Abstract
Prolonged exposure to a steady state of hypoxia causes a time-dependent increase in ventilation which persists even after return to normoxia (Dempsey & Forster, 1982). Although the precise mechanism is unknown, this persistent elevation in ventilation is critically dependent on an intact carotid chemoreflex (Forster et al, 1981; Lahiri et al., 1982; Smith et al., 1986). The goal of this research was to determine whether carotid chemoreflex control of sympathetic vasomotor outflow is similarly sensitized by short-term exposure to intermittent asphyxia. We measured ventilation, arterial pressure, and sympathetic outflow to skeletal muscle before, during, and after 20 minutes of intermittent asphyxia (combined hypoxia-hypercapnia) in healthy, awake humans.
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© 1994 Springer Science+Business Media New York
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Morgan, B.J., Crabtree, D., Skatrud, J.B. (1994). Chemoreflex Sensitization Augments Sympathetic Vasomotor Outflow in Awake Humans. In: O’Regan, R.G., Nolan, P., McQueen, D.S., Paterson, D.J. (eds) Arterial Chemoreceptors. Advances in Experimental Medicine and Biology, vol 360. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-2572-1_44
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DOI: https://doi.org/10.1007/978-1-4615-2572-1_44
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