Arterial blood studies were performed more than once on 63 patients with bronchial asthma during various phase of asthmatic attack. The degree of air way obstructive change was quantified by measuring the one second forced expiratory volume (FEV₁) and expressing this measurement as a percentage of the predicted FEV₁. Measurements performed on 13 normal adults were used as controls.
P_CO2 did not change much until very severe degree of air way obstruction was encountered, in which case P_CO2 tended to increase. In spite of the maintenance of a normal P_CO2 in most of the subjects, there was a linear fall in P_O2 with increasing severity of air way obstruction. S_O2 showed almost no changes when the degree of air way obstruction was not marked but decreased significantly when the degree became severe. PH remained fairly constant, but when the degree of air way obstruction became severe it tended to decrease. Actual bicarbonate increased some with linear relation with increasing severity of air way obstruction.
From these results, it appears that alveolar ventilation is maintained at a normal level during most asthmatic attacks, but the P_O2 falls in relation to the degree of obstruction, probably because of uneven ventilation. An elevated P_CO2 during an asthmatic attack appears to be an omnious sign.

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I) Anti-rat-lung-serum was prepared by sensitizing rabbits with rat lung homogenates emulsified in Freund's complete adjuvant. Natures of the antiserum were investigated with Ouchterlony's method in vitro and with intravenous injection to rats in vivo.
1) Studies with Ouchterlony's method showed that the antiserum contained an antibody to the common antigen between the kidney and the lung.
2) Rats died 7-10 minutes after intravenous injection of 1.0ml of the antiserum and the histological finding of the pulmonary lesions was hemorrhagic pulmonary edema.
3) With fluorescent antibody technique it was shown that the administered antiserum localized in the alveolar septa in the way of smooth linear deposit.
II) Pulmonary lesions were prepared with intra-venovs administration of reduced dosage (0.3ml) of the antiserum (absorbed with rat serum and red blood cells) for the purpose of studying the antiserum-induced pulmonary changes immunologically. The pulmonary changes by the antiserum were investigated in relation to previous sensitization of rats by subcutaneous injections of rabbit gamma-globulin.
4) After intravenous injection of reduced dosage (0.3ml) of the antiserum, round mononuclear cells infiltrated around bronchioles, blood vessels and alveolar septa. The changes exaggerated particularly around small blood vessels by previous sensitization of rats by rabbit gamma-globulin.
5) There was a slight elevation of alpha 1 globulin fraction in the group of rats with previous sensitization. No significant changes were seen in gamma globulin fraction as well as in immunoglobulin G in immunochemical assay.
6) In the pulmonary lesions, some of the infiltrated mononuclear cells were seen containing autoimmunoglobulin G in fluorescent antibody technique.
7) Autoimmunoglobulin-G-postive cells were seen around alveolar septa, which were considered to be pulmonary macrophages or large alveolar cells.

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We examined pathological changes of sarcoidosis in autopsy case in which clinical diagnosis was made.
Case: 64 year old woman, wife of a pesant.
Chief Complaint: Dyspnoea, cough, sputum, palpitation of heart, fever and eruptions of face and forearms.
Family History: Her grandmother died of pulmonary tuberculosis.
Past History: She had pain in the joints of elbows, arms, fingers, feet at the age of 20. She had first stridulous breathing at the age of 40.
Onset and Course of Present Illness: She had had the above chief complaints frequently since the age of 58. She was admitted to a certain hospital as having pulmonary tuberculosis, and the biopsy at the skin of her right fore arm was tried, and then her illness was considered sarcoidosis at the age of 60. She was admitted to the Department of Internal Medicine II, at the age of 61. She had the abve chief complaints off and on, and her conditions gradually deteriorated with corresponding changes in symptomes such as dyspnoea. She died severe dyspnoea at the age of 64 (1964).
X-ray Examination of the Chest: Chest films showed hilla enlargement which sharply demarcated, and showed irregular reticular and millialy infiltrative shadow throughout the lung fields. These findings of the chest were noticed from the age of 61.
Chief Laboratory Findings: Tuberculin reactions and Kveim tests were negative. Serum-globlin and serum calcium were almost normal.
Postmortem Examination; The main anatomical findings were small granulomas of epithelioid cells in both lungs, lymph-nodes, skin, heart and kidneys.
Lungs: Epithelioid cell granulomas were seen in the peribronchus, lobular septum, alveolar walls and pleura, and most of subpleural granulomas showed hyalin-like degeneration. Increase of collagenous fibers was seen in peribronchial lesions. The bronchial tree is filled with mucopurulent materials.
Lymph-nodes: The numerous lymph-nodes of mediastinum, trachea, bronchus, lung, neck, and pancreas-spleen showed various sizes: the small ones in the size of tip little finger and large ones in that tip of thumb. Sections through them reveal miliary, uniform granulomas including hyalin-like degeneration and Schaumann bodies.
Skin: Sarcoid granulomas were present over the fore arms and face, and were scattered in true skin.
Heart: Few granulomas were seen in the interstitial myocardium. The wall of right ventricle showed hypertrophy (light cor pulmonare).
Kidney: Few granulomas composed of giant cells and Schaumann bodies were present.
Discussion: Sarcoid granulomas show nearly uniform size and do not show necrosis, often with giant cells and hyaline-like degeneration and Schaumann bodies. Sarcoid granulomas in the skin and lungs are cured almost completely without remaining pathological changes, but relapses occur so frequently. Those lymph-nodes, however often change into hyalin-like degeneration. We consider that the initial lesion occurs within the lung, and then the lymphnodes of lung are infiltrated, and finally sarcoid granulomas appear in skin, heart, and kidney. Cause of death is relatively fresh pulmonary sarcoidosis.

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