patient is healthy now 10 years after the beginning of therapy.

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