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, E314–2 GH, University of Iowa, 200 Hawkins Dr, Iowa City, IA. E-mail virend-somers{at}uiowa.edu
Methods and Results—Using 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).
Conclusions—Increasing 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.
Whether the vagotonic effects of low-dose atropine are due to a
peripheral effect on the sinoatrial node or to a central
mechanism is not clear. If it is a central effect, it is not known
whether a similar vagotonic effect is also exerted by high-dose
atropine, because any central effect of high-dose atropine would be
masked by muscarinic blockade at the sinoatrial node. We addressed this
question by exploring how the vagotonic (low-dose) or vagolytic
(high-dose) actions of atropine affect the activity of a neural
outflow, such as muscle sympathetic nerve activity (MSNA).
Power spectral analysis of RR interval variability has been
used as an indirect marker of cardiac autonomic
regulation.6 7 8 9 Recent studies in normal subjects
have shown that MSNA variability includes low-frequency (LF) and
high-frequency (HF) components, highly coherent with those present
in RR-interval and blood-pressure variability.10
Small increases in average sympathetic activity induced by experimental
hypotension are accompanied by a relative dominance in the LF
components of both RR and MSNA variabilities and by an increase in
their LF/HF ratios. Parasympathetic activation induced by increases in
arterial pressure, conversely, is accompanied by a
reduction in MSNA and by a relative dominance of the HF oscillatory
components of RR and MSNA and a decrease in their LF/HF
ratios.10 In the present study, we obtained
simultaneous measurements of RR interval,
intra-arterial blood pressure, and MSNA and evaluated the
spectral oscillations of each of these variables during
low- and high-dose atropine in normal human subjects. We tested the
following hypotheses: (1) that the vagotonic effect of low-dose
atropine occurs at a central level and therefore increases the HF
components not only of the RR interval but also of MSNA and (2) that
despite the elimination of the HF component of the RR interval by
peripheral muscarinic blockade, central vagotonic effects
of high-dose atropine result in an increase in the HF component of
MSNA.
We recorded the ECG, intra-arterial pressure (from a
catheter inserted into the radial artery), respiration (with a
pneumatic chest belt sensitive to both frequency and amplitude), and
efferent MSNA measured directly by microneurography. MSNA was
recorded from a sympathetic nerve fascicle to muscle blood vessels
in the peroneal nerve. This technique has been extensively described in
previous studies.11 12 In brief,
recordings were obtained by percutaneous
insertion of tungsten microelectrodes into sympathetic fascicles in the
peroneal nerve. The electrodes were connected to a preamplifier, and
the nerve signal was fed through a band-pass filter and routed through
an amplitude discriminator to a storage oscilloscope and loudspeaker.
For recording and analysis, the filtered neural signal
was fed through a resistance-capacitance integrating network to obtain
a mean voltage display of the neural activity. Data were stored via an
FM tape recorder (TEAC).
Experimental Protocol
To exclude the possibility of increased blood pressure after high-dose
atropine contributing to an increased HF of
MSNA,10 we studied 4 additional subjects (men
26±2 years old) in whom arterial pressure after high-dose
atropine was maintained at slightly below the baseline level with an
intravenous infusion of nitroprusside.
Spectral Analysis
The methodology and the software for data acquisition and spectral
analysis of cardiovascular signals have been
described previously.13 Briefly, a
derivative-threshold algorithm provided the continuous series of RR
intervals (tachogram) from the ECG signal. From the continuous
arterial pressure signal, beat-by-beat systolic
(systogram) and diastolic (diastogram) values were
calculated, and the signal of respiratory activity was sampled once for
every cardiac cycle.
As described in a previous study,10 we used a
digital algorithm to automatically perform event detection and
amplitude computation of MSNA. A burst in the neural activity was
recognized on the basis of a user-defined voltage and time threshold.
For each individual sympathetic burst, the computer program provided
the time of the occurrence and its amplitude (timexvoltage area).
Simulation studies showed that this permitted an accurate automatic
computation of the average number of bursts in a time unit (minute) and
of the average burst amplitude (expressed in arbitrary units, AU). In
addition, integration of the continuous MSNA signal was performed over
the time window between 2 consecutive diastolic values
delimiting the ith cardiac cycle of period t(i)
provided by the neurogram. Accordingly, this new series of variability
measures of MSNA is synchronous with the other variability signals on a
beat-by-beat basis.
All variability series were analyzed by means of autoregressive
parametric spectral and cross-spectral
algorithms,14 which can automatically provide the
number, center frequency, and associated power of each relevant
oscillatory component. The very-low-frequency component (VLF, 0.00 to
0.03 Hz) requiring specific algorithms and longer data
series15 was not addressed in this study and,
accordingly, was considered to be a DC
component.13
The power was expressed both in absolute and in normalized units (NU),
which were obtained by dividing the power of each component by total
variance from which the VLF component had been subtracted and
multiplying this value by 100.13 16
Statistical Analysis
Spectral analysis of MSNA variability revealed 2 major
oscillatory components, LF (0.10±0.004 Hz) and HF (0.24±0.01 Hz). A
similar spectral profile was also observed in RR interval and
systolic arterial pressure (SAP) variabilities
(Figure 2
Effects of Low-Dose Atropine
Despite the absence of changes in absolute measurements of MSNA,
low-dose atropine had significant effects on spectral oscillatory
components of MSNA (Figures 2
Effects of High-Dose Atropine
Normalized LFMSNA decreased (-17±12%;
P<0.02), as did the LF/HFMSNA
(-51±21%; P<0.01), whereas normalized
HFMSNA increased (+22±3%; P<0.02).
RR interval variance was drastically reduced (-99±0.2%;
P<0.0001), accompanied by a reduction of
LFRR and HFRR in absolute
values (-96±0.1% and -99±0.1%, respectively;
P<0.0001). However, normalized LFRR
was markedly increased (+59±25%; P<0.0001), whereas
normalized HFRR was reduced (-63±12%;
P<0.0001). LF/HFRR increased markedly
(1293±540%; P<0.0001) (Figures 2
Effects of High-Dose Atropine and Intravenous
Nitroprusside
Second, we have shown that even with high-dose atropine, there is an
indication of a central parasympathetic effect that is revealed only by
examination of the HF oscillation of MSNA. This conclusion
could not have been drawn from measurements of oscillations
in RR interval variability alone because of peripheral
muscarinic blockade of the sinoatrial node with high-dose atropine.
Both low and high doses of atropine are accompanied by a relative
increase in central parasympathetic activity, reflected by a decreased
LF/HF ratio of both RR and MSNA during low-dose atropine and a
decreased LF/HF ratio of MSNA during high-dose atropine.
Effects of Low-Dose Atropine
The present study demonstrates that the decrease in heart rate
after low-dose atropine is accompanied by an increase in the HF
oscillatory components of both RR interval and MSNA variability. These
simultaneous changes suggest that low-dose atropine acts
centrally and that the parasympathetic effect of low-dose atropine
manifests as a rhythmic pattern consisting of an increase in the HF and
a decrease in the LF
oscillations.18 19
Similar findings have been reported by Tougas et
al,20 who used a mechanical rather than a
pharmacological intervention. In their study, the vagal response to
esophageal distension was accompanied by an increase of HF and a
decrease of LF in the power spectrum of heart rate variability.
Our data support earlier studies by Gilbey et
al,21 who observed an increase in single cardiac
vagal motor neuron firing activity in the nucleus ambiguus after
iontophoretic application of atropine. In studies in humans, Raczkowska
et al3 reported an increase in the magnitude of
respiratory sinus arrhythmia after low-dose atropine.
Previous reports have examined the effect of scopolamine, a muscarinic
blocker, on heart period and its variability. In studies in healthy
subjects,22 in patients after myocardial
infarction,23 and in patients with congestive
heart failure,24 scopolamine was found to
increase indices of parasympathetic activity. In patients after cardiac
transplantation and presumed cardiac denervation, Epstein et
al25 showed that low-dose atropine did not
increase RR interval, suggesting that the decrease in heart rate is not
due to direct effects of atropine on the pacemaker cells.
Effects of High-Dose Atropine
It is unlikely that the increase in arterial pressure after
high-dose atropine might have caused a reduction in the LF component of
MSNA. Indeed, even when blood pressure after high-dose atropine was
lowered to slightly below baseline levels (nitroprusside substudy), a
significant reduction in LFNU and LF/HF of MSNA
was evident in all 4 subjects.
Our findings also have implications for understanding the genesis of
the LF oscillatory components in cardiovascular
variability. Previous studies of RR
variability4 5 noted that muscarinic blockade at
the sinus node induced tachycardia, a drastic reduction of
RR variance, and reduced absolute values of both LF and HF components
of RR variability. Accordingly, reduction in the absolute value of the
LF component of RR variability after atropine has been interpreted as
evidence that this component is generated mainly by vagal mechanisms at
rest.4 5 Absolute measures of oscillatory power
are exquisitely dependent on variance of the signal. Hence, it is
likely that the reduced RR variance due to unopposed sympathetic
activity after vagal blockade with high-dose atropine results in a
reduction of the absolute LF component of RR variability. As shown in
the 15-fold magnified spectral window in the top right panel of Figure 3
Conclusions
Although both LF and HF components are present in sympathetic
discharge variability, sympathetic excitation appears to be linked to a
relative increase in the LF oscillation of sympathetic
neural outflow and RR interval variability.10 29
Similarly, LF and HF components are also present in vagal discharge
variability,6 but vagal excitation appears to be
linked to a relative increase in the HF component of sympathetic
outflow and RR variability.10 29 These rhythms
may reflect a central pattern organization in which excitation (or
sympathetic activation) is associated with increased LF rhythmicity and
inhibition (or vagal activation) with increased HF rhythmicity.
Received January 26, 1998;
revision received June 10, 1998;
accepted June 13, 1998.
© 1998 American Heart Association, Inc.
Clinical Investigation and Reports
Central Vagotonic Effects of Atropine Modulate Spectral Oscillations of Sympathetic Nerve Activity
Abstract
Top
Abstract
Introduction
Methods
Results
Discussion
References
Background—Low-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.
Key Words: vagus nerve • nervous system, autonomic • heart rate • muscles • nervous system, sympathetic
Introduction
Top
Abstract
Introduction
Methods
Results
Discussion
References
In humans, low-dose atropine decreases heart
rate1 2 and increases respiratory sinus
arrhythmia3 because of an increase in
parasympathetic activity. High doses of atropine cause blockade of
muscarinic receptors at the cardiac sinoatrial node and are
parasympatholytic, markedly increasing heart rate and decreasing heart
rate variability.4 5
Methods
Top
Abstract
Introduction
Methods
Results
Discussion
References
We studied 14 healthy human volunteers, all male, 29±2 years
old (range, 23 to 42 years). All were nonsmokers and were receiving
no medications.
Informed written consent was obtained from all subjects. The
study was approved by the Human Subject Review Committee of the
University of Iowa. All subjects were studied in a quiet, dimly lit
room at a comfortable temperature. After a period of adaptation in the
supine position, data were acquired over a 10-minute period of quiet
rest. Then 2 intravenous boluses (2 and 15 µg/kg) of
atropine were administered in a stepwise fashion, starting with the
lower dose. After each atropine bolus, 15-minute periods of
recordings were obtained (Figure 1
). This study was conducted in 10
subjects.
View larger version (24K):
[in a new window]
Figure 1. Recordings of ECG, MSNA, respiration
(RESP), and intra-arterial blood pressure (BP) in same
subject during baseline recordings, after low-dose atropine,
and after high-dose atropine. Low-dose atropine slows heart rate but
does not change overall levels of MSNA. High-dose atropine causes a
decrease in MSNA and tachycardia.
Data were analyzed off-line after analog-to-digital
conversion at a rate of 600 Hz per channel with a 12-bit converter
(Gould).
Data are expressed as mean±SEM. Responses to atropine were
tested by means of a 1-way ANOVA for repeated measures. Linear
regressions were used to determine whether any relationship existed
between changes in blood pressure and changes in spectral measurements
of MSNA. A value of P<0.05 was considered significant.
Results
Top
Abstract
Introduction
Methods
Results
Discussion
References
Baseline Conditions
In control conditions, average MSNA burst frequency and amplitude
were 25±7 bursts per minute (39±9 bursts/100 beats) and 650±150 AU,
respectively; RR interval was 1028±39 ms; and mean systolic
and diastolic arterial pressures were 115±2
and 84±3 mm Hg, respectively (Table 1).
View this table:
[in a new window]
Table 1. Mean RR Interval, MSNA Measures, and SAP at Baseline
and After Infusion of a Low and a High Dose of Atropine
(n=10) ; Table 2).
View larger version (31K):
[in a new window]
Figure 2. Spectral oscillations of RR interval,
MSNA, SAP, and respiration in a single subject during control
measurements and after low-dose and high-dose atropine. After low-dose
atropine (center), there is an increase in relative dominance of HF
component of RR interval and MSNA. After high-dose atropine (right), RR
oscillations are affected by effects of
peripheral muscarinic blockade. Nevertheless, a relative
increase in HF component of MSNA is evident. Because of blockade of
vagal effects on heart by high-dose atropine and a decrease in RR
interval variance, residual oscillatory component of RR interval is
limited predominantly to LF, as seen in 15-fold magnified window.
View this table:
[in a new window]
Table 2. Spectral Measurements of RR Interval, MSNA, and SAP
Variability During Control and After Infusion of a Low and a High Dose
of Atropine (n=10)
Bolus infusion of the low dose of atropine (2 µg/kg) did not
alter MSNA (either in burst frequency or amplitude). The RR interval
increased significantly (+9±1%; P<0.0001), whereas SAP
was unchanged (Table 1
; Figure 1). and 3).
Normalized LFMSNA power was reduced (-15±5%;
P<0.008) and normalized HFMSNA power
increased (+31±3%; P<0.007). The
LF/HFMSNA ratio decreased (-41±8%;
P<0.002). These changes in MSNA spectral profile were
mirrored by similar changes in RR interval variability. Normalized
LFRR decreased (-32±8%; P<0.004)
and normalized HFRR increased (+74±19%;
P<0.003). LF/HFRR was also reduced
(-52±10%; P<0.001). SAP variability
measures did not reveal significant changes (Table 2). The center
frequency of respiration and its variance were not significantly
modified (from 0.27±0.01 to 0.25±0.02 Hz).
View larger version (26K):
[in a new window]
Figure 3. Mean values for LF/HF ratio for RR interval
variability (left) and MSNA variability (right). Low-dose atropine
decreases LF/HF ratio of both RR interval and MSNA. This effect of
atropine is evident after high-dose atropine in MSNA
oscillations but not in RR oscillations because
of peripheral muscarinic blockade.
(*=P<0.02.)
Compared with control conditions, administration of
high-dose atropine (15 µg/kg) produced a substantial decrease in MSNA
burst frequency (-25±9%; P<0.01) as well as in RR
interval (-41±2%; P<0.0001), whereas SAP increased
slightly but significantly (+7±3%; P<0.02) (Table 1;
Figure 1). and 3). SAP variance as
well as variance and center frequency of respiration did not change
significantly (Table 2). By use of linear regressions, no significant
correlations were found between changes in SAP and alterations in
normalized LFMSNA,
HFMSNA, and
LF/HFMSNA.
In 4 subjects, we sought to exclude any possible effects of the
increased blood pressure after high-dose atropine contributing to an
increase in HF of MSNA. In 3 of these 4 subjects, infusion of
intravenous nitroprusside was used to maintain blood
pressure slightly below baseline. In the fourth subject, blood pressure
after high-dose atropine was lower than the baseline even without the
use of nitroprusside. For all subjects, blood pressure at baseline was
116±3 mm Hg, and after high-dose atropine (and
intravenous nitroprusside in 3 subjects) it was 110±5
mm Hg. MSNA was significantly decreased when expressed as bursts per
100 beats (-35±7%; P<0.04) but not when expressed as
bursts per minute (from 19±6 to 22±5). Normalized
LFMSNA decreased (-48±10%;
P<0.03). HFMSNA increased, but not
significantly, from 36±8 to 45±6 NU (P=0.3). A significant
decrease in LF/HFMSNA (-61±13%;
P<0.05) was also evident in these 4 subjects.
Discussion
Top
Abstract
Introduction
Methods
Results
Discussion
References
This study shows, first, that the vagotonic effect of low-dose
atropine (slowing of heart rate) is accompanied by a relative increase
in the HF components of both RR interval and MSNA variabilities.
Changes in the oscillatory properties of MSNA occur in the absence of
any clear changes in burst frequency of MSNA.
The mechanism by which low-dose atropine slows heart rate is not
clear. It has been suggested that the bradycardia is due to the
stimulation of pacemaker muscarinic M1
receptors17 or to a direct effect on
pacemaker cells, independent of muscarinic
receptors1 ; however, such a mechanism would be
unlikely to enhance the HF rhythmicity of RR-interval variability.
The increased normalized HF component, decreased normalized LF
component, and decreased LF/HF ratio of MSNA oscillations
after low-dose atropine are also evident after high-dose atropine.
However, these vagotonic effects of high-dose atropine are apparent
only by examination of the alteration in MSNA oscillations.
These findings are consistent, in part, with data from Katona
et al,26 who showed that atropine increased
cardiac vagal efferent activity in anesthetized dogs in a
dose-response fashion. We were unable to demonstrate, however, that
high-dose atropine reduced the LF/HF ratio of MSNA beyond the level
achieved with low-dose atropine. , after high-dose atropine all remaining power in the RR interval
variability is condensed into the LF component, leading to high values
of normalized LF power (see Table 2). These findings are similar to
those noted by Bernardi and colleagues27 after
atropine administration in normal subjects and by Rimoldi et
al28 in studies in conscious dogs. Thus, an
alternative conclusion is that the relative sympathetic predominance in
RR modulation after high-dose atropine is evident from the marked
increase in the normalized LF of RR variability and in the LF/HF ratio
of RR variability.
Central parasympathetic activation induced by blockade of
inhibitory muscarinic receptors of central vagal nuclei
causes bradycardia and induces a relative predominance of the HF
oscillatory components not only of the RR interval but also of MSNA.
Although high-dose atropine blocks vagal activity at the cardiac level,
causing tachycardia, a central muscarinic receptor blockade
causing vagal activation is suggested by a relative increase in the HF
component of MSNA. Thus, central parasympathetic activation may also
modulate the oscillatory components of sympathetic traffic directed to
peripheral blood vessels.
Acknowledgments
These studies were supported by an American Heart Association
Grant-in-Aid, NIH grant HL-14388, and an NIH Sleep Academic
Award (Dr Somers). We thank Linda Bang and Isabella Ghirardelli for
expert typing of the manuscript.
References
Top
Abstract
Introduction
Methods
Results
Discussion
References
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 R. Furlan, A. Porta, F. Costa, J. Tank, L. Baker, R. Schiavi, D. Robertson, A. Malliani, and R. Mosqueda-Garcia Oscillatory Patterns in Sympathetic Neural Discharge and Cardiovascular Variables During Orthostatic Stimulus Circulation, February 29, 2000; 101(8): 886 - 892. [Abstract] [Full Text] [PDF]
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D. L. Eckberg Mathematical Treatment of Autonomic Oscillations Circulation, October 12, 1999; 100 (15): e63 - e63. [Full Text] [PDF]
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J. A. Taylor, C. W. Myers, N. Montano, C. Cogliati, A. Porta, M. Pagani, A. Malliani, K. Narkiewicz, F. M. Abboud, and V. K. Somers Mathematical Treatment of Autonomic Oscillations - 2 • Response Circulation, October 12, 1999; 100 (15): e64 - e64. [Full Text] [PDF]
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E. R. Azevedo and J. D. Parker Parasympathetic Control of Cardiac Sympathetic Activity : Normal Ventricular Function Versus Congestive Heart Failure Circulation, July 20, 1999; 100(3): 274 - 279. [Abstract] [Full Text] [PDF]
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F. Iellamo, P. Pizzinelli, M. Massaro, G. Raimondi, G. Peruzzi, and J. M. Legramante Muscle Metaboreflex Contribution to Sinus Node Regulation During Static Exercise : Insights From Spectral Analysis of Heart Rate Variability Circulation, July 6, 1999; 100(1): 27 - 32. [Abstract] [Full Text] [PDF]
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D. P. Holschneider, O. U. Scremin, D. R. Chialvo, K. Chen, and J. C. Shih Heart rate dynamics in monoamine oxidase-A- and -B-deficient mice Am J Physiol Heart Circ Physiol, May 1, 2002; 282(5): H1751 - H1759. [Abstract] [Full Text] [PDF]
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