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Department of Physiology and Biophysics, University of Nebraska College of Medicine, Omaha, Nebraska 68198-4575
The present study aimed to determine whether
peripheral and/or central chemoreflex function is altered in chronic
heart failure (CHF) and whether altered chemoreflex function
contributes to sympathetic activation in CHF. A rabbit model of
pacing-induced CHF was employed. The development of CHF (3-4 wk of
pacing) was characterized by an enlarged heart, an attenuated
contractility, and an elevated central venous pressure. Renal
sympathetic nerve activity (RSNA) and minute volume (MV) of ventilation
in response to stimulation of peripheral chemoreceptors by
isocapnic/hypoxic gases were measured in the conscious state. It was
found that the baseline RSNA at normoxia was higher in CHF rabbits than
in sham rabbits (35.00 ± 4.03 vs. 20.75 ± 2.87% of maximum,
P < 0.05). Moreover, the magnitudes
of changes in RSNA and MV in response to stimulation of the peripheral
chemoreceptors and the slopes of RSNA-arterial
PO2 and MV-arterial
PO2 curves were greater in CHF than
in sham rabbits. Inhibition of the peripheral chemoreceptors by
inhalation of 100% O2 decreased
RSNA in CHF but not in sham rabbits. The central chemoreflex function,
as evaluated by the responses of RSNA and MV to hyperoxic/hypercapnic gases, was not different between sham and CHF rabbits. These data suggest that an enhancement of the peripheral chemoreflex occurs in the
rabbit model of pacing-induced CHF and that the enhanced peripheral
chemoreflex function contributes to the sympathetic activation in the
CHF state.
renal sympathetic nerve activity; minute ventilation; hypoxia; hypercapnia
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