Combined hypoxia and hypercapnia evokes long-lasting sympathetic
activation in humans.
Morgan, Barbara J., David C. Crabtree, Mari Palta, James B. Skatrud.
Departments of Kinesiology, Medicine and Preventive Medicine,
University of Wisconsin and the Middleton Memorial Veterans Hospital,
Madison, Wisconsin 53706
APStracts 2:0111A, 1995.
We studied ventilatory and neurocirculatory responses to combined
hypoxia (arterial O2 saturation, 80%) and hypercapnia (PetCO2, +5
mmHg) in awake humans. This asphyxic stimulus produced a substantial
increase in minute ventilation (6.9+/-0.4 to 20.0+/-1.5 liters/min)
which promptly subsided upon return to room air breathing. During
asphyxia, muscle sympathetic nerve activity (intraneural
microelectrodes) increased to 220+/-28% of the room air baseline.
Approximately two-thirds of this sympathetic activation persisted
after return to room air breathing for the duration of our
measurements (20 min in 8 subjects, 1 hr in 2 subjects). In contrast,
neither ventilation nor sympathetic outflow changed during time
control experiments. A 20-min exposure to hyperoxic hypercapnia also
caused a sustained increase in sympathetic activity, but unlike the
after effect of asphyxia, this effect was short-lived and coincident
with continued hyperpnea. In summary, relatively brief periods of
asphyxic stimulation cause substantial increases in sympathetic
vasomotor outflow which outlast the chemical stimuli. These findings
provide a potential explanation for the chronically-elevated
sympathetic nervous system activity which accompanies sleep apnea
syndrome.
Received 16 November 1994; accepted in final form 3 March 1995.
APS Manuscript Number A1170-4.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 21 March 1995.