BACKGROUND: Sympathetic activation in heart failure may be due to an increase in sympathetic excitatory influences or to a decrease in inhibitory signals to the brain stem. Chemoreflex sensitivity may be increased in patients with heart failure. The present study tested the hypothesis that tonic activation of excitatory chemoreceptor afferents contributes to the elevated sympathetic activity in heart failure. METHODS AND RESULTS: We recorded sympathetic nerve activity to muscle circulation from the peroneal nerve of 12 chronic heart failure patients while the patients were breathing room air and during deactivation of the chemoreceptors while the patients were breathing a 100% O2 gas mixture. All patients except 2 were in class III of the New York Heart Association functional classification. Left ventricular ejection fraction defined by radionuclide ventriculography was 24 +/- 2% (mean +/- SE). We also obtained measurements of resting sympathetic nerve activity in 9 healthy control subjects to document that sympathetic nerve activity was elevated in heart failure subjects. Resting sympathetic nerve activity was 59 +/- 5 bursts/min in heart failure patients versus 36 +/- 4 bursts/min in control subjects (P < .01). In heart failure patients, oxygen administration increased oxygen saturation from 94 +/- 0.9% to 99 +/- 0.3% (P < .0001). This increase in oxygen saturation did not affect resting muscle sympathetic nerve activity (798 +/- 122 U/min while patients breathed room air and 824 +/- 35 U/min during 100% O2 breathing) or blood pressure. CONCLUSIONS: Increased efferent sympathetic activity to muscle circulation in patients with heart failure is not explained by tonic activation of excitatory chemoreflex afferents.
BACKGROUND: Sympathetic activation in heart failure may be due to an increase in sympathetic excitatory influences or to a decrease in inhibitory signals to the brain stem. Chemoreflex sensitivity may be increased in patients with heart failure. The present study tested the hypothesis that tonic activation of excitatory chemoreceptor afferents contributes to the elevated sympathetic activity in heart failure. METHODS AND RESULTS: We recorded sympathetic nerve activity to muscle circulation from the peroneal nerve of 12 chronic heart failurepatients while the patients were breathing room air and during deactivation of the chemoreceptors while the patients were breathing a 100% O2 gas mixture. All patients except 2 were in class III of the New York Heart Association functional classification. Left ventricular ejection fraction defined by radionuclide ventriculography was 24 +/- 2% (mean +/- SE). We also obtained measurements of resting sympathetic nerve activity in 9 healthy control subjects to document that sympathetic nerve activity was elevated in heart failure subjects. Resting sympathetic nerve activity was 59 +/- 5 bursts/min in heart failurepatients versus 36 +/- 4 bursts/min in control subjects (P < .01). In heart failurepatients, oxygen administration increased oxygen saturation from 94 +/- 0.9% to 99 +/- 0.3% (P < .0001). This increase in oxygen saturation did not affect resting muscle sympathetic nerve activity (798 +/- 122 U/min while patients breathed room air and 824 +/- 35 U/min during 100% O2 breathing) or blood pressure. CONCLUSIONS: Increased efferent sympathetic activity to muscle circulation in patients with heart failure is not explained by tonic activation of excitatory chemoreflex afferents.