(Circulation. 1996;93:1527-1532.)
© 1996 American Heart Association, Inc.
Articles |
Fundamental Relations Between Short-term RR Interval and Arterial Pressure Oscillations in Humans
From the Departments of Medicine and Physiology, Hunter Holmes McGuire Department of Veterans Affairs Medical Center, Virginia Commonwealth University, Medical College of Virginia, Richmond.
Correspondence to J. Andrew Taylor, PhD, HRCA Research and Training Institute, Hebrew Rehabilitation Center for Aged, 1200 Centre St, Boston, MA 02131. E-mail ataylor@mail.hrca.harvard.edu.
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Abstract |
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Background One of the principal explanations for respiratory sinus arrhythmia is that it reflects arterial baroreflex buffering of respiration-induced arterial pressure fluctuations. If this explanation is correct, then elimination of RR interval fluctuations should increase respiratory arterial pressure fluctuations.
Methods and Results We measured RR interval and arterial pressure fluctuations during normal sinus rhythm and fixed-rate atrial pacing at 17.2±1.8 (SEM) beats per minute greater than the sinus rate in 16 healthy men and 4 healthy women, 20 to 34 years of age. Measurements were made during controlled-frequency breathing (15 breaths per minute or 0.25 Hz) with subjects in the supine and 40° head-up tilt positions. We characterized RR interval and arterial pressure variabilities in low-frequency (0.05 to 0.15 Hz) and respiratory-frequency (0.20 to 0.30 Hz) ranges with fast Fourier transform power spectra and used cross-spectral analysis to determine the phase relation between the two signals. As expected, cardiac pacing eliminated beat-to-beat RR interval variability. Against expectations, however, cardiac pacing in the supine position significantly reduced arterial pressure oscillations in the respiratory frequency (systolic, 6.8±1.8 to 2.9±0.6 mm Hg2/Hz, P=.017). In contrast, cardiac pacing in the 40° tilt position increased arterial pressure variability (systolic, 8.0±1.8 to 10.8±2.6, P=.027). Cross-spectral analysis showed that 40° tilt shifted the phase relation between systolic pressure and RR interval at the respiratory frequency from positive to negative (9±7° versus -17±11°, P=.04); that is, in the supine position, RR interval changes appeared to lead arterial pressure changes, and in the upright position, RR interval changes appeared to follow arterial pressure changes.
Conclusions These results demonstrate that respiratory sinus arrhythmia can actually contribute to respiratory arterial pressure fluctuations. Therefore, respiratory sinus arrhythmia does not represent simple baroreflex buffering of arterial pressure.
Key Words: waves • nervous system, autonomic • reflex • physiology • Fourier analysis
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Introduction |
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One of the principal explanations for respiratory RR interval fluctuations, or respiratory sinus arrhythmia, is that they represent baroreflex buffering of arterial pressure changes induced by the mechanical effects of breathing on intrathoracic pressures, venous return to the heart, and ventricular preload and afterload.1 2 3 4 5 6 7 Prospective testing of this hypothesis has been difficult in humans. The most obvious way to discern the relation between respiratory RR interval and arterial pressure fluctuations is to obtain measurements with and without RR interval fluctuations. Investigators have fixed RR interval in two ways: they have given large atropine doses to healthy subjects3 4 6 8 9 10 or paced the heart in patients with cardiac pacemakers.8 Neither approach is entirely satisfactory. Cholinergic blockade with atropine not only stabilizes the RR interval but also increases arterial pressure3 4 6 8 10 ; pressure elevations may affect arterial compliance11 and thereby change the magnitude of arterial pressure variability, independent of RR interval changes. Therefore, this physiology may be studied more simply by fixed-rate cardiac pacing. However, patients with pacemakers usually have heart disease, which may alter the relation between arterial pressure and RR interval. The only available data on cardiac pacing in healthy hearts are derived from dogs and suggest that respiratory sinus arrhythmia generates respiratory-frequency fluctuations in arterial pressure.12 13 Thus, the fundamental relation between RR interval and arterial pressure oscillations in humans remains uncertain.
We circumvented the problems with human research simply by studying healthy volunteers with and without atrial pacing with an esophageal electrode. Our atrial pacing paradigm during controlled-frequency breathing allowed us to characterize arterial pressure oscillations in the presence and absence of respiratory sinus arrhythmia without affecting average arterial pressures. We tested the hypothesis that if heart rate variability represents baroreflex buffering of arterial pressure, abolition of heart rate variability should augment arterial pressure variability. Our study yields opposite results and suggests that respiratory sinus arrhythmia contributes importantly to arterial pressure fluctuations in supine humans.
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Methods |
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Subjects
We studied 16 healthy men and 4 healthy women, 20 to 34 years of age. None were on medications, all were nonsmokers, and all had average levels of physical activity. This study was approved by the institutional review boards for human experimentation of the Hunter Holmes McGuire Department of Veterans Affairs Medical Center and the Medical College of Virginia. All subjects gave their written informed consent to participate.
Measurements and Protocol
We measured RR intervals from lead II of the ECG. We estimated
beat-to-beat arterial pressure from the middle
phalanx of the middle finger of the left hand with a
photoplethysmograph (Finapres, model 2300, Ohmeda). This device has
been validated for power spectral analysis of
arterial pressure variability.14 We also
measured brachial arterial pressure with an oscillometric
device (Dinamap, Critikon) placed on the right arm. A bellows around
the subject's upper abdomen was connected to a strain-gauge
pressure transducer to indicate respiratory excursions.
We paced the heart at a constant rate with transesophageal electrical stimuli sufficient to override normal sinus rhythm consistently. A bipolar electrode (TAPSUL or TAPCATH, Arzco) was introduced either orally or nasally and positioned in the esophagus behind the left atrium. The location of the electrode was considered adequate when the atrial electrogram voltage was equal to or greater than the QRS voltage and when a satisfactory paced rhythm was maintained. Transesophageal atrial pacing is sometimes associated with significant discomfort; adequate pacing without undue discomfort at stimuli <20 mA was achieved in 70% of the trials (see below).
Measurements were made during 7 minutes of controlled-frequency breathing (15 breaths per minute, 0.25 Hz) with normal sinus and paced rhythm. Cardiac pacing was set at a rate that minimized the number of breakthrough sinus beats (17.2±1.8 beats per minute [mean±SEM] greater than sinus rate). Measurements were made with subjects in both the supine and 40° passive head-up tilt positions. Paced rhythm was not achieved in all subjects in both positions; data were obtained on a total of 14 subjects in the supine position and 14 subjects in the 40° head-up tilt position.
Data Analysis and Statistics
The ECG, respiration, and beat-to-beat
arterial pressure waveforms were recorded on FM tape
and subsequently digitized at 1000 samples per second for off-line
analysis with signal processing software (CODAS, Dataq
Instruments; DADiSP, DSP Development Corp). The recording speed
and digitizing rate of these data allowed accurate measurement of RR
intervals to the nearest millisecond.
Consistent cardiac pacing was difficult to achieve; therefore, the 4 minutes with the highest ratio of paced to sinus rhythm RR intervals were extracted from the 7 minutes of pacing for data analysis. On average, normal sinus rhythm accounted for only 3% of all cardiac intervals evaluated (range, 0% to 12%), and the occurrence of normal sinus rhythm during pacing did not have a consistent, time-dependent pattern in any subject. The corresponding 4-minute period was extracted from the 7 minutes of normal sinus rhythm for comparison.
The means and SDs for the RR interval and systolic and diastolic pressures were calculated from the beat-to-beat values. Frequency domain analysis of variability was performed on beat-to-beat RR intervals, beat-to-beat systolic and diastolic pressures, and the respiratory signal. A power spectrum analysis technique based on the Welch algorithm of averaging periodograms was used.15 The 240-second time series of beat-to-beat RR interval and systolic pressure were interpolated at 4 Hz to obtain equidistant time intervals and then divided into three equal overlapping segments. Each segment was detrended, Hanning filtered, and fast Fourier transformed to its frequency representation squared. The periodograms were averaged to produce the spectrum estimate. This method yielded a frequency resolution of 0.0042 Hz. The areas under power spectra in the low and respiratory frequencies (defined as 0.05 to 0.15 and 0.20 to 0.30 Hz) were integrated and used for statistical comparisons.
Coherence and phase between systolic pressure and RR interval variabilities during normal sinus rhythm were assessed by cross-spectral analysis based on models previously described.5 16 When the coherence function exceeds 0.5 (range, 0 to 1) at any frequency, the phase function provides a statistically reliable estimate of the time relations between the two signals. A negative phase suggests that changes in input (systolic pressure) precede changes in output (RR interval); a positive phase suggests the converse.16 We interpreted a negative phase as suggestive of a baroreflex link between RR interval and systolic pressure because of known baroreflex latencies; pressure changes provoke RR interval changes with latencies as short as 0.24 second.17
The results from a 2x2 ANOVA of the data from those subjects who could be paced in both the supine and 40° tilt positions (n=8) did not differ from the results of paired and unpaired Student's t tests of all subjects' data (n=14). Therefore, we used Student's paired t test to assess the effects of cardiac pacing and Student's unpaired t test to assess the effects of 40° tilt. A value of P=.05 was considered significant. All values are given as mean±SEM.
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Results |
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Breathing frequency was well controlled for all conditions in all subjects: respiratory power was always centered near 0.25 Hz and concentrated within 0.20 to 0.30 Hz. During normal sinus rhythm, RR interval and all indexes of RR interval variability were less in the 40° tilt than in the supine position (the Table
).
Forty-degree tilt did not affect average arterial pressures
or respiratory-frequency arterial pressure variability;
however, 40° tilt did increase low-frequency arterial
pressure variability. Fig 1 is a tracing from a
representative subject. As expected, RR interval was
less, with essentially no beat-to-beat variability during
cardiac pacing. Average data from all subjects are depicted in Figs 2 through 4 and are given in the Table. Cardiac pacing in both the supine
and 40° tilt positions had no effect on average arterial
pressures. However, cardiac pacing had significant effects on
arterial pressure oscillations in the
respiratory frequency (Fig 2). In the supine position,
elimination of sinus arrhythmia decreased
respiratory-frequency systolic and diastolic
(not shown) pressure variabilities by 44% and 31% (both
P<.05). In contrast, in the 40° tilt position,
elimination of sinus arrhythmia increased
respiratory-frequency arterial pressure variabilities.
Systolic variability increased by 40%, and
diastolic variability increased by >100% (both
P<.05). In the supine position, elimination of RR interval
fluctuations did not alter low-frequency arterial
pressure variabilities. In the 40° tilt position, elimination of RR
interval fluctuations did not alter low-frequency systolic
pressure variability but almost doubled low-frequency
diastolic pressure variability.
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Cross-spectral analysis provided further insight to the
position-dependent relation between arterial pressure
and RR interval variabilities during normal sinus rhythm (Fig 3
). There was significant coherence between
systolic pressure and RR interval variabilities in both low and
respiratory frequencies in both positions (average coherence >0.72).
The phase of the systolic pressure–RR interval relation in the
low-frequency range was not different in the supine and 40° tilt
positions (-44±8° versus -48±4°). However, the phase
of the systolic pressure–RR interval relation in the
respiratory frequency was positive in the supine position but negative
in the 40° tilt position (9±7 versus -17±11,
P=.04). These results suggest that systolic pressure
variations in the low frequency precede RR interval variations,
regardless of whether subjects are supine or tilted. In contrast, the
phase estimates suggest that systolic pressure variations in
the respiratory frequency follow those in RR interval when subjects are
supine but precede those in RR interval when subjects are tilted.
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Discussion |
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Our data provide unique insight to fundamental relations between RR interval and arterial pressure oscillations in humans. The effects of cardiac pacing indicate that RR interval fluctuations subserve a conventional baroreflex role in buffering arterial pressure fluctuations only when mechanical influences on arterial pressure (eg, respiration, central blood volume) are greater than those in healthy supine humans.
These results clearly demonstrate that RR interval fluctuations at the respiratory and low frequencies do not dampen, and in fact can augment, arterial pressure fluctuations in supine humans. Respiratory-frequency systolic pressure variations follow RR interval variations, and respiratory arterial pressure variability is decreased by fixed-rate atrial pacing. Although low-frequency systolic pressure variations precede RR interval variations, these pressure oscillations are unaffected by fixed-rate atrial pacing. In contrast, both respiratory-frequency and low-frequency RR interval fluctuations dampen arterial pressure fluctuations in tilted humans. Systolic pressure variations in the respiratory and low frequencies precede those in RR interval, and arterial pressure variability is increased by fixed-rate atrial pacing. These data suggest that body position in part determines the mechanisms for the linkage between arterial pressure and RR interval.
Respiratory-Frequency Oscillations
Respiration-synchronous fluctuations in intrathoracic pressure
provoke fluctuations in stroke volume,2 which contribute
to respiratory-frequency arterial pressure variability
in humans.1 3 4 Presumably, this arterial
pressure fluctuation provokes parallel changes in arterial
baroreceptor activity and increases and decreases in cardiac vagal
outflow, resulting in respiratory sinus
arrhythmia.5 7 10 16 By this reasoning,
respiratory sinus arrhythmia arises from a baroreflex mechanism
that should counteract stroke volume fluctuations and reduce
arterial pressure fluctuations.3
Investigation of this hypothesis in healthy humans has relied on muscarinic blockade to reduce RR interval variability.3 4 6 8 9 10 However, muscarinic blockade also increases arterial pressure3 4 6 8 10 and decreases beat-to-beat sympathetic vasomotor outflow,18 both of which affect arterial compliance.11 Altered arterial compliance may explain the increased arterial pressure variability with muscarinic blockade in humans.3 9 10 Fixed-rate atrial pacing, a simpler way to prevent RR interval variability, reduces respiratory-frequency arterial pressure variability in dogs.12 13 We found that fixed-rate atrial pacing reduces respiratory-frequency arterial pressure oscillations in supine humans. In contrast, we found that fixed-rate atrial pacing increases arterial pressure oscillations in tilted subjects. These findings may be explained by the position-dependent phase relations between systolic pressure and RR interval at the respiratory frequency. The phase relation in the supine position was positive, suggesting that systolic pressure oscillations followed those in RR interval. Conversely, the phase in the tilted position was negative, suggesting that systolic pressure oscillations preceded those in RR interval. A similar phase shift in the systolic pressure–RR interval relation with orthostatic stress was described previously.19 A phase shift induced by orthostasis may indicate engagement of the arterial baroreflex; reductions in effective blood volume reduce aortic baroreceptive areas,20 resulting in arterial baroreceptor engagement. This suggests that respiratory sinus arrhythmia buffers respiratory arterial pressure oscillations in upright humans but augments arterial pressure oscillations in supine humans.
This interpretation of our data agrees with the closed-loop models of systolic pressure variability formulated by Saul et al6 and Turjanmaa et al.21 These investigators proposed that the contribution of RR interval variability to respiratory variance in arterial pressure was greater than the contribution of pressure to interval. Furthermore, Saul et al6 suggested that the mechanical influences of respiration on arterial pressure are greater in the upright than the supine position and in the upright position alter RR interval through the baroreflex. Our data, considered with proposed models of respiratory-frequency cardiovascular variability, underscore the mutable nature of the links between respiration, arterial pressure, and RR interval.
Low-Frequency Oscillations
Arterial pressure Mayer waves, occurring at an
interval of about 10 seconds or 0.10 Hz in humans, are presumed to
result from rhythmic, sympathetic vasomotor
activity.1 22 23 24 RR interval oscillations at
this same frequency are mediated by both cardiac sympathetic and
cardiac vagal outflows12 and are thought to
represent arterial baroreflex responses to pressure
oscillations.10 12 16 Our data demonstrate
that in supine humans, low-frequency RR interval
oscillations follow but do not dampen arterial
pressure oscillations; elimination of RR interval
variability does not increase low-frequency arterial
pressure oscillations. However, when vascular sympathetic
outflow was increased by 40° tilt,25 elimination of
low-frequency RR interval variability augmented the
diastolic pressure Mayer waves. This effect may not have
been seen in systolic pressure because of the greater dampening
of changes in RR interval on diastolic pressure; in
reaction to a higher systolic pressure, a longer RR interval
provides a longer diastolic runoff time, resulting in a
lower diastolic pressure.16 Therefore,
elimination of this dampening effect by cardiac pacing markedly
enhanced low-frequency diastolic pressure variability
but had minimal effect on systolic variability. Similar to the
results from respiratory-frequency arterial pressure
variability, these data indicate that low-frequency RR interval
oscillations buffer low-frequency arterial
pressure oscillations only in upright humans. Our results
in supine humans fit best with the hypothesis that low-frequency
arterial pressure oscillations result from a
latency in baroreflex-induced changes in vascular sympathetic
outflow—in other words, a pressure-pressure feedback
loop.26 Our data do not exclude an arterial
baroreflex link between low-frequency systolic pressure and
RR interval oscillations; however, we demonstrated such a
link only when sympathetic outflow was augmented.
Study Limitations
Although we found a high coherence between RR interval and
systolic pressure fluctuations at both the low and respiratory
frequencies, phase estimates provide only gross indexes of the time
relation between two signals. In a respiratory-frequency cycle of 4
seconds, a positive phase relation could indicate that the RR interval
output precedes the systolic pressure input with a
feed-forward delay between 0 and 2 seconds or that the RR interval
output follows the systolic pressure input with a feedback
delay between 2 and 4 seconds. We interpreted a positive phase relation
at the respiratory frequency as RR interval leading systolic
pressure within 2 seconds. The alternative, that systolic
pressure leads RR interval within 2 to 4 seconds, cannot be explained
on the basis of known baroreflex latencies; the vagal
baroreceptor–cardiac reflex latency is less than 1
second.17 However, it may be that our estimates of phase,
which are not entirely consistent with either feedback or
feed-forward delays indicate that baroreflex and mechanical links
between RR interval and systolic pressure are inconstant and
that the dominant influence determines the phase relation. Nonetheless,
our findings of a positive phase in the supine position and a negative
phase in the 40° tilt position are consistent with the
effects of cardiac pacing on respiratory arterial pressure
oscillations.
Study Implications
These data underscore theoretical limitations of time and
frequency domain measures of baroreflex function derived from
spontaneous, parallel changes in arterial pressure and RR
interval. Short-term changes in systolic pressure and RR
interval have been proposed to be cause-and-effect events
linked through the baroreflex.27 28 The majority of these
short-term changes are concentrated within a narrow frequency range
(
0.04 to 0.3 Hz), which prominently includes both low- and
respiratory-frequency oscillations.29
However, our data in supine humans minimize a direct baroreflex
buffering role for these short-term RR interval
oscillations. Alternatively, the close relation between the
amplitudes of arterial pressure and RR interval
variabilities may simply reflect the simultaneous effect of
respiration on cardiac vagal outflow30 and
arterial pressure,2 possibly explaining the
high baroreflex sensitivity derived from beat-to-beat
changes.31 Although measures of spontaneous baroreflex
function may be appropriate in some conditions, our cardiac pacing data
bring into question measures of baroreflex function derived from either
spectral or beat-to-beat analyses in supine humans.
These data also underscore an important point for quantifying
cardiovascular variability with power spectral
analysis. Appropriate techniques to quantify
cardiovascular variability continue to be a topic of
debate.32 33 34 Dividing the power of the respiratory- and
low-frequency components by the total power across all frequencies
(ie, normalizing) has been proposed as the most relevant measure of
variability.35 Fig 4 shows the result of
analyzing RR interval variability data in a
representative subject (see Fig 1) according to the
suggested autoregressive technique.35 Our results are
significantly altered by this analysis; monotonic cardiac
pacing in the supine position does not alter respiratory sinus
arrhythmia measured in normalized units (73±9 versus 77±6,
P=.734). Only the absolute measure of variability reflected
the elimination of heart rate oscillations by cardiac
pacing; normalizing power at the respiratory frequency to total power
artificially increased the remaining small component. It may be argued
that normalized units and absolute units yield complementary
information; one cannot be considered without taking the other into
account. Yet, even in response to a more
physiological condition, 40° tilt, we found a
striking divergence in the results from the two autoregressive
measures. Absolute low-frequency RR interval power decreased by
30%, whereas normalized power increased by 21% from supine to tilt.
Thus, results from both artificial manipulation of
cardiovascular variability by cardiac pacing and the
normal physiological response to tilt demonstrate
that these two measures may not be complementary and explicitly
emphasize the need to quantify frequency-specific
oscillations with absolute values derived from power
spectral analysis.
Conclusions
Our results challenge the concept that short-term fluctuations
in RR interval are linked inextricably to those in arterial
pressure through the arterial baroreflex. We found that
elimination of respiratory sinus arrhythmia diminished
respiratory-frequency arterial pressure fluctuations
and therefore do not buffer these arterial pressure
fluctuations in supine humans. We conclude that respiratory sinus
arrhythmia may be mediated by the baroreflex only when the
mechanical effects of respiration on arterial pressure are
greater than those in supine humans.
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Acknowledgments |
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This research was supported by the National Institute on Aging (grant AG05636-01), the NHLBI (grant HL-22296), the Department of Veterans Affairs, and the National Aeronautics and Space Administration (grants NAS9-16046 and NAG9-412). We thank Jeffery B. Hoag for his technical assistance in completing these studies.
Received July 11, 1995; revision received October 26, 1995; accepted November 5, 1995.
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A. Silvani, D. Grimaldi, S. Vandi, G. Barletta, R. Vetrugno, F. Provini, G. Pierangeli, C. Berteotti, P. Montagna, G. Zoccoli, et al. Sleep-dependent changes in the coupling between heart period and blood pressure in human subjects Am J Physiol Regulatory Integrative Comp Physiol, May 1, 2008; 294(5): R1686 - R1692. [Abstract] [Full Text] [PDF]
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K. D. Monahan Effect of aging on baroreflex function in humans Am J Physiol Regulatory Integrative Comp Physiol, July 1, 2007; 293(1): R3 - R12. [Abstract] [Full Text] [PDF]
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H. van de Vooren, M. G. J. Gademan, C. A. Swenne, B. J. TenVoorde, M. J. Schalij, and E. E. Van der Wall Baroreflex sensitivity, blood pressure buffering, and resonance: what are the links? Computer simulation of healthy subjects and heart failure patients J Appl Physiol, April 1, 2007; 102(4): 1348 - 1356. [Abstract] [Full Text] [PDF]
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A. Kamiya, J. Hayano, T. Kawada, D. Michikami, K. Yamamoto, H. Ariumi, S. Shimizu, K. Uemura, T. Miyamoto, T. Aiba, et al. Low-frequency oscillation of sympathetic nerve activity decreases during development of tilt-induced syncope preceding sympathetic withdrawal and bradycardia Am J Physiol Heart Circ Physiol, October 1, 2005; 289(4): H1758 - H1769. [Abstract] [Full Text] [PDF]
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K. Okazaki, K.-i. Iwasaki, A. Prasad, M. D. Palmer, E. R. Martini, Q. Fu, A. Arbab-Zadeh, R. Zhang, and B. D. Levine Dose-response relationship of endurance training for autonomic circulatory control in healthy seniors J Appl Physiol, September 1, 2005; 99(3): 1041 - 1049. [Abstract] [Full Text] [PDF]
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P. E. Hammer and J. P. Saul Resonance in a mathematical model of baroreflex control: arterial blood pressure waves accompanying postural stress Am J Physiol Regulatory Integrative Comp Physiol, June 1, 2005; 288(6): R1637 - R1648. [Abstract] [Full Text] [PDF]
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G. Nollo, L. Faes, A. Porta, R. Antolini, and F. Ravelli Exploring directionality in spontaneous heart period and systolic pressure variability interactions in humans: implications in the evaluation of baroreflex gain Am J Physiol Heart Circ Physiol, April 1, 2005; 288(4): H1777 - H1785. [Abstract] [Full Text] [PDF]
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D. D. O'Leary, J. K. Shoemaker, M. R. Edwards, and R. L. Hughson Spontaneous beat-by-beat fluctuations of total peripheral and cerebrovascular resistance in response to tilt Am J Physiol Regulatory Integrative Comp Physiol, September 1, 2004; 287(3): R670 - R679. [Abstract] [Full Text] [PDF]
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I. Fietze, D. Romberg, M. Glos, S. Endres, H. Theres, C. Witt, and V. K. Somers Effects of positive-pressure ventilation on the spontaneous baroreflex in healthy subjects J Appl Physiol, March 1, 2004; 96(3): 1155 - 1160. [Abstract] [Full Text] [PDF]
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B. R. Baldridge, D. E. Burgess, E. E. Zimmerman, J. J. Carroll, A. G. Sprinkle, R. O. Speakman, S.-G. Li, D. R. Brown, R. F. Taylor, S. Dworkin, et al. Heart rate-arterial blood pressure relationship in conscious rat before vs. after spinal cord transection Am J Physiol Regulatory Integrative Comp Physiol, September 1, 2002; 283(3): R748 - R756. [Abstract] [Full Text] [PDF]
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G. Nollo, L. Faes, A. Porta, B. Pellegrini, F. Ravelli, M. Del Greco, M. Disertori, and R. Antolini Evidence of unbalanced regulatory mechanism of heart rate and systolic pressure after acute myocardial infarction Am J Physiol Heart Circ Physiol, September 1, 2002; 283(3): H1200 - H1207. [Abstract] [Full Text] [PDF]
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R. Zhang, K. Iwasaki, J. H Zuckerman, K. Behbehani, C. G Crandall, and B. D Levine Mechanism of blood pressure and R-R variability: insights from ganglion blockade in humans J. Physiol., August 15, 2002; 543(1): 337 - 348. [Abstract] [Full Text] [PDF]
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H.-K. Liu, S.-J. Guild, J. V. Ringwood, C. J. Barrett, B. L. Leonard, S.-K. Nguang, M. A. Navakatikyan, and S. C. Malpas Dynamic baroreflex control of blood pressure: influence of the heart vs. peripheral resistance Am J Physiol Regulatory Integrative Comp Physiol, August 1, 2002; 283(2): R533 - R542. [Abstract] [Full Text] [PDF]
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M. A Cohen and J A. Taylor Short-term cardiovascular oscillations in man: measuring and modelling the physiologies J. Physiol., August 1, 2002; 542(3): 669 - 683. [Abstract] [Full Text] [PDF]
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P. Kaushal and J. A. Taylor Inter-relations among declines in arterial distensibility, baroreflex function and respiratory sinus arrhythmia J. Am. Coll. Cardiol., May 1, 2002; 39(9): 1524 - 1530. [Abstract] [Full Text] [PDF]
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S. D. Beske, G. E. Alvarez, T. P. Ballard, and K. P. Davy Reduced cardiovagal baroreflex gain in visceral obesity: implications for the metabolic syndrome Am J Physiol Heart Circ Physiol, February 1, 2002; 282(2): H630 - H635. [Abstract] [Full Text] [PDF]
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S. C. Malpas Neural influences on cardiovascular variability: possibilities and pitfalls Am J Physiol Heart Circ Physiol, January 1, 2002; 282(1): H6 - H20. [Abstract] [Full Text] [PDF]
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D. W. Wray, K. J. Formes, M. S. Weiss, A. H. O-Yurvati, P. B. Raven, R. Zhang, and X. Shi Vagal cardiac function and arterial blood pressure stability Am J Physiol Heart Circ Physiol, November 1, 2001; 281(5): H1870 - H1880. [Abstract] [Full Text] [PDF]
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M. Elstad, K. Toska, K. H Chon, E. A Raeder, and R. J Cohen Respiratory sinus arrhythmia: opposite effects on systolic and mean arterial pressure in supine humans J. Physiol., October 1, 2001; 536(1): 251 - 259. [Abstract] [Full Text] [PDF]
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L. J. Badra, W. H. Cooke, J. B. Hoag, A. A. Crossman, T. A. Kuusela, K. U. O. Tahvanainen, and D. L. Eckberg Respiratory modulation of human autonomic rhythms Am J Physiol Heart Circ Physiol, June 1, 2001; 280(6): H2674 - H2688. [Abstract] [Full Text] [PDF]
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J. W. Hamner, R. J. Morin, J. L. Rudolph, and J. A. Taylor Inconsistent link between low-frequency oscillations: R-R interval responses to augmented Mayer waves J Appl Physiol, April 1, 2001; 90(4): 1559 - 1564. [Abstract] [Full Text] [PDF]
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J. M. Legramante, G. Raimondi, M. Massaro, and F. Iellamo Positive and Negative Feedback Mechanisms in the Neural Regulation of Cardiovascular Function in Healthy and Spinal Cord-Injured Humans Circulation, March 6, 2001; 103(9): 1250 - 1255. [Abstract] [Full Text] [PDF]
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R. Zhang, K. Behbehani, C. G. Crandall, J. H. Zuckerman, and B. D. Levine Dynamic regulation of heart rate during acute hypotension: new insight into baroreflex function Am J Physiol Heart Circ Physiol, January 1, 2001; 280(1): H407 - H419. [Abstract] [Full Text] [PDF]
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K.-I. Iwasaki, R. Zhang, J. H. Zuckerman, J. A. Pawelczyk, and B. D. Levine Effect of head-down-tilt bed rest and hypovolemia on dynamic regulation of heart rate and blood pressure Am J Physiol Regulatory Integrative Comp Physiol, December 1, 2000; 279(6): R2189 - R2199. [Abstract] [Full Text] [PDF]
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A. Just, J. Faulhaber, and H. Ehmke Autonomic cardiovascular control in conscious mice Am J Physiol Regulatory Integrative Comp Physiol, December 1, 2000; 279(6): R2214 - R2221. [Abstract] [Full Text] [PDF]
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C. G. Crandall, R. Zhang, and B. D. Levine Effects of whole body heating on dynamic baroreflex regulation of heart rate in humans Am J Physiol Heart Circ Physiol, November 1, 2000; 279(5): H2486 - H2492. [Abstract] [Full Text] [PDF]
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A. Porta, G. Baselli, O. Rimoldi, A. Malliani, and M. Pagani Assessing baroreflex gain from spontaneous variability in conscious dogs: role of causality and respiration Am J Physiol Heart Circ Physiol, November 1, 2000; 279(5): H2558 - H2567. [Abstract] [Full Text] [PDF]
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D. Chemla, E. Aptecar, J.-L. Hebert, C. Coirault, D. Loisance, Y. Lecarpentier, and A. Nitenberg Short-term variability of pulse pressure and systolic and diastolic time in heart transplant recipients Am J Physiol Heart Circ Physiol, July 1, 2000; 279(1): H122 - H129. [Abstract] [Full Text] [PDF]
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J. P. Fauvel, C. Cerutti, P. Quelin, M. Laville, M. P. Gustin, C. Z. Paultre, and M. Ducher Mental Stress-Induced Increase in Blood Pressure Is Not Related to Baroreflex Sensitivity in Middle-Aged Healthy Men Hypertension, April 1, 2000; 35(4): 887 - 891. [Abstract] [Full Text] [PDF]
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D. Mesangeau, D. Laude, and J.-L. Elghozi Early detection of cardiovascular autonomic neuropathy in diabetic pigs using blood pressure and heart rate variability Cardiovasc Res, March 1, 2000; 45(4): 889 - 899. [Abstract] [Full Text] [PDF]
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J M Serrador, H C Finlayson, and R L Hughson Physical activity is a major contributor to the ultra low frequency components of heart rate variability Heart, December 1, 1999; 82(6): 9e - 9. [Abstract] [Full Text]
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M. V. Pitzalis, F. Massari, C. Forleo, A. Fioretti, R. Colombo, C. Balducci, F. Mastropasqua, and P. Rizzon Respiratory Systolic Pressure Variability During Atrial Fibrillation and Sinus Rhythm Hypertension, November 1, 1999; 34(5): 1060 - 1065. [Abstract] [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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D. P. Francis, L. C. Davies, M. Piepoli, M. Rauchhaus, P. Ponikowski, and A. J. S. Coats Origin of Oscillatory Kinetics of Respiratory Gas Exchange in Chronic Heart Failure Circulation, September 7, 1999; 100(10): 1065 - 1070. [Abstract] [Full Text] [PDF]
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J. M Karemaker Autonomic integration: the physiological basis of cardiovascular variability J. Physiol., June 1, 1999; 517(2): 316 - 316. [Full Text] [PDF]
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W. H Cooke, J. B Hoag, A. A Crossman, T. A Kuusela, K. U O Tahvanainen, and D. L Eckberg Human responses to upright tilt: a window on central autonomic integration J. Physiol., June 1, 1999; 517(2): 617 - 628. [Abstract] [Full Text] [PDF]
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J. M. Legramante, G. Raimondi, M. Massaro, S. Cassarino, G. Peruzzi, and F. Iellamo Investigating Feed-Forward Neural Regulation of Circulation From Analysis of Spontaneous Arterial Pressure and Heart Rate Fluctuations Circulation, April 6, 1999; 99(13): 1760 - 1766. [Abstract] [Full Text] [PDF]
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T. Laitinen, J. Hartikainen, L. Niskanen, G. Geelen, and E. Lansimies Sympathovagal balance is major determinant of short-term blood pressure variability in healthy subjects Am J Physiol Heart Circ Physiol, April 1, 1999; 276(4): H1245 - H1252. [Abstract] [Full Text] [PDF]
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R. P. Sloan, P. A. Shapiro, E. Bagiella, M. M. Myers, and J. M. Gorman Cardiac Autonomic Control Buffers Blood Pressure Variability Responses to Challenge: A Psychophysiologic Model of Coronary Artery Disease Psychosom Med, January 1, 1999; 61(1): 58 - 68. [Abstract] [Full Text] [PDF]
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M. Malik and D. L Eckberg Sympathovagal Balance: A Critical Appraisal • Response Circulation, December 8, 1998; 98(23): 2643 - 2644. [Full Text] [PDF]
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J. A. Taylor, D. L. Carr, C. W. Myers, and D. L. Eckberg Mechanisms Underlying Very-Low-Frequency RR-Interval Oscillations in Humans Circulation, August 11, 1998; 98(6): 547 - 555. [Abstract] [Full Text] [PDF]
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R. L. Cooley, N. Montano, C. Cogliati, P. van de Borne, W. Richenbacher, R. Oren, and V. K. Somers Evidence for a Central Origin of the Low-Frequency Oscillation in RR-Interval Variability Circulation, August 11, 1998; 98(6): 556 - 561. [Abstract] [Full Text] [PDF]
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R. A. Henry, I-L. Lu, L. A. Beightol, and D. L. Eckberg Interactions between CO2 chemoreflexes and arterial baroreflexes Am J Physiol Heart Circ Physiol, June 1, 1998; 274(6): H2177 - H2187. [Abstract] [Full Text] [PDF]
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M. V. Pitzalis, F. Mastropasqua, F. Massari, A. Passantino, R. Colombo, A. Mannarini, C. Forleo, and P. Rizzon Effect of respiratory rate on the relationships between RR interval and systolic blood pressure fluctuations: a frequency-dependent phenomenon Cardiovasc Res, May 1, 1998; 38(2): 332 - 339. [Abstract] [Full Text] [PDF]
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M. V. Pitzalis, F. Mastropasqua, A. Passantino, F. Massari, L. Ligurgo, C. Forleo, C. Balducci, F. Lombardi, and P. Rizzon Comparison Between Noninvasive Indices of Baroreceptor Sensitivity and the Phenylephrine Method in Post–Myocardial Infarction Patients Circulation, April 14, 1998; 97(14): 1362 - 1367. [Abstract] [Full Text] [PDF]
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J. A. Taylor, T. D. Williams, D. R. Seals, and K. P. Davy Low-frequency arterial pressure fluctuations do not reflect sympathetic outflow: gender and age differences Am J Physiol Heart Circ Physiol, April 1, 1998; 274(4): H1194 - H1201. [Abstract] [Full Text] [PDF]
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P. B. Persson Spectrum analysis of cardiovascular time series Am J Physiol Regulatory Integrative Comp Physiol, October 1, 1997; 273(4): R1201 - R1210. [Abstract] [Full Text] [PDF]
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L. A. Lipsitz, R. Morin, M. Gagnon, D. Kiely, and A. Medina Vasomotor instability preceding tilt-induced syncope: does respiration play a role? J Appl Physiol, August 1, 1997; 83(2): 383 - 390. [Abstract] [Full Text] [PDF]
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M. Piepoli, P. Sleight, S. Leuzzi, F. Valle, G. Spadacini, C. Passino, J. Johnston, and L. Bernardi Origin of Respiratory Sinus Arrhythmia in Conscious Humans : An Important Role for Arterial Carotid Baroreceptors Circulation, April 1, 1997; 95(7): 1813 - 1821. [Abstract] [Full Text]
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