1. Pneumonia as an opportunistic infection
Pneumonia caused by gram negative bacilli (GNB) which belong to Enterobacteriaceae is found increasingly in recent years. It occurs in most cases nosocomially in patients with severe diseases such as malignant tumor, malignat lymphoma, leukemia, etc. and treated with anticancer drugs, immunosuppressive substances, radiation, adrnocortical steroids etc.
Pneumonia caused by Pneumocystis carinii is also an opportunistic infections and occurs in patients treated with long-term, large dose steroids, immunosuppressive substances etc. for leukemia, malignant lymphoma, organ implantation etc.
The causative protozoa, Pneumocystis carinii can be found by Gomori's methonamine silver stain in needle-puncture fluid and in needle- or pen biopsied specimen.
Intramuscular or intravenous injection of pentamidine isothianate 4mg/kg/day for one to two weeks is effective in nearly the half of the cases.
2. Causative bacteria in pneumonia
From a few reports in recent years it can be inferred that the causative bacteria in primary simple pneumonia (pneumonia in patients without severe complications) is still Str. pneumoniae or Hemophilus influenzae and both of them have few resistant strains against common antibiotics.
3. Causative bacteria in broncho-pulmonary infections
The endeavour to find out or to determine the causative bacteria in pneumonia by many authors was tabulated and our method, the so-called Washculture method of sputum was introduced.
4. Experimental model for the study of pharmacokinetics of antibiotics
The pharmacokinetics of antibiotisc in diseased organ tissue must be different from that of experimental healthy in these rabbit lung were introuduced and discussed.

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Serum N-acetyl-β-glucosaminidase (GL) activity, monoamine oxidase (MAO) activity, and hydroxyproline concentration were determined during the progress of experimental pulmonary fibrosis in rabbits monthly for 4 months. The rabbits received intravenous injections of N-methyl-N-nitrosourethane (MNU) (1mg/Kg of body weight, 6 times a month for 5 to 9 months). GL and MAO activities, and hydroxyproline concentration of the pulmonary tissue of the MNU-treated rabbits were also determined.
Results obtained were as follows.
1) The values of GL activity in serum from rabbits before treatment ranged from 2.8 to 7.5 units per dl with a mean value of 5.3 units. The serum GL activity rose remarkably and ranged from 7.8 to 20.4 units with a mean value of 14.2 units after 6 injections of MNU, when the animals treated with MNU were considered to be at the stage of the interstitial pneumonitis. Significantly high GL activity continued for the 4 months of the experimental period.
2) Serum MAO activity in the MNU-treated rabbits increased as the pulmonary fibrosis advanced.
3) Serum hydroxyproline concentration in the MNU-treated rabbits decreased gradually with the development of experimental pulmonary fibrosis.
4) A fairly good correlation was seen between the severity of the histopathological pulmonary fibrosis and hydroxyproline concentration of the lung tissue.
5) There was atypical proliferation of the bronchioloalveolar epithelium associated with foci of severe pulmonary fibrosis in rabbits treated with MNU fro 9 months.
6) GL and MAO activity of lung tissue homogenate of the rabbits treated with MNU were also determined. The values of GL activity in fibrotic lung tissue ranged from 14.1 to 25.1 units per mg of lung tissue. The values of MAO activity ranged from 27.0 to 79.4 units per 5mg of lung tissue.

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As previously reported, the in vivo buffer value of cerebrospinal fluid (CSF) in acute respiratory acidosis is larger than that of arterial blood, and the buffer mechanism becomes more active as the PCO₂ of the system increases.
To investigate this special buffering mechanism of CSF, we tried to evaluate the role of carbonic anhydrase which is present to a high degree in the central nervous system.
Nine mongrel dogs were anesthetized and mechanically ventilated under muscle relaxation. After two hours of normal ventilation, 50mg/kg of acetazolamide was injected intravenously and the inspired gas was changed from air to 6% CO₂ gas mixture. After maintenance of this condition for two hours, the inspired gas was turned to 12% CO₂ gas mixture and again maintained for two hours. At the end of each stage, arterial blood and mixed venous blood were sampled anaerobically through catheters, and PO₂, PCO₂ and pH values were measured by electrodes. At the same time, CSF was sampled anaerobically through a needle fixed at the cisterna magna, PO₂, PCO₂ and pH values were measured by electrodes and TCO₂ was measured by a Van Slyke gaschromatograph system.
The in vivo buffer values, Δ[HCO₃^-]ΔpH, were calculated using the results of stage 1 and stage 2 (step 1), and from the results of stage 2 and stage 3 (step 2), and they were 10.5±3.0 slykes in the first step and 14.7±3.2 slykes in the second step for arterila blood and 17.2±2.4 slykes and 17.0±3.3 slykes at each step for CSF.
Comparing with the buffer value of the control group (10.7±1.3 slykes in step 1 and 9.8±3.7 slykes in Step 2 for arterial blood, 21.9±3.3 slykes and 43.8±3.7 slykes at each step for CSF), we found that the in vivo buffer value of CSF against acute respiratory acidosis decreased markedly by means of inhibition of carbonic anhydrase of the central nervous systhem by acetazolamide, and the tendency of marked increase of the buffer value at high PCO₂ levels is almost completely abolished. From these observations, we concluded that the carbonic anhydrase system plays an important role in the buffering mechanism of CSF in respiratory acidosis.

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Prostaglandins (PGs), first identified in human and bovine seminal plasma, are also found in considerable amounts in the lungs, kidneys, thymus, brain, pancreas and irises of various mammals. PGE₁ and PGE₂ induce dilation, and PGF_2α constriction in both the tracheobronchial system and the pulmonary vasculature.
The present investigation was conducted to explore the effect of PGs and mixtures of PGs on the cyclic nucleotide contents of guinea-pgi lung and tracheal tissues.
Male guinea-pigs, weighfng 250-300g, were used. Radioimmunoassay was used to determine cyclic nucleotide contents of lung and tracheal tissues.
1) The cyclic AMP contents of guinea-pig tracheal tissues increased dose dependently by incubating them with PGE₂ and PGF_2α. The increase of cyclic AMP with PGE₂ is greater than with PGF_2α.
2) The cyclic AMP contents of guinea-pig lung tissues increased dose dependently by incubating them with PGE₂ and PGF_2α. The increase of cyclic AMP with PGE₂ is graeter than with PGE_2α.
3) The cyclic GMP contents of guinea-pig lung and tracheal tissues increased by incubating them with PGF_2α, but did not show any change by incubating them with PGE₂.
4) The cyclic AMP contents of guinea-pig lung and tracheal tissues showed minimum values when incubated with mixture ratios of 3:7-1:9 PGE₂ and PGF_2α.

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Serum lysozyme was determined by the lysoplate technique in 130 patients with sarcoidosis, and it was 405.8±245.7μg/ml in these patients which was significantly higher than that in normal controls (181.3±31.3μg/ml). The serum lysozyme in 95 patients with manifested lesions (449.7±264.8μg/ml) was significantly higher than in 49 patients in remission (274.6±103.4μg/ml). The serum lysozyme was 388.9±231.1μg/ml in 27 patients with BILL alone, 435.3±256.7μg/ml in 17 patients with BHL and other mediastinal lymphnode enlargement, 476.7±240.4μg/ml in 30 patients with pulmonary involvement without extrathoracic lesions, 424.3±274.4μg/ml in 26 patients with ocular lesions, and 492.9±229.0μg/ml in 7 patients with skin lesions. The serum lysozyme paralleled the extent of the disease and decreased on corticosteroid therapy.
High lysozyme activity was detected in 3 lymphnodes with epithelioid cell granulomas and in 4 lymphnodes with histiocytic proliferation, while could not be detected in 3 normal lymphnodes.
The source of increased serum lysozyme was suspected to be the granulmoas of sarcoidosis, especially the epithelioid cells.

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The present study evaluates whether or not there are macrophage activating factors in pulmonary washings (PW) obtained from normal rabbit lung. Activation of alveolar macrophages in culture was measured by morphological alterations, by adherence to glass, and by the amount of nitroblue tetrazolium (NBT) reduction which reflect the enhanced oxidative metabolism of macrophages.
PW were freed of cells and added to the monolayers of alveolar macrophages. At one hour after incubation with PW, many more cells were attached on glass, spread out and showed enhanced NBT reduction. The maximal effects of PW on macrophage activation were obtained at 6 and 12 hours after incubation with PW. The results suggested that there was the macrophage activating factor in PW obtained from normal rabbit lung. To find the factor, PW were passed through a Sepharose 4B colum. The factor was found to be in the fourth fraction (Fr-IV). From the results of immunoelectrophoresis and the molecular weight of the fraction, it was hypothesized that respiratory IgG in PW was the factor. When IgG in Fr-IV was removed by affinity chromatography, the residual solutions that were free from IgG had no activities. On the other hand, IgG obtained from Fr-IV had similar effects on alveolar macrophages as PW or whole Fr-IV. The effects of IgG on alveolar macrophages was dosedependent and minimal responses to 1×10⁶cells/ml were obtained at a protein concentration of 20μg per ml of culture medium. The molecular weight of respiratory IgG was about 160, 000 daltons when estimated by the method of Andrews with Sephadex G-200. These data showed that the factor in PW which spread out alveolar macrophages morphologically, increased adherence of alveolar macrophages to glass and enhanced NBT reduction by alveolar macrophages was respiratory IgG. Immunoglobulin in the third farction of PW through a Sepharose 4B had no effect on alveolar macrophages. It was thought to be secretory IgA from molecular weight and immunoelectrophoreresis estimations. Lymphokines which were used as a control stimulant had no effect on alveolar macrophages with respect to the morphological alterations and NBT reduction during the observation time of 24 hours.
The results reported here may suggest that alveolar macrophages activated by respiratory IgG or serum IgG play important roles in the defense machanisms of the lower respiratory tract in normal or inflammatory states.

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初診時21オ女性. 10年前より体動時息切れと胸部X線上両下野内側の浸潤影. X線所見徐々に悪化. バチ状指あり, ラ音なし. 肺機能は拘束, 拡散障害, 開胸生検でDIPの診断. ステロイド治療後, 自覚症, X線所見, 肺機能共やや改善し現在健在.

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