The plasma levels of DKB were measured in ten subjects following bronchofiberscopic bronchial lavage with a 300mg dose of the drug diluted by 60ml saline solution (bronchial lavage method) and nine subjects following inhalation of a 300mg dose via intermittent positive pressure breathing (IPPB method). All the subjects had respiratory infections.
The highest mean concentration of DKB was 6.17μg/ml at 120 minutes after bronchial lavage and 0.62μg/ml at 15 and 30 minutes after inhalation via IPPB.
The bronchial lavage method with a 300mg dose of the drug produced a concentration of the drug about ten times higher than the IPPB method with a 300mg dose and almost the same concentration as intramuscular administration of a 100mg dose of the drug. Via the bronchial lavage method, the concentration of the drug in the lung tissue and sputum can easily exceed the level of MIC without side effects. Via intramuscular administration, if the pathogenic microorganism is relatively resistant to the drug, it might not attain the level of MIC without side effects.
Therefore, we expect that this will become a powerful new method in treatment of intractable infectious diseases of the respiratory tract.
However, optimal administration dose of the drug should be discussed thoroughly considering the effect on the disease and the direct injury of the mucosa of the respiratory tract.

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Two hundred and sixty-three subjects with chronic respiratory diseases were repeatedly studied by means of routine spirometry over a period of more than two years (average 4.8 years), during which at least three observations were performed. These tests were carried out at reasonably stable stages of illness.
The annual change in each parameter was estimated by least-squares regression of obtained values against time. The mean annual change in each group of patients with each clinically determined pulmonary disease was calculated by averaging these slopes. Results were compared with our data obtained from sixty-three healthy control subjects.
Patients with chronic pulmonary emphysema and diffuse fibrotic change in the lungs showed greater decreases in ventilatory function values than did the healthy subjects during the period of observation. In patients with emphysema, the mean annual changes were decreases of 0.027l/m/yr for VC/Ht, 0.055l/m/yr for FVC/Ht, 1.01%/yr for % VC, 0.058l/yr for FEV_1.0, 1.42l/min/yr for MVV, 1.44%/yr for %MVV, and 0.90%/yr for the air trapping index. In patients with diffuse fibrotic change in the lungs, there were also decreases of 0.042 for VC/Ht, 0.050 for FVC/Ht, 1.73 for % VC, 0.065 for FEV_1.0, and 0.63 for MVV. These changes were statistically significant (p<0.05) compared with data in the healthy subjects. Patients with bronchial asthma, bronchiectasis, and pulmonary tuberculosis generally showed no further deterioration than did the healthy subjects.
Observed variation of ventilatory parameters was represented by the residual standard deviation of the regression line. The coefficient of variation in patients with asthma, emphysema, and bronchiectasis exceeded 10% in all parameters obtained, which was greater than in healthy subjects.

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Pulmonary effects produced by exposure to a low concentration of ozone were investigated utilizing 53 pentobarbitalized adult rabbits. Thirty five rabbits respired room air containing ozone ranging frome 0.25 to 1.1ppm for 12hr. The lungs were examined for functional and pathological changes at 6 hrs (15 rabbits), 1 day (7 rabbits), 3 days (6 rabbits), and 7 days (7 rabbits) thereafter. The remaining 18 rabbits were not exposed to ozone and served as controls. Closing volume and lung volumes were measured by use of the single breath oxygen test. Significant changes were observed in the slope of phase III (ΔN₂%), closing volume %(CV%), closing capacity %(CC%), residual volume %(RV%), standardized vital capacity (%VC), and standardized residual volume (%RV), though the peak stage of these changes varied for each factor. ΔN₂% showed a maximal increase at 6hrs, followed by a rather rapid recovery. In contrast, the CC%, CV%, and RV% attained their highest values at one day and gradually recovered to levels close to control values by seven days. Since the functional changes reported were closely correlated with concurrent pathological findings, we conclude that the former reliably reflect the abnormalities of peripheral airway disease.

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The effects of hyperoxygenation on carbohydrate metabolism were examined in 30 patients with chronic respiratory failure based on chronic obstructive pulmonary disease. Glycolytic metabolites and related substances were analyzed before and after 1 hour of pure oxygen inhalation. Decrease in blood glucose (4.2%) and lactate (27.2%) and increase in 2, 3-diphosphoglycerate (DPG, 5.0%) and lactic dehydrogenase (LDH)-3 (17.3%) were seen after oxygen inhalation in patients with moderate hypoxemia (n=14, mean PaO₂=51mmHg). These metabolites except for 2, 3-DPG did not change in patients with slight hypoxemia (n=16, mean PaO₂=67.4mmHg). Pyruvate, free fatty acid, LDH activity, LDH-1, 2, 4, and 5, and immunoreactive insulin did not change during hyperoxygenation. These results suggest that metabolic alteration due to hyperoxygenation is extremely rapid in patients with deteriorated lung function. Combined effects of tissue hyperoxygenation and concurrent respiratory acidosis are mechanisms probably involved. Increase in LDH-3 is especially noted perhaps because it may leak from lung tissue injured by oxygen.

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To maintain an adequate level of arterial oxygen tension (PaO₂), it is not necessary to remark that one of the most essential is the balance between ventilation and perfusion in the lung. This study tested how rapidly and effectively PaO₂ recovers when an acutely distorted imbalance is repaired. The lungs of 31 mongrel dogs, anesthetized with sodium pentobarbital were divided with Carlens' tracheal divider under mechanical ventilation with 100 percent oxygen in a supine position. Arterial and mixed venous blood were consecutively sampled every one to three minutes and analysed with an electrode blood gas analyzer (IL 213), with simultaneous monitoring for other vital signs. With obstruction of the left main bronchus and induction of absorption atelectasis of the left lung, PaO₂ decreased to the level of 81.1±32.4mmHg (QS/QT 45.8±13.6%) in about ten minutes from a control arterial tension level (PaO₂ 620±38mmHg, Qs/Qt 3.9±2.9%). However, PaO₂ recove red almost instantaneously to the control level (PaO₂ 576±56mmHg, QS/QT 5.5±2.2%) when the ipsilateral pulmonary artery was obstructed at the trunk of the pulmonary artery with a balloon tip cardiac catheter. The magnitude of the PaO₂ elevation by pulmonary artery obstruction was entirely dependent on at where the pulmonary artery was obstructed. When the pulmonary artery was obstructed in the peripheral portion, the rec overy of PaO₂ was not sufficient (PaO₂ 203.2±116.1mmHg, QS/QT 31.4±11.1%). These results suggest that the level of PaO₂ during acute im balance of ventilation and perfusion in the lung is entirely dependent on the geometrical balance between vascularand alveolar compartments and there is no active nervous or humoral regulation to readjust their balance in either the plumonary vasculature or ariway system.

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We have studied the response of gas exchange parameters, e.g. arterial oxygen (O₂) and carbon dioxide (CO₂) tension, alveolar O₂ and CO₂ tension, and alveolar to arterial pressure differences for O₂ and CO₂, to muscular exercise aiming to establish a means of evaluating exercise tests and applying the rescults to clinical diagnosis.
Five healthy male subjects, ranging in age from 20 to 22yrs. were directed to exercise using a bicycle ergometer at three work loads i.e. light work with oxygen consumption (V_O2) 1l/min, moderate (V_O2=2l/min), and heavy (V_O2=3l/min) work. When steady states were achieved at rest and at each work load, arterial blood samples were taken through an indwelling catheter in the radial artery, and the P_O2, P_CO2 and pH were measured immediately by an electrode system. At the same time, expired gas was collected in a Douglas bag for the measurement of minuite ventilation and mean expired O₂ and CO₂ concentrations. During rest and exerc ise, O₂ and CO₂ tension of expirated air were continuously measured by a mass spectrometer. Heart rate and esophageal temperature were also monitored throughout the experiment.
End-tidal O₂ tension, assumed equivalent to alveolar O₂ tension, decreased slightly from the level at rest at the light work load, and then increased gradually when the work load increased. On the other hand, arterial oxygen tension decreased 6mmHg from the resting level at the light work load and stayed at the same level in spite of the increase in work intensity. Therefore, end-tidal to arterial oxygen tension difference (A-aD_O2), which was 11.3±1.1mmHg at rest, decreased to 7.6±1.3mmHg at light exercise and then increased finally up to 22.3±2.8mmHg at heavy exercise. Limited oxygen diffusion through the alveolar membrane, as a result of remarkable decrease of P_VO2 and contact time, was considered as the reason for the increase of A-aD_O2 during heavy exercise.
As a result of this experiment, the following ideas were suggested for clinical applications: 1) end-tidal sampling for estimating alveolar O₂ tension has definite advantages over using the alveolar equation, both from a theoretical and also from a technical point of view. 2) the pattern of A-aD_O2 changes due to the increase of work load would be a valuable measure to evaluate the gas exchange during exercise and could be used to categorize potieuts of pulmonary diseases. 3) A-aD_O2 during light exercise is a good index to differentiate normal and impaired gas exchange since it shows a minimal value in healthy sub jects. 4) Alveolar oxygen tension during exercise could be approximated by using arterial values alone and assuming R from arterial bicarbonate concentration.

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A 42-year-old man was admitted to the emergency ward of our hospital, because of disturbance of consciousness and chest pain. He was hit on his chest by a man in a drunken brawl, 10 days prior to the admission.
His chest X-rays on admission showed abnormal mediastinal widening and a fracture of the sternum, but pulmonary angiogram and aortogram revealed no evidence of involvement of great vessels. The abnormal mediastinal widening which was diagnosed to be the traumatic mediastinal hematoma, reduced in size gradually for first 10 days in the hospital, but began to enlarge again thereafter.
The mediastinal hematoma was removed by surgery on the 19th day of the admission.

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