The author discussed respiration physiology found on patients accompanied by predominantly-impaired alveolar gas exchange in terms of alveolar-arterial gas tension differences both for oxygen and nitrogen or of other respiratory parameters. The author's emphasis was placed upon the facts that (1) impaired physiology of arterial hypoxemia without CO₂ retension to be seen on patients with pulmonary diseases, (2) clinical significance of “bronchiolitis syndrome” with referrence to its respiratory impairment, (3) increasing prevalence of such predominant impairment of alveolar gas exchange probably due to ventilation-perfusion ratio uneveness with/or without diffusion impairment, and (4) characteristic features of these patients with regard to their response against therapeutic agents.
Normal standards for the alveolar-arterial gas tension differences (AaDs) were established as following: Mean and standard error of estimates for AaDo₂ obtained on the 57 supine healthy subjects breathing room air was 4.45±0.42 torr and those for aAD_N2 obtained on the 242 healthy subjects was 4.03±0.20 torr. aADN₂ obtained on 114 healthy subjects, whose age wers 41 years or over, was 5.30±0.31 torr. (mean±1 S. E. E.)
The author described impaired respiration physiology on patients with “bronchiolitis syndrome”, whose main subjective complaints were paroxysmal coughing, pain or dullness on chest and shortness of breath. On most of the patients crepitant rales or small moist rales were audible. The patients revealed abnormal AaDs without consistent CO₂ retension although they demonstrated ventilatory capacity within normal limits. Those who were accompanied by the “bronchiolitis syndrome” did not responded to the bronchodilators of isoproterenol derivatives. Oral administration of either prednisolone or d, 1, -alpha-tocopheryl nicotinate was found effective to improve their abnormally increased AaDs.
Consistently increased AaDs were also obtained on patients with collagen diseases, patients treated with BLEOMYCIN (an anticancer agent) and on those who were exposed against environmental oxidants of various concentration higher than 0.10PPM.
AaDo₂ and aAD_N2 were compared with 3Hz effective compliance, flow-volume characteristics, closing capacity, carbon monoxide pulmonary diffusing capacity, and other respiratory parameters to assess their diagnostic significance. Mathematical analysis of AaDs was performed using NOVA-01 minicomputor system based on a two-compartmental model, upon which uneven ventilation-perfusion ratio distribution was assumed. The data obtained on this theoretical calculation enabled the author to estimate quantitatively the contribution of uneven ventilation-perfusion ratio distribution to arterial hypoxemia or to abnormally increased AaDs to be seen on the pulmonary patients.

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The in vitro and in vivo tests for blood lymphocytes from 43 patients with asbestosis and 46 normal adults were performed. These tests included blood lymphocyte counts, lymphocyte transformation, with and without PHA-P, population of E-and EAC-Rosettes forming cells and skin response by PPD and PHA-P injection. Serum immunoglobulin levels were also quantitated and following results were obtained.
1) The mean counts of blood lymphocytes in asbestosis patients of grade I, II and III disclosed 1206, 1620 and 1669/mm³ respectively, while that of normal controls was 2154/mm³. In 9 cases of associated neoplasm there was remarkable lymphopenia.
2) PHA-P response (³H-thymidine uptake) of blood lymphocytes from asbestosis patients was depressed with the degree of diffuse reticulations of the lungs, compared with those of normal controls.
3) PHA-P and PPD skin tests showed less reaction in asbestosis than those in minimal tuberculosis.
4) The population of E-Rosette forming cells in blood lymphocytes of asbestosis patients was decreased, while that of EAC-Rosettes forming cells was increased.
5) In almost cases of asbestosis, the serum levels of IgG and IgA showed significant elevation.

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To verify the applicability of the beta-adrenergic receptor theory on tracheobronchial hypersensitivity in patients with bronchial asthma the author measured cyclic AMP content in the lungs and bronchi. Guinea pig, dog, rabbit, rat, and mouse were used in the present study with radio-immunoassay technique using [³H]-labelled cyclic AMP.
1) Difference of cyclic AMP content in trachea, bronchus and in lungs was consistent with regard to the species of animals. Cyclic AMP content in dogs or in mouse was the highest, which was followed by that in rat, rabbit and that of guinea pig.
2) Cyclic AMP content in the airway of guinea pig was 1/4 of that in dog and the content in rabbit was 3/5 of that in dog.
3) No consistent difference of cyclic AMP content in mucous tissue of the trachea, main bronchus and in lobar bronchus to each other was evident. Content of cyclic AMP in the segmental bronchi was as low as 75±14% of that in bronchi (p<0.02) and that in the lungs was 38±4% of that in trachea.
4) Based on the measurement of cyclic AMP content on different tracheal component, especailly with regard to the membranous wall component, the author concluded that cyclic AMP in the airways is mainly distributed in the tracheal smooth muscle. Cyclic AMP content in the tracheal muscle was over ten folds of that in the heart muscle.
5) 10 minutes after IP administration of some beta-stimulants of 1mg/kg body weight on guinea pig cyclic AMP content in the airways increased up to 3-6 folds of the initial value. 60 minutes after administration of Salbutamol or of Metaproterenol no consistent change in cyclic AMP content in the airways was evident while it decreased to 50% of the peak value when Isoproterenol was given. 10 minutes after IP administration of Propranolol of 2mg/kg body weight cyclic AMP content decreased to 41±17% of the initial value.
6) 10 minutes after IP administration of Aminophyllin of 100mg/kg body weight, Papaverine of 10mg/kg body weight, Prednisolone of 1mg/kg, or of Prostaglandin E. of 0.1mg/kg body weight cyclic AMP content in the airways increased 2-3 folds of its initial content.
The author presumed, based on these data, that the cyclic AMP theory could be applied upon the bronchopulmonary system.

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A case of “primary mediastinal choriocarcinoma with teratoma” was described.
Main symptomes and signs of the patient were cough, bloody sputum, chest pain and gynecomastia. Chorionic gonadotropin in the serum was markedly elevated. On chest X-ray film large massive shadows protruding from the right hilar portion and multiple nodular shadows in the both lung fields were found. He died with evidence of progression after 2 weeks of admission.
Pathologically, anterior mediastinal tumor, metastatized to the lungs and various organs, was comprised the elements of choriocarcinoma, fetal cartilage, and glandular, epidermoid tissue accompaning marked necrosis with hemorrhage.

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