(Circulation. 1999;100:e63.)
© 1999 American Heart Association, Inc.
Circulation Electronic Pages |
Mathematical Treatment of Autonomic Oscillations
Hunter Holmes McGuire Department of Veterans Affairs Medical Center, and Medical College of Virginia at Virginia Commonwealth University, Richmond, Va
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To the Editor:
Montano et al1 measured RR interval and muscle sympathetic nerve activity (MSNA) autoregressive spectral power before and after small- and large-dose atropine and drew inferences regarding human central autonomic mechanisms. I have several questions for the authors, as well as comments.
Your finding that low-dose atropine does not alter low-frequency RR-interval spectral power (Table 2) is at variance with results published by Ikuta et al,2 which document significant increases. Your observation also is at variance with one of your principal conclusions (Abstract), that low-dose atropine decreases low-frequency RR-interval spectral power. In the absence of changes of measured low-frequency RR-interval spectral power, the reduction of normalized low-frequency RR-interval spectral power that you report simply signifies that low-dose atropine increases respiratory sinus arrhythmia.3
You report that low-dose atropine does not alter MSNA. This confirms an observation we made earlier.4 You report also that high-dose atropine reduces muscle sympathetic nerve burst frequency, expressed as bursts/100 heart beats and bursts/min. Our study4 also showed that large-dose atropine significantly reduces sympathetic activity expressed as bursts/100 heart beats. However, contrary to your observations, we found that large-dose atropine does not significantly alter sympathetic activity expressed as bursts/min. This finding was supported by a related observation that large-dose atropine does not alter antecubital vein plasma norepinephrine concentrations (which correlate well with MSNA).5 Can you explain the disparity between your results and ours?
You present only "normalized" MSNA; therefore, it is impossible to determine whether measured MSNA frequency or amplitude spectral power changed in high or low ranges or both. I am aware of substantial uncertainty regarding what high- and low-frequency MSNA oscillations signify individually. My sense is that when you divide one by the other (and thereby "normalize" them), you enter largely uncharted territory. The notion that a change of this quotient documents central parasympathetic modulation of sympathetic oscillations is provocative. However, high-dose atropine is a complex intervention that profoundly alters autonomic function; there may be several alternative explanations for your results.
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1. Montano N, Cogliati C, Porta A, Pagani M, Malliani A, Narkiewicz K, Abboud FM, Birkett C, Somers VK. Central vagotonic effects of atropine modulate spectral oscillations of sympathetic nerve activity. Circulation. 1998;98:1394–1399.
2. Ikuta Y, Shimoda O, Kano T. Quantitative assessment of the autonomic nervous system activities during atropine-induced bradycardia by heart rate spectral analysis. J Auton Nerv Syst. 1995;52:71–76.[Medline] [Order article via Infotrieve]
3. Raczkowska M, Eckberg DL, Ebert TJ. Muscarinic cholinergic receptors modulate vagal cardiac responses in man. J Auton Nerv Syst. 1983;7:271–278.[Medline] [Order article via Infotrieve]
4. Porter TR, Eckberg DL, Fritsch JM, Rea RF, Beightol LA, Schmedtje JF Jr, Mohanty PK. Autonomic pathophysiology in heart failure patients: sympathetic-cholinergic interrelations. J Clin Invest. 1990;85:1362–1371.
5. Wallin BG, Sundlöf G, Eriksson B-M, Dominiak P, Grobecker H, Lindblad LE. Plasma noradrenaline correlates to sympathetic muscle nerve activity in normotensive man. Acta Physiol Scand. 1981;111:69–73.[Medline] [Order article via Infotrieve]
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