JAPANESE CIRCULATION JOURNAL
Online ISSN : 1347-4839
Print ISSN : 0047-1828
ISSN-L : 0047-1828
Effects of Reserpine upon Respiratory Functions, with Special Reference to Its Participation in the Increase of Anoxemia
SHOJI KAWABATA
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JOURNAL FREE ACCESS

1968 Volume 32 Issue 2 Pages 201-210

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Abstract
In the previous paper published from this department, it was reported that intramuscular reserpine administration to pulmonary and cardiac patients resulted in decrease of pulmonary artery pressure. It was found in addition, through the study at that time, that arterial oxygen saturation (SaO2) also decreased in most of these cases. It was aimed, therefore, in this presentation to estimate the effects of reserpine upon ventilation, ventilation perfusion relationship in the lung, diffusing capacity of the lung and metabolic rate, for further analysis of the factors participating to the reserpine induced decrease in SaO2. Materials and Methods In 15 patients with chronic pulmonary disease (6 with chronic pulmonary emphysema, 6 with bronchial asthma, 1 with bronchiectasis, 1 with pulmonary fibrosis, and 1 with chronic bronchitis) and 15 patients with chronic cardiac disease (3 with mitral stenosis, 3 with mitral insufficiency, 1 with mitral steno-insufficiency, 2 with aortic stenosis, 2 with atrial septal defect, and 4 with pulmonic stenosis), right heart catheterization was performed, then 1 to 2mg reserpine was injected intramuscularly. Respiratory functions and pulmonary circulations were studied before and 90 minutes after reserpine injection. Results Arterial oxygen saturation (SaO2) decreased in 24 cases after reserpine administration. In patients with chronic pulmonary disease, 13 cases showed decrease in SaO2 and the change was within a range of 4 to -13 (average -5.7) per cent. In patients with chronic cardiac disease, 11 showed decrease in SaO2 and the change was within a range of 2 to -7 (average -2.1) per cent. In 4 cases with pulmonic stenosis the decrease in SaO2 was only 0.8 per cent on an average. I. Changes in ventilatory functions, oxygen uptake and respiratory dead space and its relations to the changes in SaO2.
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© Japanese Circulation Society
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