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 CO
2 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 AaDo
2 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. aADN
2 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 CO
2 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.
AaDo
2 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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