Clin Auton Res (2002) 12 : 137–138 DOI 10.1007/s10286-002-0033-y
Brian E. Hunt
EDITORIAL
Sympathetic surges?
Increased sympathetic outflow invariably accompanies many pathophysiologies such as heart failure, and is often related to the medical prognosis in these patient populations. However, the afferent input(s) responsible for activation of the sympathetic system are not clearly understood. Though likely the result of numerous effectors, an abundance of data from both animal and human models implicate autonomic reflex systems. In this issue of Clinical Autonomic Research, Macefield and Elam share some intriguing observations regarding the apparent inability of the baroreflex to inhibit basal sympathetic outflow in patients with congestive heart failure and obstructive sleep apnea [3]. Furthermore, the authors speculate on a chemoreflex origin for these baroreflex resistant surges in sympathetic outflow. If the author’s hypothesis is proven true, these observations may significantly add to the sparse data on autonomic reflex control of sympathetic outflow in heart failure patients. However, the lack of quantification and small sample renders the authors’ conclusions speculative. The raw neurogram is characterized by random electrical ‘noise’ producing a broad band of indiscernible activity from which discernable positive and negative neural spikes emerge. Efferent sympathetic outflow transmitted along C-fibers, generate negative spikes in the neurogram. Since first used to identify peripheral sympathetic nervous activity in the late 1960’s [2], the neurogram typically undergoes significant post-processing before analysis, including full wave rectification and integration. Although this provides a waveform from which pulse synchronous bursting (i. e., sympathetic activity) can be discerned, this process also am-
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Brian Hunt, Ph. D. () Research and Training Institute, HRCA Boston MA 02131, USA Tel.: +1-6 17/3 63-85 42 Fax: +1-6 17/3 63-89 36 E-Mail:
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plifies or exaggerates characteristics of the raw signal such as burst amplitude, baseline shifts, etc. [1]. Thus, the inclusion of both raw and integrated data by Macefield and Elam provides the reader an excellent opportunity to compare the integrated waveform and raw signal to determine the most likely origin of these surges in sympathetic outflow. The raw neurogram provided by Macefield and Elam shows periodic widening in the central band. Continued sympathetic firing during systole could generate the type of neurogram shown. Alternatively, increased noise also may result in similar neurogram characteristics. Identification of single sympathetic neurons, which typically fire during diastole and which are also active during systole when the ‘surges’ of activity occur, would favor the authors’ neural hypothesis. Interestingly, the integrated signal shows the average amplitude of each burst during a purported surge is similar to those during ‘normal’ firing, simply offset to the rest of the neurogram. This pattern of sympathetic bursting within the integrated neurogram is common, even in healthy adults, and often linked to the mechanics of ventilation [1]. If the apparent surges do indeed represent baroreflex resistant sympathetic outflow, then their origins are of considerable interest. The apparent association between the Cheyne-Stokes respiratory pattern and the purported surges in sympathetic activity may suggest an important role of the chemoreflex, with periodic chemoreflex input augmenting sympathetic activity. However, the fact the surges were not sustained throughout the hypopneas makes this hypothesis tenuous. Moreover, the obvious association between blood pressure oscillations and sympathetic activity provides evidence that the physiological link between blood pressure and sympathetic activity remains intact and active in these patients. The small number of subjects, lack of quantification, and equally plausible alternative explanations should alert the reader to interpret the observations presented
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by Macefield and Elam cautiously. However, future investigations designed to control PaCO2 and/or account for the mechanics of respiration, in which rigorous standards are applied to data analysis, may indeed confirm
these authors were among the first to recognize a physiological link between chemoreflex and baroreflex sympathetic control in patient populations such as heart failure.
References 1. Delius W, Hagbarth KE, Hongell A, Wallin BG (1972) General characteristics of sympathetic activity in human muscle nerves. Acta Physiol Scand 84: 65–81
2. Hagbarth KE, Vallbo AB (1968) Pulse and respiratory grouping of sympathetic impulses in human musclenerves. Acta Physiol Scand 74:96–108
3. Macefield VG, Elam M (2002) Prolonged surges of baroreflex-resistant muscle sympathetic drive during periodic breathing. Clin Auton Res 12:165–169
