Central volume expansion is pivotal for sustained decrease in heart rate during seated to supine posture change

2001 ◽  
Vol 281 (3) ◽  
pp. H1274-H1279 ◽  
Author(s):  
Bettina Pump ◽  
Tsutomu Kamo ◽  
Anders Gabrielsen ◽  
Peter Bie ◽  
Niels Juel Christensen ◽  
...  
Keyword(s):  
Heart Rate ◽  
Pulse Pressure ◽  
Volume Expansion ◽  
Arterial Pulse ◽  
Carotid Baroreceptor ◽  
Posture Change ◽  
Arterial Pulse Pressure ◽  
Baroreceptor Stimulation ◽  
Central Volume ◽  
Carotid Baroreceptor Stimulation

During prolonged, static carotid baroreceptor stimulation by neck suction (NS) in seated humans, heart rate (HR) decreases acutely and thereafter gradually increases. This increase has been explained by carotid baroreceptor adaptation and/or buffering by aortic reflexes. During a posture change from seated to supine (Sup) with similar carotid stimulation, however, the decrease in HR is sustained. To investigate whether this discrepancy is caused by changes in central blood volume, we compared ( n = 10 subjects) the effects of 10 min of seated NS (adjusted to simulate carotid stimulation of a posture change), a posture change from seated to Sup, and the same posture change with left atrial (LA) diameter maintained unchanged by lower body negative pressure (Sup + LBNP). During Sup, the prompt decreases in HR and mean arterial pressure (MAP) were sustained. HR decreased similarly within 30 s of NS (65 ± 2 to 59 ± 2 beats/min) and Sup + LBNP (65 ± 2 to 58 ± 2 beats/min) and thereafter gradually increased to values of seated. MAP decreased similarly within 5 min during Sup + LBNP and NS (by 7 ± 1 to 9 ± 1 mmHg) and thereafter tended to increase toward values of seated subjects. Arterial pulse pressure was increased the most by Sup, less so by Sup + LBNP, and was unchanged by NS. LA diameter was only increased by Sup. In conclusion, static carotid baroreceptor stimulation per se causes the acute (<30 s) decrease in HR during a posture change from seated to Sup, whereas the central volume expansion (increased LA diameter and/or arterial pulse pressure) is pivotal to sustain this decrease. Thus the effects of central volume expansion override adaptation of the carotid baroreceptors and/or buffering of aortic reflexes.

Cardiac autonomic control during balloon carotid angioplasty and stenting

2003 ◽  
Vol 81 (10) ◽  
pp. 944-951 ◽  
Author(s):  
Laurence Mangin ◽  
Claire Medigue ◽  
Jean-Claude Merle ◽  
Isabelle Macquin-Mavier ◽  
Philippe Duvaldestin ◽  
...  
Keyword(s):  
Heart Rate ◽  
Internal Carotid ◽  
Autonomic Control ◽  
Frequency Domain Method ◽  
Carotid Angioplasty ◽  
Sinus Arrhythmia ◽  
Time Frequency ◽  
Carotid Baroreceptor ◽  
Baroreceptor Stimulation ◽  
Carotid Baroreceptor Stimulation

Hemodynamic alterations during balloon carotid angioplasty (BCA) and stenting have been ascribed to the consequences of direct carotid baroreceptor stimulation during balloon inflation. BCA with stenting in patients with carotid atheromatous stenoses offers a unique opportunity for elucidating the cardiovascular autonomic response to direct transient intravascular stimulation of the baroreceptors. We analysed the consequences of BCA on the autonomic control of heart rate and on breathing components in nine patients with atheromatous stenoses involving the bifurcation and the internal carotid. A time–frequency domain method, the smoothed pseudo-Wigner–Ville transform (SPWVT), was used to evaluate the spectral parameters (i.e., the instantaneous amplitude and centre frequency (ICF) of the cardiovascular and respiratory oscillations). Those parameters and their dynamics (8 and 24 h later) were evaluated during and after the procedure. BCA stimulates baroreceptors in all patients, which markedly reduces heart rate and blood pressure. Vagal baroreflex activation altered the respiratory sinus arrhythmia in terms of amplitude and frequency (ICF HF RR shifted from 0.27 ± 0.03 to 0.23 ± 0.04 Hz pre-BCA vs. BCA, respectively; p < 0.01). Both the high- and low-frequency amplitudes of heart rate oscillations were altered during carotid baroreceptor stimulation, strongly supporting a contribution of the baroreflex to the generation of both oscillations of heart rate. Carotid baroreceptors stimulation increased the inspiratory time (Ti) (1.5 ± 0.5 to 2.3 ± 0.6 s pre-BCA vs. BCA, respectively; p < 0.01). In awake patients, BCA with stenting of atheromatous stenosis involving the bifurcation and internal carotid causes marked changes in the cardiac autonomic and respiratory control systems.Key words: carotid angioplasty, heart rate variability, autonomic nervous system, respiration, spectral analysis.

Smoking impairs baroreflex sensitivity in humans

1997 ◽  
Vol 273 (3) ◽  
pp. H1555-H1560 ◽  
Author(s):  
G. Mancia ◽  
A. Groppelli ◽  
M. Di Rienzo ◽  
P. Castiglioni ◽  
G. Parati
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Systolic Blood Pressure ◽  
Baroreflex Sensitivity ◽  
Pulse Interval ◽  
Average Systolic Blood Pressure ◽  
Carotid Baroreceptor ◽  
Baroreceptor Stimulation ◽  
Finger Blood Pressure ◽  
Carotid Baroreceptor Stimulation

In 10 healthy smokers, finger blood pressure was recorded continuously for 1 h in a supine control condition and for 1 h while smoking four cigarettes, one every 15 min. Smoking increased average systolic blood pressure (+19%, P < 0.01) and its variability and reduced pulse interval (reciprocal of heart rate, -22%, P < 0.01) and its variability. Baroreflex sensitivity, as assessed by the slope of spontaneous hypertension/bradycardia or hypotension/tachycardia sequences and by the alpha-coefficient (squared ratio between pulse interval and systolic blood pressure spectral powers at 0.1 Hz) was significantly decreased (P < 0.01) during smoking, whereas there were no effects of smoking on the reflex changes in pulse interval induced by carotid baroreceptor stimulation through a neck suction device. Sham smoking by a drinking straw had no effects on any of the above parameters. Thus, when assessed in the absence of laboratory maneuvers in daily life conditions, baroreflex sensitivity is markedly impaired by smoking. This impairment may contribute to the smoking-induced increase in blood pressure and heart rate as well as to the concomitant alterations in their variability.

15.9 MODELLING ARTERIAL PULSE PRESSURE FROM HEART RATE DURING SYMPATHETIC ACTIVATION

2016 ◽  
Vol 16 (C) ◽  
pp. 88
Author(s):  
Bjorn van der Ster ◽  
Berend Westerhof ◽  
Wim Stok ◽  
Feras Hatib ◽  
Jos Settels ◽  
...  
Keyword(s):  
Heart Rate ◽  
Pulse Pressure ◽  
Sympathetic Activation ◽  
Arterial Pulse ◽  
Arterial Pulse Pressure

scholarly journals Modeling Arterial Pulse Pressure From Heart Rate During Sympathetic Activation by Progressive Central Hypovolemia

2018 ◽  
Vol 9 ◽  
Author(s):  
Björn J. P. van Der Ster ◽  
Nicolaas H. Sperna Weiland ◽  
Berend E. Westerhof ◽  
Wim J. Stok ◽  
Johannes J. van Lieshout
Keyword(s):  
Heart Rate ◽  
Pulse Pressure ◽  
Sympathetic Activation ◽  
Arterial Pulse ◽  
Arterial Pulse Pressure

Mechanisms of inhibition of vasopressin release during moderate antiorthostatic posture change in humans

1999 ◽  
Vol 277 (1) ◽  
pp. R229-R235 ◽  
Author(s):  
Bettina Pump ◽  
Anders Gabrielsen ◽  
Niels Juel Christensen ◽  
Peter Bie ◽  
Morten Bestle ◽  
...  
Keyword(s):  
Lower Body Negative Pressure ◽  
Plasma Norepinephrine ◽  
Simultaneous Application ◽  
Vasopressin Release ◽  
Carotid Baroreceptor ◽  
Posture Change ◽  
Baroreceptor Stimulation ◽  
Vasopressin Secretion ◽  
Sinus Pressure ◽  
Carotid Baroreceptor Stimulation

The hypothesis was tested that the carotid baroreceptor stimulation caused by a posture change from upright seated with legs horizontal (Seat) to supine (Sup) participates in the suppression of arginine vasopressin (AVP) release. Ten healthy males underwent this posture change for 30 min without or with simultaneous application of lower body negative pressure (LBNP) adjusted to maintain left atrial diameter (LAD) at the Seat level. Throughout Sup, mean arterial pressure and heart rate decreased from 98 ± 2 to 91 ± 2 mmHg and from 63 ± 2 to 55 ± 2 beats/min ( P < 0.05), respectively, whereas the corresponding decreases during Sup + LBNP were attenuated and of shorter duration (98 ± 2 to 93 ± 2 mmHg and 62 ± 2 to 58 ± 3 beats/min, P < 0.05). During Sup, LAD increased from 30 ± 1 to 33 ± 1 mm, and arterial pulse pressure (PP) increased from 40 ± 2 to 47 ± 2 mmHg, whereas plasma AVP decreased from 0.9 ± 0.2 to 0.5 ± 0.1 pg/ml ( P < 0.05), and plasma norepinephrine (NE) decreased from 176 ± 20 to 125 ± 16 pg/ml ( P < 0.05). During Sup + LBNP, there were no changes in LAD, PP, plasma AVP, or NE. In conclusion, vasopressin secretion is suppressed during an antiorthostatic posture change, which increases carotid sinus pressure, PP, and LAD. The suppression is absent when PP and LAD are prevented from increasing and is thus critically dependent on at least one of these stimuli.

Cardiovascular effects of static carotid baroreceptor stimulation during water immersion in humans

2001 ◽  
Vol 280 (6) ◽  
pp. H2607-H2615 ◽  
Author(s):  
Bettina Pump ◽  
Makoto Shiraishi ◽  
Anders Gabrielsen ◽  
Peter Bie ◽  
Niels Juel Christensen ◽  
...  
Keyword(s):  
Water Immersion ◽  
Cardiovascular Effects ◽  
Plasma Norepinephrine ◽  
Xiphoid Process ◽  
Carotid Baroreceptor ◽  
Posture Change ◽  
Supine Posture ◽  
Baroreceptor Stimulation ◽  
Pressure Receptor ◽  
Carotid Baroreceptor Stimulation

We hypothesized that the more-pronounced hypotensive and bradycardic effects of an antiorthostatic posture change from seated to supine than water immersion are caused by hydrostatic carotid baroreceptor stimulation. Ten seated healthy males underwent five interventions of 15-min each of 1) posture change to supine, 2) seated water immersion to the Xiphoid process (WI), 3) seated neck suction (NS), 4) WI with simultaneous neck suction (−22 mmHg) adjusted to simulate the carotid hydrostatic pressure increase during supine (WI + NS), and 5) seated control. Left atrial diameter increased similarly during supine, WI + NS, and WI and was unchanged during control and NS. Mean arterial pressure (MAP) decreased the most during supine (7 ± 1 mmHg, P < 0.05) and less during WI + NS (4 ± 1 mmHg) and NS (3 ± 1 mmHg). The decrease in heart rate (HR) by 13 ± 1 beats/min ( P < 0.05) and the increase in arterial pulse pressure (PP) by 17 ± 4 mmHg ( P< 0.05) during supine was more pronounced ( P < 0.05) than during WI + NS (10 ± 2 beats/min and 7 ± 2 mmHg, respectively) and WI (8 ± 2 beats/min and 6 ± 1 mmHg, respectively, P < 0.05). Plasma vasopressin decreased only during supine and WI, and plasma norepinephrine, in addition, decreased during WI + NS ( P < 0.05). In conclusion, WI + NS is not sufficient to decrease MAP and HR to a similar extent as a 15-min seated to supine posture change. We suggest that not only static carotid baroreceptor stimulation but also the increase in PP combined with low-pressure receptor stimulation is a possible mechanism for the more-pronounced decrease in MAP and HR during the posture change.

Influence of cardiopulmonary receptors on the bradycardic responses to carotid baroreceptor stimulation in man

1987 ◽  
Vol 72 (5) ◽  
pp. 639-645 ◽  
Author(s):  
G. Parati ◽  
G. Grassi ◽  
P. Coruzzi ◽  
Luisa Musiari ◽  
Antonella Ravogli ◽  
...  
Keyword(s):  
Heart Rate ◽  
Central Venous Pressure ◽  
Venous Pressure ◽  
Receptor Activity ◽  
Right Atrial ◽  
Central Venous ◽  
Carotid Baroreceptor ◽  
Atrial Catheter ◽  
Baroreceptor Stimulation ◽  
Carotid Baroreceptor Stimulation

1. Animal studies have shown that arterial baroreflexes are modulated by reflexes originating from the cardiopulmonary volume receptors, and that this modulation consists of a reduction of the inhibitory influence exerted by arterial baroreceptors on the heart and peripheral circulation. This has not been confirmed in man, however, in whom no reduction in the bradycardic response to carotid baroreceptor stimulation has been observed after the mild increase in central venous pressure (right atrial catheter) and cardiopulmonary receptor activity provided by passive leg raising. 2. In seven normotensive subjects carotid baroreceptors were gradedly stimulated by progressively increasing carotid transmural pressure through a neck chamber device, the resulting reflex lengthening in R–R interval being measured in the two–three cardiac cycles immediately after the baroreceptor stimulus. This manoeuvre was performed in control conditions and repeated during a head-out water immersion which increased central venous pressure (right atrial catheter) from 1.5 ± 0.2 to 12.0 ± 0.9 mmHg (mean ± SE), thereby providing a marked increase in the cardiopulmonary receptor stimulus. 3. In the control condition graded stimulation of the baroreceptors caused a progressive lengthening in R–R interval, the maximal effect being + 477.4 ± 57.2 ms. Immersion increased the R–R interval from 774.2 ± 3.2 to 961.6 ± 5.8 ms (P < 0.01) and reduced mean arterial pressure (cuff measurement) from 96.0 ± 1.0 to 82.3 ± 0.9 mmHg. The changes in R–R interval induced by carotid baroreceptor stimulation were virtually identical with those observed in the absence of immersion. However, owing to the lower baseline heart rate during immersion, this meant a lesser degree of reflex bradycardia to carotid baroreceptor stimulation (maximal reduction − 30.5 ± 3.0 beats/min and −19.3 ± 3.1 beats/min before and during immersion respectively). 4. Thus, although the baroreflex sensitivity as expressed by changes in R–R interval is altered, the arterial baroreceptor ability to modulate heart rate (and perhaps cardiac output) is reduced when cardiopulmonary receptor activity is markedly increased. This may have implications in a number of physiological and pathophysiological settings.

Variability of the haemodynamic responses to laboratory tests employed in assessment of neural cardiovascular regulation in man

1985 ◽  
Vol 69 (5) ◽  
pp. 533-540 ◽  
Author(s):  
Gianfranco Parati ◽  
Guido Pomidossi ◽  
Agustin Ramirez ◽  
Bruno Cesana ◽  
Giuseppe Mancia
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Test Performance ◽  
Blood Pressure Response ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Cardiovascular Regulation ◽  
Pressor Test ◽  
Carotid Baroreceptor ◽  
Baroreceptor Stimulation

1. In man evaluation of neural cardiovascular regulation makes use of a variety of tests which address the excitatory and reflex inhibitory neural influences that control circulation. Because interpretation of these tests is largely based on the magnitude of the elicited haemodynamic responses, their reproducibility in any given subject is critical. 2. In 39 subjects with continuous blood pressure (intra-arterial catheter) and heart rate monitoring we measured (i) the blood pressure and heart rate rises during hand-grip and cold-pressor test, (ii) the heart rate changes occurring during baroreceptor stimulation and deactivation by injection of phenylephrine and trinitroglycerine, and (iii) the heart rate and blood pressure changes occurring with alteration in carotid baroreceptor activity by a neck chamber. Each test was carefully standardized and performed at 30 min intervals for a total of six times in each subject. 3. The results showed that the responses to any test were clearly different from one another and that this occurred in all subjects studied. For the group as a whole the average response variability (coefficient of variation) ranged from 10.2% for the blood pressure response to carotid baroreceptor stimulation to 44.2% for the heart rate response to cold-pressor test. The variability of the responses was not related to basal blood pressure or heart rate, nor to the temporal sequence of the test performance. 4. Thus tests employed for studying neural cardiovascular control in man produce responses whose reproducibility is limited. This phenomenon may make it more difficult to define the response magnitude typical of each subject, as well as its comparison in different conditions and diseases.

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