Effects of Acute Hypoxia and Exercise on the Pulmonary Circulation
The effects of acute hypoxia, of graded exercise, or both, on the pulmonary circulation were studied in 17 normal subjects. In 3 of these subjects, and in 3 patients with restricted vascular beds, the effects of these stimuli were compared during successive test periods.
In 7 normal subjects, moderate exercise, associated with an increase in cardiac output of approximately 25 per cent, resulted in an average rise in pulmonary arterial mean pressure of 3 mm.Hg. More strenuous exercise in the same subjects, associated with a further increase in cardiac output of approximately 25 per cent, did not elicit further increment in pulmonary arterial mean pressure.
In contrast, 10 subjects with normal pulmonary circulations, who responded to acute hypoxia with an average reduction of arterial oxygen saturation of 17 per cent, manifested an average increase in cardiac output of 5 per cent and an average rise in mean pulmonary arterial pressure of 4 mm.Hg. The critical level of arterial blood oxygen saturation for a significant rise in pulmonary arterial pressure was 85 per cent: in 6 subjects, with arterial blood O2 saturation reduced below this level, the average pulmonary artery pressure rise was 7 mm. Hg.
In the 3 subjects with normal pulmonary circulations who performed exercise and were exposed to acute hypoxia, the contrasting effects of these stimuli on the pulmonary circulation were striking. In the 3 patients with restricted vascular beds exposed successively to both stimuli, the rise in pulmonary arterial mean pressure appeared to be linearly related to the increase in pulmonary blood flow.
In 1 subject, the surgical resection of the preganglionic fibers and ganglia which supply sympathetic efferent nerves to the pulmonary vascular tree was without effect on the responses of the pulmonary circulation to acute hypoxia and to exercise.
The present study failed to identify the mechanism and the site of action of acute hypoxia on the pulmonary circulation.
- © 1960 American Heart Association, Inc.