Abstract
The ventilatory response to isocapnic moderate hypoxia in humans is biphasic, consisting of an initial brisk increase followed by a gradual decrease in ventilation, namely hypoxic ventilatory depression (HVD)1. A similar biphasic response in the heart rate (HR) during sustained hypoxia was also observed in our previous study2. Although some mechanisms of the HVD have been proposed (the increase in inhibitory neuromodulators in the central nervous systems3, adaptation of the peripheral chemoreceptors4, increase in brain blood flow5 etc.), little has been known about the circulatory parameters, especially about stroke volume (SV) and cardiac output (CO) behaviors during sustained hypoxia in humans. Accurate measurement of SV (and CO) is difficult noninvasively, during sustained hypoxic exposure. In order to compare the effect of sustained mild hypoxia (SpO2 = 80%) on ventilatory vs. circulatory responses, healthy young humans were exposed to sustained hypoxia (end-tidal Po2 = 55∼60 mmHg) for 20 min, applying a newly developed apparatus for measuring CO (pulse dye densitometry).
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References
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© 2004 Kluwer Academic/Plenum Publishers, New York
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Kobayashi, T., Masuda, A., Sakakibara, Y., Tanaka, M., Masuyama, S., Honda, Y. (2004). Relationship Between Ventilatory and Circulatory Responses to Sustained Mild Hypoxia in Humans. In: Champagnat, J., Denavit-Saubié, M., Fortin, G., Foutz, A.S., Thoby-Brisson, M. (eds) Post-Genomic Perspectives in Modeling and Control of Breathing. Advances in Experimental Medicine and Biology, vol 551. Springer, Boston, MA. https://doi.org/10.1007/0-387-27023-X_36
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DOI: https://doi.org/10.1007/0-387-27023-X_36
Publisher Name: Springer, Boston, MA
Print ISBN: 978-0-306-48507-7
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