The purpose of this study is to assess the efficiency of ASAHI-Hollow Fiber Gas Exchanger by extracorporeal circuit for improving acute respiratory insufficiency.
The gas exchanger has 8000 hollow fibers made of cuproammonium rayon, the thickness of the fiber wall is 20μ, inside diameter 260μ, length 17.0cm. The total surface area for gas transfer is 1.0m² and the priming volume of the gas exchanger is 115.0ml. 12 dogs (9-13kg) were administered with sodium pentobarbital and hexafluorenium bromide, intubated and ventilated with a volume cycled respirator. The state of acute respiratory insufficiency was brought about by reducing the displacement capacity of the respirator. A-V shunt was placed in the femoral artery and femoral vein and the dog was heparinized.
The extracorporeal circuit consisted of a roller pump, the gas exchanger and a heat exchanger. The volume flow of blood through the gas exchanger was kept at 90-350ml/min.
The results ohteined were:
1) O₂ and CO₂ transfer rates were 8.5ml/min/m₂ and 17.0ml/min/m₂ respectively at the blood flow of 350ml/min.
2) Excepting mild hemolysis, no significant change was observed in blood components.
3) The experimental hypoxemia was eliminated by the gas exchanger, while it could not necessarily be said that the hypercapnia was sufficiently eliminated.

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Immunology has made significant advances in recent years and many questions have been resolved with regard to the local immune mechanism in various organs. However, immune mechanisms in lung tissue have not been sufficiently understood.
Therefore, 95 autopsy or biopsy specimens of lung and bronchial tissue were studied in order to obtain informations about the local immune mechanism in human lungs.
Antisera obtained from immunized rabbits with immunoglobulins (IgA, IgG and IgM) were labeled with conjugated FITC or Rhodamine. Following a single and double direct staining using fluorescent antibody techniques, the distribution and localization of immunogloblins (IgG, IgA and IgM) were systematically investigated.
Antisera obtained from immunized rabbits with immunoglobulins (IgA, IgG and IgM) were labeled with conjugated FITC or Rhodamine. Following a single and double direct staining using fluorescent antibody techniques, the distribution and localization of immunogloblins (IgG, IgA and IgM) were systematically investigated.
The results obtained were as follows.
In the normal lung tissue, IgA was predominantly distributed in the bronchial area, while IgG was predominantly distributed in the alveolar area. The boundary between the IgA and IgG regions existed probably in the bronchiolar area. IgM showed no partfcular distribution and was traced in small amounts in the adult lung tissue except for perinatal periods. The distribution of lysozyme was similar to IgA in the bronchial areas and to peroxidase in the alveolar areas. IgG was localized in the connective tissue and secretion to the airway was not usually observed. When inflammation developed in the alveolar area, IgG tended to increase significantly. IgA was mostly localized in the apical portion of mucosai epithelial cells, their intercellular spaces, bronchial ciliary cells and bronchial glands. IgM was mainly observed in the mucous glands and the mucous layer at the main bronchus and secretion into the airway was also noted. Ig bearing cells were small in number as expected and each cell responded to only one of the immunoglobulins. The IgG bearing cells were present to a greater extent than IgA-bearing cells. Each type of Ig-bearing cell was observed in the foetus lung, thymus and spleen at 24 question weeks. There was a poor immune response in the hilar lymph nodes and Ig bearing cells were only present in less than 10% of total cells in the lymph node. Each type of Ig-bearing cell increased significantly around the interstitial vessels in various lung diseases, especially in primary lung cancer, and the distribution ratio of IgG, IgA and IgM was 2-3, 2, and 0.4 respectively. The distribution of IgA and lysozyme suggested that the bronchial glands would be a source of IgA and lysozyme.
The above results indicated that a multi-immune defence system by IgG and IgA might exist in the lung; IgA being active in the bronchial area, especially in the mucous lining and IgG in the alveolar area.

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Although silicosis is characterized by proliferation of fibrous tissues in the lung, it is well known that some of the patients with silicosis show emphysematous changes in the lung. To confirm the relationship between the low serum antiprotease activity and the relatively high incidence of emphysema combined with silicosis, the serum alpha-1-antitrypsin level was measured in 79 patients with silicosis, (there were none with silicotuberculosis), using Eriksson's trypsin inhibition method and the single radial immunodiffusion method. The results were discussed by comparing with chest X-ray findings and data of pulmonary function tests.
Of the 79 patients with silicosis examined, 5 showed a low serum alpha-1-antitrypsin level below normal range in both methods. However, all of the 5 patients showed an intermediate level of alpha-1-antitrypsin. Cases suggesting homozygous alpha-1-antitrypsin deficiency were not recognized in our study.
The average age of the patients with low and normal alpha-1-antitrysin on initial admission to the hospital was 44 and 53 years respectively, the difference being significant.
Roentgenological examination of the chest showed the patients with low serum alpha-1-antitrypsin exhibited emphysematous changes more frequently than the patients with normal alpha-1-antitrypsin level.
According to the respiratory function tests, the patients with low antitrypsin had a higher incidence of lowered FEV 1.0% and of elevated %RV than the normal alpha-1-antitrypsin group.
From these results, it was proved that the low serum alpha-1-antitrypsin level in silicotic patients was more closely associated with combined emphysema than the normal alpha-1-antitrypsin level.

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The patient was a 43-year-old woman complaining of progressive dyspnea and fever. Rales in the lungs and clubbing of the fingers were seen at clinical examinations. Chest roentgenogram showed nodulary opacities in the midle and lower lung fields giving a ground-glass appearance. Corticosteroids and antibiotics produced no response and she died on the 24th admission day.
Histological findings of the autopsy lung were as follows. The alveolar septa were thickened with infiltration of lymphocytes, plasma cells as well as proliferating fibroblasts and alveolar pneumocytes. In the alveoli, there were numerous bizarre multinucleated giant cells with a high phagocitic activity which Liebow considered “cannibalistic”. The cause of the disease was not disclosed by the patient's history and results of examinations. This report may show the first GIP case in Japan.

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A 21 year-old primipara aspirated gastric contents into the lungs during anesthesia for cesarian operation and had dyspnea and cyanosis. Her chest X-ray showed pictures indistinguishable from those of interstitial pneumonitis and pulmonary edema.
After the diagnosis of aspiration pneumonitis-“Mendelson's syndrome” was made, this obstetric complication disappeared rapidly with administration of corticosteroids and antibiotics in large doses.

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