From the Centro L.I.T.A. di Vialba, Centro Ricerche Cardiovascolari, CNR,
Medicina Interna II, Ospedale "L. Sacco," Università di
Milano, Italy (N.M., C.C., A.P., M.P., A.M.) and the Cardiovascular Division,
Department of Internal Medicine, College of Medicine, University of Iowa, Iowa
City (K.N., F.M.A., C.B., V.K.S.).
Correspondence to Virend K. Somers, MD, PhD, Department of Internal Medicine, Cardiovascular Division, E3142 GH, University of Iowa, 200 Hawkins Dr, Iowa City, IA. E-mail virend-somers{at}uiowa.edu
BackgroundLow-dose atropine
causes bradycardia either by acting on the sinoatrial node or by its
effects on central muscarinic receptors increasing vagal activity. Any
central muscarinic effects of high-dose atropine on RR interval are
masked by peripheral muscarinic blockade at the sinoatrial
node, which causes tachycardia. Effects of central
parasympathetic activation on sympathetic activity are not
known.
Methods and ResultsUsing power spectral analysis of RR
interval, intra-arterial blood pressure, respiration, and
muscle sympathetic nerve activity (MSNA), we examined the effects of
both low (2 µg/kg IV) and high (15 µg/kg IV) doses of atropine.
After low-dose atropine, RR increased by 9±1%
(P<0.0001), the low-frequency (LF) component (in
normalized units, NU) of RR variability decreased by -32±8%, and the
high-frequency (HF)NU component increased (+74±19%);
hence, LF/HF of RR variability fell by 52±10% (all
P<0.01). Although overall MSNA did not change,
LFNU of MSNA decreased (-15±5%), HFNU of
MSNA increased (+31±3%), and LF/HF of MSNA fell (-41±8%) (all
P<0.01). After high-dose atropine, LFNU of
MSNA decreased (-17±12%), HFNU of MSNA increased
(+22±3%), and LF/HF of MSNA fell (-51±21%) (all
P<0.02).
ConclusionsIncreasing central parasympathetic activity with
low-dose atropine is associated with an increase in the HF and a
decrease in the LF oscillations of both RR interval and
MSNA variability. High-dose atropine similarly induces an increase in
the HF and a decrease in the LF components of MSNA variability. Thus,
central parasympathetic activation is able to modulate the oscillatory
characteristics of sympathetic nerve traffic to peripheral
blood vessels.
© 1998 American Heart Association, Inc.
Clinical Investigation and Reports
Central Vagotonic Effects of Atropine Modulate Spectral Oscillations of Sympathetic Nerve Activity
Key Words: vagus nerve nervous system, autonomic heart rate muscles nervous system, sympathetic
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