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Department of Medicine, University of California, San Diego, La Jolla, California 92093-0623
Chronic exposure
to hypoxia results in a time-dependent increase in ventilation called
ventilatory acclimatization to hypoxia. Increased
O2 sensitivity of arterial
chemoreceptors contributes to ventilatory acclimatization to hypoxia,
but other mechanisms have also been hypothesized. We designed this
experiment to determine whether central nervous system processing of
peripheral chemoreceptor input is affected by chronic hypoxic exposure.
The carotid sinus nerve was stimulated supramaximally at different
frequencies (0.5-20 Hz, 0.2-ms duration) during recording of
phrenic nerve activity in two groups of anesthetized, ventilated,
vagotomized rats. In the chronically hypoxic group (7 days at 80 Torr
inspired PO2), phrenic burst
frequency (fR, bursts/min) was
significantly higher than in the normoxic control group with carotid
sinus nerve stimulation frequencies >5 Hz. In the chronically hypoxic
group, peak amplitude of integrated phrenic nerve activity
(
Phr, percent baseline) or change in
Phr was
significantly greater at stimulation frequencies between 5 and 17 Hz,
and minute phrenic activity (
Phr × fR) was significantly greater at
stimulation frequencies >5 Hz. These experiments show that chronic
hypoxia facilitates the translation of arterial chemoreceptor afferent
input to ventilatory efferent output through a mechanism in the central
nervous system.
hypoxic ventilatory response; acclimatization; central nervous system
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