What question did this study set out to answer?

This study aims to determine whether tonic activation of chemoreflex afferents contributes to elevated sympathetic nerve activity in heart failure.

September 15, 1996Circulation

Tonic Chemoreflex Activation Does Not Contribute to Elevated Muscle Sympathetic Nerve Activity in Heart Failure

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Why the study?

Does deactivation of chemoreceptors with 100% O2 reduce muscle sympathetic nerve activity in patients with chronic heart failure?

This study aims to determine whether tonic activation of chemoreflex afferents contributes to elevated sympathetic nerve activity in heart failure.
Recorded sympathetic nerve activity from the peroneal nerve in 12 chronic heart failure patients.
Measured resting sympathetic nerve activity and oxygen saturation during room air and pure oxygen breathing.
Compared findings with 9 healthy control subjects for baseline data.
Resting sympathetic nerve activity was significantly elevated in heart failure patients (59 +/- 5 bursts/min) compared to controls (36 +/- 4 bursts/min, P < .01).
Oxygen administration increased oxygen saturation from 94 +/- 0.9% to 99 +/- 0.3% (P < .0001), but did not affect muscle sympathetic nerve activity (798 +/- 122 U/min vs. 824 +/- 35 U/min).
Tonic activation of excitatory chemoreflex afferents does not explain increased sympathetic nerve activity in heart failure.

Does deactivation of chemoreceptors with 100% O2 reduce muscle sympathetic nerve activity in patients with chronic heart failure?

Population

12 chronic heart failure patients (10 in NYHA class III, mean LVEF 24 +/- 2%) and 9 healthy control subjects.

Intervention

Breathing a 100% O2 gas mixture to deactivate chemoreceptors

Comparator

Breathing room air

Outcome

Muscle sympathetic nerve activity recorded from the peroneal nervesurrogate

Elevated sympathetic activity in heart failure is not explained by tonic activation of excitatory chemoreflex afferents.

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Hyperoxia does not suppress sympathetic activity in heart failure; leaves open non-chemoreflex mechanisms and does not support routine oxygen use.

Borne et al. (1996) studied this question.

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Hyperoxia does not suppress sympathetic activity in heart failure; leaves open non-chemoreflex mechanisms and does not support routine oxygen use.