Increase in vagal activity during hypotensive lower-body negative pressure in humans

1988 ◽  
Vol 255 (1) ◽  
pp. R149-R156 ◽  
Author(s):  
K. Sander-Jensen ◽  
J. Mehlsen ◽  
C. Stadeager ◽  
N. J. Christensen ◽  
J. Fahrenkrug ◽  
...  
Keyword(s):  
Heart Rate ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Venous Pressure ◽  
Initial Increase ◽  
Vagal Activity ◽  
Lower Body ◽  
Central Venous ◽  
Subsequent Decrease ◽  
Before And After

Progressive central hypovolemia is characterized by a normotensive, tachycardic stage followed by a reversible, hypotensive stage with slowing of the heart rate (HR). We investigated circulatory changes and arterial hormone concentrations in response to lower-body negative pressure (LBNP) in six volunteers before and after atropine administration. LBNP of 55 mmHg initially resulted in an increase in HR from 55 +/- 4 to 90 +/- 5 beats/min and decreases in mean arterial pressure (MAP) from 94 +/- 4 to 81 +/- 5 mmHg, in central venous pressure from 7 +/- 1 to -3 +/- 1 mmHg, and in cardiac output from 6.1 +/- 0.5 to 3.7 +/- 0.11/min. Concomitantly, epinephrine and norepinephrine levels increased. After 8.2 +/- 2.3 min of LBNP, the MAP had decreased to 41 +/- 7 mmHg and HR had decreased to 57 +/- 3 beats/min. Vasopressin increased from 1.2 +/- 0.3 to 137 +/- 45 pg/ml and renin activity increased from 1.45 +/- 4.0 to 3.80 +/- 1.0 ng.ml-1.h-1 with no further changes in epinephrine, norepinephrine, and vasoactive intestinal polypeptide. A tardy rise in pancreatic polypeptide indicated increased vagal activity. After atropine. LBNP also caused an initial increase in HR, which, however, remained elevated during the subsequent decrease in MAP to 45 +/- 6 mmHg occurring after 8.1 +/- 2.4 min.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Reductions in central venous pressure by lower body negative pressure or blood loss elicit similar hemodynamic responses

2014 ◽  
Vol 117 (2) ◽  
pp. 131-141 ◽  
Author(s):  
Blair D. Johnson ◽  
Noud van Helmond ◽  
Timothy B. Curry ◽  
Camille M. van Buskirk ◽  
Victor A. Convertino ◽  
...  
Keyword(s):  
Heart Rate ◽  
Blood Loss ◽  
Central Venous Pressure ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Venous Pressure ◽  
Lower Body ◽  
Central Venous ◽  
Stimulus Response ◽  
Response Slope

The purpose of this study was to compare hemodynamic and blood analyte responses to reduced central venous pressure (CVP) and pulse pressure (PP) elicited during graded lower body negative pressure (LBNP) to those observed during graded blood loss (BL) in conscious humans. We hypothesized that the stimulus-response relationships of CVP and PP to hemodynamic responses during LBNP would mimic those observed during BL. We assessed CVP, PP, heart rate, mean arterial pressure (MAP), and other hemodynamic markers in 12 men during LBNP and BL. Blood samples were obtained for analysis of catecholamines, hematocrit, hemoglobin, arginine vasopressin, and blood gases. LBNP consisted of 5-min stages at 0, 15, 30, and 45 mmHg of suction. BL consisted of 5 min at baseline and following three stages of 333 ml of hemorrhage (1,000 ml total). Individual r2 values and linear regression slopes were calculated to determine whether the stimulus (CVP and PP)-hemodynamic response trajectories were similar between protocols. The CVP-MAP trajectory was the only CVP-response slope that was statistically different during LBNP compared with BL (0.93 ± 0.27 vs. 0.13 ± 0.26; P = 0.037). The PP-heart rate trajectory was the only PP-response slope that was statistically different during LBNP compared with BL (−1.85 ± 0.45 vs. −0.46 ± 0.27; P = 0.024). Norepinephrine, hematocrit, and hemoglobin were all lower at termination in the BL protocol compared with LBNP ( P < 0.05). Consistent with our hypothesis, LBNP mimics the hemodynamic stimulus-response trajectories observed during BL across a significant range of CVP in humans.

Cardiovascular responses to lower body negative pressure before and after 4 h of head-down bed rest and seated control in men and women

2012 ◽  
Vol 113 (10) ◽  
pp. 1604-1612 ◽  
Author(s):  
H. Edgell ◽  
A. Grinberg ◽  
N. Gagné ◽  
K. R. Beavers ◽  
R. L. Hughson
Keyword(s):  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Venous Pressure ◽  
Bed Rest ◽  
Time Of Day ◽  
Lower Body ◽  
Central Venous ◽  
Men And Women ◽  
Cardiovascular Deconditioning ◽  
Before And After

Cardiovascular deconditioning after a 4-h head-down bed rest (HDBR) might be a consequence of the time of day relative to pre-HDBR testing, or simply 4 h of confinement and inactivity rather than the posture change. Ten men and 11 women were studied during lower body negative pressure (LBNP) before and after 4-h HDBR and 4-h seated posture (SEAT) as a control for time of day and physical inactivity effects to test the hypotheses that cardiovascular deconditioning was a consequence of the HDBR posture, and that women would have a greater deconditioning response. Following HDBR, men and women had lower blood volume, higher heart rate with a greater increase during LBNP, a greater decrease of stroke volume during LBNP, lower central venous pressure, smaller inferior vena cava diameter, higher portal vein resistance index with a greater increase during LBNP, but lower forearm vascular resistance, lower norepinephrine, and lower renin. Women had lower vasopressin and men had higher vasopressin after HDBR, and women had lower pelvic impedance and men higher pelvic impedance. Following SEAT, brachial vascular resistance was reduced, thoracic impedance was elevated, the reduction of central venous pressure during LBNP was changed, women had higher angiotensin II whereas men had lower levels, and pelvic impedance increased in women and decreased in men. Cardiovascular deconditioning was greater after 4-h HDBR than after SEAT. Women and men had similar responses for most cardiovascular variables in the present study that tested the responses to LBNP after short-duration HDBR compared with a control condition.

Differential sympathetic nerve and heart rate spectral effects of nonhypotensive lower body negative pressure

2001 ◽  
Vol 281 (2) ◽  
pp. R468-R475 ◽  
Author(s):  
John S. Floras ◽  
Gary C. Butler ◽  
Shin-Ichi Ando ◽  
Steven C. Brooks ◽  
Michael J. Pollard ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Stroke Volume ◽  
Negative Pressure ◽  
Sympathetic Nerve ◽  
Lower Body Negative Pressure ◽  
Muscle Sympathetic Nerve Activity ◽  
Venous Pressure ◽  
Harmonic Component ◽  
Lower Body

Lower body negative pressure (LBNP; −5 and −15 mmHg) was applied to 14 men (mean age 44 yr) to test the hypothesis that reductions in preload without effect on stroke volume or blood pressure increase selectively muscle sympathetic nerve activity (MSNA), but not the ratio of low- to high-frequency harmonic component of spectral power (PL/PH), a coarse-graining power spectral estimate of sympathetic heart rate (HR) modulation. LBNP at −5 mmHg lowered central venous pressure and had no effect on stroke volume (Doppler) or systolic blood pressure but reduced vagal HR modulation. This latter finding, a manifestation of arterial baroreceptor unloading, refutes the concept that low levels of LBNP interrogate, selectively, cardiopulmonary reflexes. MSNA increased, whereas PL/PH and HR were unchanged. This discordance is consistent with selectivity of efferent sympathetic responses to nonhypotensive LBNP and with unloading of tonically active sympathoexcitatory atrial reflexes in some subjects. Hypotensive LBNP (−15 mmHg) increased MSNA and PL/PH, but there was no correlation between these changes within subjects. Therefore, HR variability has limited utility as an estimate of the magnitude of orthostatic changes in sympathetic discharge to muscle.

Comparison of muscle sympathetic responses to hemorrhage and lower body negative pressure in humans

1991 ◽  
Vol 70 (3) ◽  
pp. 1401-1405 ◽  
Author(s):  
R. F. Rea ◽  
M. Hamdan ◽  
M. P. Clary ◽  
M. J. Randels ◽  
P. J. Dayton ◽  
...  
Keyword(s):  
Negative Pressure ◽  
Sympathetic Nerve Activity ◽  
Lower Body Negative Pressure ◽  
Muscle Sympathetic Nerve Activity ◽  
Venous Pressure ◽  
Lower Body ◽  
Central Venous ◽  
Nerve Activity ◽  
Percent Change ◽  
Sympathetic Responses

We compared changes in muscle sympathetic nerve activity (SNA) during graded lower body negative pressure (LBNP) and 450 ml of hemorrhage in nine healthy volunteers. During LBNP, central venous pressure (CVP) decreased from 6.1 +/- 0.4 to 4.5 +/- 0.5 (LBNP -5 mmHg), 3.4 +/- 0.6 (LBNP -10 mmHg), and 2.3 +/- 0.6 mmHg (LBNP -15 mmHg), and there were progressive increases in SNA at each level of LBNP. The slope relating percent change in SNA to change in CVP during LBNP (mean +/- SE) was 27 +/- 11%/mmHg. Hemorrhage of 450 ml at a mean rate of 71 +/- 5 ml/min decreased CVP from 6.1 +/- 0.5 to 3.7 +/- 0.5 mmHg and increased SNA by 47 +/- 11%. The increase in SNA during hemorrhage was not significantly different from the increase in SNA predicted by the slope relating percent change in SNA to change in CVP during LBNP. These data show that nonhypotensive hemorrhage causes sympathoexcitation and that sympathetic responses to LBNP and nonhypotensive hemorrhage are similar in humans.

Aortic baroreflex control of heart rate during hypertensive stimuli: effect of fitness

1993 ◽  
Vol 74 (4) ◽  
pp. 1555-1562 ◽  
Author(s):  
X. Shi ◽  
J. M. Andresen ◽  
J. T. Potts ◽  
B. H. Foresman ◽  
S. A. Stern ◽  
...  
Keyword(s):  
Heart Rate ◽  
Steady State ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Venous Pressure ◽  
Lower Body ◽  
Baroreflex Control ◽  
Fitness Level ◽  
Neck Pressure ◽  
Sinus Pressure

We examined the aortic baroreflex control of heart rate (HR) in seven healthy young men of average fitness (AF) and seven of high fitness (HF). The fitness level was determined by maximal oxygen uptake (AF = 42.9 +/- 1.1, HF = 62.3 +/- 1.8 ml.kg-1.min-1). Aortic baroreflex control of HR was determined during a steady-state increase of mean arterial pressure (MAP; AF, +15.0 +/- 2.1 and HF, +18.3 +/- 0.8 mmHg) with phenylephrine (PE) infusion combined with positive neck pressure (NP; AF, 18 +/- 2.0 and HF, 20 +/- 0.8 mmHg) to counteract the increased carotid sinus pressure and with low levels of lower body negative pressure to counteract the increased central venous pressure. There was no group difference in the increased MAP or NP, nor was there stage difference in MAP within either group during PE infusion. However, the isolated cardiac-aortic baroreflex gains (i.e., delta HR/delta MAP) were significantly less in the HF (0.16 +/- 0.02 and 0.14 +/- 0.03 beats.min-1.mmHg-1) than in the AF (0.52 +/- 0.08 and 0.59 +/- 0.07 beats.min-1.mmHg-1) subjects at PE + NP and PE + NP + lower body negative pressure. We concluded that during steady-state increases in MAP, the sensitivity of aortic baroreflex control of HR was significantly less in the HF than in the AF subjects.

Effect of central venous pressure on arterial baroreflex control of heart rate

1979 ◽  
Vol 236 (1) ◽  
pp. H42-H47 ◽  
Author(s):  
A. Takeshita ◽  
A. L. Mark ◽  
D. L. Eckberg ◽  
F. M. Abboud
Keyword(s):  
Central Venous Pressure ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Sinus Node ◽  
Venous Pressure ◽  
Lower Body ◽  
Arterial Baroreflex ◽  
Central Venous ◽  
Baroreceptor Stimulation ◽  
Arterial Baroreceptor

There is considerable evidence that the level of afferent cardiopulmonary receptor activity modulates sinus node responses to arterial baroreflex stimulation in experimental animals. We tested the hypothesis that this reflex interaction occurs also in man by measuring sinus node responses to arterial baroreceptor stimulation with phenylephrine injection or neck suction, before and during changes of central venous pressure provoked by lower body negative pressure or leg and lower trunk elevation. Variations of central venous pressure between 1.1 and 9.0 mmHg did not influence arterial baroreflex mediated bradycardia. Baroreflex sinus node responses were augmented by intravenous propranolol, but the level of responses after propranolol was comparable during the control state, lower body negative pressure, and leg and trunk elevation. Sinus node responses to very brief baroreceptor stimuli applied during the transitions of central venous pressure also were comparable in the three states. We conclude that physiological variations of central venous pressure do not influence sinus node responses to arterial baroreceptor stimulation in man.

scholarly journals Cerebral blood velocity regulation during progressive blood loss compared with lower body negative pressure in humans

2015 ◽  
Vol 119 (6) ◽  
pp. 677-685 ◽  
Author(s):  
Caroline A. Rickards ◽  
Blair D. Johnson ◽  
Ronée E. Harvey ◽  
Victor A. Convertino ◽  
Michael J. Joyner ◽  
...  
Keyword(s):  
Blood Loss ◽  
Arterial Pressure ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Venous Pressure ◽  
Blood Velocity ◽  
Lower Body ◽  
Central Venous ◽  
Cerebral Blood Velocity ◽  
Level 3

Lower body negative pressure (LBNP) is often used to simulate blood loss in humans. It is unknown if cerebral blood flow responses to actual blood loss are analogous to simulated blood loss during LBNP. Nine healthy men were studied at baseline, during three levels of LBNP (5 min at −15, −30, and −45 mmHg), and during three levels of blood loss (333, 667, and 1,000 ml). LBNP and blood loss conditions were randomized. Intra-arterial mean arterial pressure (MAP) during LBNP was similar to that during blood loss ( P ≥ 0.42). Central venous pressure (2.8 ± 0.7 vs. 4.0 ± 0.8, 1.2 ± 0.6 vs. 3.5 ± 0.8, and 0.2 ± 0.9 vs. 2.1 ± 0.9 mmHg for levels 1, 2, and 3, respectively, P ≤ 0.003) and stroke volume (71 ± 4 vs. 80 ± 3, 60 ± 3 vs. 74 ± 3, and 51 ± 2 vs. 68 ± 4 ml for levels 1, 2, and 3, respectively, P ≤ 0.002) were lower during LBNP than blood loss. Despite differences in central venous pressure, middle cerebral artery velocity (MCAv) and cerebrovascular conductance were similar between LBNP and blood loss at each level (MCAv at level 3: 62 ± 6 vs. 66 ± 5 cm/s, P = 0.37; cerebrovascular conductance at level 3: 0.72 ± 0.05 vs. 0.73 ± 0.05 cm·s−1·mmHg−1, P = 0.53). While the slope of the MAP-MCAv relationship was slightly different between LBNP and blood loss (0.41 ± 0.03 and 0.66 ± 0.04 cm·s−1·mmHg−1, respectively, P = 0.05), time domain gain between MAP and MCAv at maximal LBNP/blood loss ( P = 0.23) and low-frequency MAP-mean MCAv transfer function coherence, gain, and phase were similar ( P ≥ 0.10). Our results suggest that cerebral hemodynamic responses to LBNP to −45 mmHg and blood loss up to 1,000 ml follow a similar trajectory, and the arterial pressure-cerebral blood velocity relationship is not altered from baseline under these conditions.

Response of vasopressin and norepinephrine to lower body negative pressure in humans

1982 ◽  
Vol 243 (6) ◽  
pp. H970-H973 ◽  
Author(s):  
S. R. Goldsmith ◽  
G. S. Francis ◽  
A. W. Cowley ◽  
J. N. Cohn
Keyword(s):  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Venous Pressure ◽  
Plasma Norepinephrine ◽  
Lower Body ◽  
Central Venous ◽  
Nervous System Activity ◽  
Normal Humans ◽  
Cardiopulmonary Receptors ◽  
Control State

To examine the contributions of cardiopulmonary and sinoaortic baroreceptors to the nonosmotic release of arginine vasopressin (AVP) in normal humans, we subjected nine individuals without evidence of hypertension or heart disease to graded, lower body negative pressure (LBNP). We also studied the effects of this maneuver on sympathetic nervous system activity using plasma norepinephrine (NE) as an index. Heart rate (HR), mean arterial pressure (MAP), pulse pressure (PP), and central venous pressure (CVP) were measured in the control state and during two consecutive levels of increasingly intense LBNP. At each stage blood was sampled for AVP and NE. AVP was analyzed by radioimmunoassay, NE by a radioenzymatic method. During the first level of LBNP, CVP decreased with no change in HR, MAP, or PP. NE increased from 147 +/- 47 to 212 +/- 53 (SD) pg/ml, P less than 0.01, whereas AVP (5.0 +/- 1.0 pg/ml) did not change. With increased suction CVP fell further, HR increased, and PP narrowed, but MAP did not change. NE further increased to 291 +/- 58 pg/ml (P less than 0.01), but AVP still did not change significantly. One subject became markedly hypotensive, and his AVP increased from 2.6 to 81 pg/ml. A fall in CVP that results in sympathetic activation presumably via cardiopulmonary receptors does not therefore increase AVP levels; a further fall in CVP that leads to modest unloading of the sinoaortic baroreceptor and further increased sympathetic activity also fails to stimulate AVP. Hypotension, however, is accompanied by a rapid and profound increase in circulating AVP.

scholarly journals Validation of lower body negative pressure as an experimental model of hemorrhage

2014 ◽  
Vol 116 (4) ◽  
pp. 406-415 ◽  
Author(s):  
Carmen Hinojosa-Laborde ◽  
Robert E. Shade ◽  
Gary W. Muniz ◽  
Cassondra Bauer ◽  
Kathleen A. Goei ◽  
...  
Keyword(s):  
Experimental Model ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Cardiovascular Response ◽  
Venous Pressure ◽  
Blood Gases ◽  
Plasma Renin ◽  
Lower Body ◽  
Central Venous ◽  
Shed Blood

Lower body negative pressure (LBNP), a model of hemorrhage (Hem), shifts blood to the legs and elicits central hypovolemia. This study compared responses to LBNP and actual Hem in sedated baboons. Arterial pressure, pulse pressure (PP), central venous pressure (CVP), heart rate, stroke volume (SV), and +dP/d t were measured. Hem steps were 6.25%, 12.5%, 18.75%, and 25% of total estimated blood volume. Shed blood was returned, and 4 wk after Hem, the same animals were subjected to four LBNP levels which elicited equivalent changes in PP and CVP observed during Hem. Blood gases, hematocrit (Hct), hemoglobin (Hb), plasma renin activity (PRA), vasopressin (AVP), epinephrine (EPI), and norepinephrine (NE) were measured at baseline and maximum Hem or LBNP. LBNP levels matched with 6.25%, 12.5%, 18.75%, and 25% hemorrhage were −22 ± 6, −41 ± 7, −54 ± 10, and −71 ± 7 mmHg, respectively (mean ± SD). Hemodynamic responses to Hem and LBNP were similar. SV decreased linearly such that 25% Hem and matching LBNP caused a 50% reduction in SV. Hem caused a decrease in Hct, Hb, and central venous oxygen saturation (ScvO2). In contrast, LBNP increased Hct and Hb, while ScvO2 remained unchanged. Hem caused greater elevations in AVP and NE than LBNP, while PRA, EPI, and other hematologic indexes did not differ between studies. These results indicate that while LBNP does not elicit the same effect on blood cell loss as Hem, LBNP mimics the integrative cardiovascular response to Hem, and validates the use of LBNP as an experimental model of central hypovolemia associated with Hem.

Noise-Enhanced Heart Rate and Sympathetic Nerve Responses to Oscillatory Lower Body Negative Pressure in Humans

2001 ◽  
Vol 86 (2) ◽  
pp. 559-564 ◽  
Author(s):  
Ichiro Hidaka ◽  
Shin-Ichi Ando ◽  
Hideaki Shigematsu ◽  
Koji Sakai ◽  
Soko Setoguchi ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Stochastic Resonance ◽  
Negative Pressure ◽  
Sympathetic Nerve ◽  
Carotid Sinus ◽  
Lower Body Negative Pressure ◽  
Arterial System ◽  
Lower Body ◽  
Cardiopulmonary Baroreceptors

By injecting noise into the carotid sinus baroreceptors, we previously showed that heart rate (HR) responses to weak oscillatory tilt were enhanced via a mechanism known as “stochastic resonance.” It remains unclear, however, whether the same responses would be observed when using oscillatory lower body negative pressure (LBNP), which would unload the cardiopulmonary baroreceptors with physically negligible effects on the arterial system. Also, the vasomotor sympathetic activity directly controlling peripheral resistance against hypotensive stimuli was not observed. We therefore investigated the effects of weak (0 to approximately −10 mmHg) oscillatory (0.03 Hz) LBNP on HR and muscle sympathetic nerve activity (MSNA) while adding incremental noise to the carotid sinus baroreceptors via a pneumatic neck chamber. The signal-to-noise ratio of HR, cardiac interbeat interval, and total MSNA were all significantly improved by increasing noise intensity, while there was no significant change in the arterial blood pressure in synchronized with the oscillatory LBNP. We conclude that the stochastic resonance, affecting both HR and MSNA, results from the interaction of noise with the signal in the brain stem, where the neuronal inputs from the arterial and cardiopulmonary baroreceptors first come together in the nucleus tractus solitarius. Also, these results indicate that the noise could induce functional improvement in human blood pressure regulatory system in overcoming given hypotensive stimuli.

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