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.

Active recovery attenuates the fall in sweat rate but not cutaneous vascular conductance after supine exercise

2004 ◽  
Vol 96 (2) ◽  
pp. 668-673 ◽  
Author(s):  
Thad E. Wilson ◽  
Robert Carter ◽  
Michael J. Cutler ◽  
Jian Cui ◽  
Michael L. Smith ◽  
...  
Keyword(s):  
Heart Rate ◽  
Central Venous Pressure ◽  
Sweat Rate ◽  
Venous Pressure ◽  
Thoracic Impedance ◽  
Active Recovery ◽  
Central Venous ◽  
Cycle Exercise ◽  
Vascular Conductance ◽  
Cutaneous Vascular Conductance

The purpose of this study was to identify whether baroreceptor unloading was responsible for less efficient heat loss responses (i.e., skin blood flow and sweat rate) previously reported during inactive compared with active recovery after upright cycle exercise (Carter R III, Wilson TE, Watenpaugh DE, Smith ML, and Crandall CG. J Appl Physiol 93: 1918-1929, 2002). Eight healthy adults performed two 15-min bouts of supine cycle exercise followed by inactive or active (no-load pedaling) supine recovery. Core temperature (Tcore), mean skin temperature (Tsk), heart rate, mean arterial blood pressure (MAP), thoracic impedance, central venous pressure ( n = 4), cutaneous vascular conductance (CVC; laser-Doppler flux/MAP expressed as percentage of maximal vasodilation), and sweat rate were measured throughout exercise and during 5 min of recovery. Exercise bouts were similar in power output, heart rate, Tcore, and Tsk. Baroreceptor loading and thermal status were similar during trials because MAP (90 ± 4, 88 ± 4 mmHg), thoracic impedance (29 ± 1, 28 ± 2 Ω), central venous pressure (5 ± 1, 4 ± 1 mmHg), Tcore (37.5 ± 0.1, 37.5 ± 0.1°C), and Tsk (34.1 ± 0.3, 34.2 ± 0.2°C) were not significantly different at 3 min of recovery between active and inactive recoveries, respectively; all P > 0.05. At 3 min of recovery, chest CVC was not significantly different between active (25 ± 6% of maximum) and inactive (28 ± 6% of maximum; P > 0.05) recovery. In contrast, at this time point, chest sweat rate was higher during active (0.45 ± 0.16 mg·cm-2·min-1) compared with inactive (0.34 ± 0.19 mg·cm-2·min-1; P < 0.05) recovery. After exercise CVC and sweat rate are differentially controlled, with CVC being primarily influenced by baroreceptor loading status while sweat rate is influenced by other factors.

Alteration in heart rate response to hemorrhage in conscious dogs with volume overload

1978 ◽  
Vol 235 (4) ◽  
pp. H422-H428
Author(s):  
M. M. LeWinter ◽  
J. S. Karliner ◽  
J. W. Covell
Keyword(s):  
Heart Rate ◽  
Central Venous Pressure ◽  
Pulse Pressure ◽  
Pressure Pulse ◽  
Heart Rate Response ◽  
Parasympathetic Nervous System ◽  
Venous Pressure ◽  
Volume Overload ◽  
Conscious Dogs ◽  
Central Venous

The heart rate response to hemorrhage was studied in conscious dogs before and up to 2 mo after the establishment of volume overload due to systemic arteriovenous (a-v) fistulas. Before a-v fistula, heart rate increased markedly during hemorrhage. When hemorrhage was preceded by dextran infusion, bleeding resulted in a gradual reduction in heart rate. The a-v fistula caused marked increases in resting heart rate, central venous pressure, pulse pressure, and blood volume. During hemorrhage, heart rate initially remained constant, but then declined abruptly from the resting value of 121 +/- 3.7 beats/min to a nadir of 89 +/- 6.5 beats/min (P less than 0.01). Although mean arterial pressure decreased markedly, there was no significant change in pulse pressure, and central venous pressure tended to stabilize with the heart rate decline. The abrupt heart rate decline was prevented by atropine but unaltered by propranolol. The response was observed as early as 5 days after a-v fistula. We conclude that an alteration in the heart rate response to hemorrhage appears early during volume overload. This alteration appears to be reflex in nature and to be mediated by the parasympathetic nervous system.

ANP-mediated volume depletion attenuates renal responses in humans

1992 ◽  
Vol 263 (6) ◽  
pp. R1303-R1308 ◽  
Author(s):  
T. J. Ebert ◽  
L. Groban ◽  
M. Muzi ◽  
M. Hanson ◽  
A. W. Cowley
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Central Venous Pressure ◽  
Sodium Excretion ◽  
Healthy Subjects ◽  
Venous Pressure ◽  
Urine Volume ◽  
Positive Pressure ◽  
Plasma Norepinephrine ◽  
Central Venous

Brief low-dose infusions of atrial natriuretic peptide (ANP) that emulate physiological plasma concentrations in humans have little if any effect on renal excretory function. This study explored the possibility that ANP-mediated reductions in cardiac filling pressures (through ANP's rapid effect on capillary dynamics) could attenuate its purported renal effects. Protocol A consisted of 16 healthy subjects (ages 19-27 yr old) who underwent three consecutive 45-min experimental sequences: 1) placebo, 2) ANP (10 ng.kg-1 x min-1), and 3) ANP alone (n = 8) or ANP with simultaneous lower body positive pressure (LBPP, n = 8). Electrocardiogram and direct measures of arterial and central venous pressures were continuously monitored. Blood was sampled at the end of each 45-min sequence before subjects stood to void. Compared with control (placebo), ANP produced a hemoconcentration and increased plasma norepinephrine, but did not change heart rate, blood pressure, plasma levels of renin, aldosterone, or vasopressin, or renal excretion of volume or sodium. In subjects receiving LBPP to maintain central venous pressure during the last 45 min of ANP infusion, norepinephrine did not increase and urine volume and sodium excretion increased (P < 0.05). In a second study (protocol B), five healthy subjects received a placebo infusion for 45 min followed by two consecutive 45-min infusions of ANP (10 ng.kg-1 x min-1). Central venous pressure was maintained (LBPP) at placebo baseline throughout the two ANP infusion periods. Urine volume and sodium excretion rates increased progressively and significantly during both ANP infusion periods (P < 0.05) without significant changes in creatinine clearance, blood pressure, or heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Microcirculatory Perfusion during Volume Therapy

1995 ◽  
Vol 82 (4) ◽  
pp. 975-982. ◽  
Author(s):  
Wolfgang Funk ◽  
Verena Baldinger
Keyword(s):  
Heart Rate ◽  
Oxygen Partial Pressure ◽  
Partial Pressure ◽  
Central Venous Pressure ◽  
Venous Pressure ◽  
Tissue Perfusion ◽  
Volume Replacement ◽  
Surface Oxygen ◽  
Tissue Oxygen ◽  
Central Venous

Background Because of the passage of water and salt molecules into the interstitial space, volume replacement with crystalloid solutions requires an amount at least four times that of lost blood. The resulting tissue edema may interfere with nutritive capillary perfusion and oxygen delivery. To prove this hypothesis, the effects of isovolemic hemodilution (hematocrit 30%) with Ringer's lactate solution or dextran 60 on tissue perfusion and oxygenation were investigated in awake Syrian golden hamsters. Methods Experiments were performed by using a chronic dorsal skinfold window giving access to skeletal muscle tissue (musculus cutaneus) with in vivo microscopy, quantitative video image analysis, and surface oxygen partial pressure electrodes. Central venous and arterial pressures were measured by means of chronically implanted jugular venous and carotid catheters. Results Isovolemic exchange of blood with dextran caused no significant changes in arterial or central venous pressure, heart rate, capillary flow velocity, functional capillary density, or surface oxygen partial pressure during the 1-h observation period. A volume of Ringer's solution equal to four times of the amount of blood lost maintained arterial pressure and heart rate when central venous pressure was kept at predilution control values. However, tissue perfusion determined by counting perfused capillaries per terminal arteriole was reduced by 62%, and mean tissue oxygen partial pressure decreased from 19 to 8 mmHg. Conclusions In this model, volume replacement with artificial colloids yielded hemodynamic stability and adequate tissue oxygen supply, whereas administration of crystalloids alone jeopardized tissue perfusion and oxygenation.

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.

Baroreceptor-mediated suppression of osmotically stimulated vasopressin in normal humans

1988 ◽  
Vol 65 (3) ◽  
pp. 1226-1230 ◽  
Author(s):  
S. R. Goldsmith
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Central Venous Pressure ◽  
Venous Pressure ◽  
Positive Pressure ◽  
Lower Body ◽  
Central Venous ◽  
Lower Body Positive Pressure ◽  
Body Positive

Increases in central venous pressure and arterial pressure have been reported to have variable effects on normal arginine vasopressin (AVP) levels in healthy humans. To test the hypothesis that baroreceptor suppression of AVP secretion might be more likely if AVP were subjected to a prior osmotic stimulus, we investigated the response of plasma AVP to increased central venous pressure and mean arterial pressure after hypertonic saline in six normal volunteers. Plasma AVP, serum osmolality, heart rate, central venous pressure, mean arterial pressure, and pulse pressure were assessed before and after a 0.06 ml.kg-1.min-1-infusion of 5% saline give over 90 min and then after 10 min of 30 degrees head-down tilt and 10 min of head-down tilt plus lower-body positive pressure. Hypertonic saline increased plasma AVP. After head-down tilt, which did not change heart rate, pulse pressure, or mean arterial pressure but did increase central venous pressure, plasma AVP fell. Heart rate, pulse pressure, and central venous pressure were unchanged from head-down tilt values during lower-body positive pressure, whereas mean arterial pressure increased. Plasma AVP during lower-body positive pressure was not different from that during tilt. Osmolality increased during the saline infusion but was stable throughout the remainder of the study. These data therefore suggest that an osmotically stimulated plasma AVP level can be suppressed by baroreflex activation. Either the low-pressure cardiopulmonary receptors (subjected to a rise in central venous pressure during head-down tilt) or the sinoaortic baroreceptors (subjected to hydrostatic effects during head-down tilt) could have been responsible for the suppression of AVP.(ABSTRACT TRUNCATED AT 250 WORDS)

Central venous pressure in humans during short periods of weightlessness

1987 ◽  
Vol 63 (6) ◽  
pp. 2433-2437 ◽  
Author(s):  
P. Norsk ◽  
N. Foldager ◽  
F. Bonde-Petersen ◽  
B. Elmann-Larsen ◽  
T. S. Johansen
Keyword(s):  
Heart Rate ◽  
Central Venous Pressure ◽  
Supine Position ◽  
Parabolic Flight ◽  
Venous Pressure ◽  
Central Venous Catheters ◽  
Sitting Position ◽  
Central Venous ◽  
Pressure Transducers ◽  
Gauge Pressure

Central venous pressure (CVP) was measured in 14 males during 23.3 +/- 0.6 s (mean +/- SE) of weightlessness (0.00 +/- 0.05 G) achieved in a Gulfstream-3 jet aircraft performing parabolic flight maneuvers and during either 60 or 120 s of +2 Gz (2.0 +/- 0.1 Gz). CVP was obtained using central venous catheters and strain-gauge pressure transducers. Heart rate (HR) was measured simultaneously in seven of the subjects. Measurements were compared with values obtained inflight at 1 G with the subjects in the supine (+1 Gx) and upright sitting (+1 Gz) positions, respectively. CVP was 2.6 +/- 1.5 mmHg during upright sitting and 5.0 +/- 0.7 mmHg in the supine position. During weightlessness, CVP increased significantly to 6.8 +/- 0.8 mmHg (P less than 0.005 compared with both upright sitting and supine inflight). During +2 Gz, CVP was 2.8 +/- 1.4 mmHg and only significantly lower than CVP during weightlessness (P less than 0.05). HR increased from 65 +/- 7 beats/min at supine and 70 +/- 5 beats/min during upright sitting to 79 +/- 7 beats/min (P less than 0.01 compared with supine) during weightlessness and to 80 +/- 6 beats/min (P less than 0.01 compared with upright sitting and P less than 0.001 compared with supine) during +2 Gz. We conclude that the immediate onset of weightlessness induces a significant increase in CVP, not only compared with the upright sitting position but also compared with the supine position at 1 G.

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.

scholarly journals Central venous pressure from common iliac vein reflects right atrial pressure

1998 ◽  
Vol 45 (8) ◽  
pp. 798-801 ◽  
Author(s):  
Abdulaziz Alzeer ◽  
Subhash Arora ◽  
Ziauddin Ansari ◽  
Desouky F. Fayed ◽  
Mohamed Naguib
Keyword(s):  
Central Venous Pressure ◽  
Venous Pressure ◽  
Iliac Vein ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Common Iliac Vein ◽  
Central Venous

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.

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