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.

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)

Lower body negative pressure exercise plus brief postexercise lower body negative pressure improve post-bed rest orthostatic tolerance

2007 ◽  
Vol 103 (6) ◽  
pp. 1964-1972 ◽  
Author(s):  
Donald E. Watenpaugh ◽  
Deborah D. O'Leary ◽  
Suzanne M. Schneider ◽  
Stuart M. C. Lee ◽  
Brandon R. Macias ◽  
...  
Keyword(s):  
Negative Pressure ◽  
Acute Exercise ◽  
Treadmill Exercise ◽  
Orthostatic Intolerance ◽  
Lower Body Negative Pressure ◽  
Bed Rest ◽  
Orthostatic Tolerance ◽  
Lower Body ◽  
Before And After ◽  
Head Up Tilt

Orthostatic intolerance follows actual weightlessness and weightlessness simulated by bed rest. Orthostasis immediately after acute exercise imposes greater cardiovascular stress than orthostasis without prior exercise. We hypothesized that 5 min/day of simulated orthostasis [supine lower body negative pressure (LBNP)] immediately following LBNP exercise maintains orthostatic tolerance during bed rest. Identical twins (14 women, 16 men) underwent 30 days of 6° head-down tilt bed rest. One of each pair was randomly selected as a control, and their sibling performed 40 min/day of treadmill exercise while supine in 53 mmHg (SD 4) [7.05 kPa (SD 0.50)] LBNP. LBNP continued for 5 min after exercise stopped. Head-up tilt at 60° plus graded LBNP assessed orthostatic tolerance before and after bed rest. Hemodynamic measurements accompanied these tests. Bed rest decreased orthostatic tolerance time to a greater extent in control [34% (SD 10)] than in countermeasure subjects [13% (SD 20); P < 0.004]. Controls exhibited cardiac stroke volume reduction and relative cardioacceleration typically seen after bed rest, yet no such changes occurred in the countermeasure group. These findings demonstrate that 40 min/day of supine LBNP treadmill exercise followed immediately by 5 min of resting LBNP attenuates, but does not fully prevent, the orthostatic intolerance associated with 30 days of bed rest. We speculate that longer postexercise LBNP may improve results. Together with our earlier related studies, these ground-based results support spaceflight evaluation of postexercise orthostatic stress as a time-efficient countermeasure against postflight orthostatic intolerance.

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.

Effect of hindlimb suspension on cardiovascular responses to sympathomimetics and lower body negative pressure

1990 ◽  
Vol 68 (1) ◽  
pp. 355-362 ◽  
Author(s):  
J. M. Overton ◽  
C. M. Tipton
Keyword(s):  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Cardiovascular Responses ◽  
Male Rats ◽  
Hindlimb Suspension ◽  
Lower Body ◽  
Baroreflex Control ◽  
Cardiovascular Deconditioning ◽  
Treatment Conditions ◽  
Before And After

To determine whether hindlimb suspension is associated with the development of cardiovascular deconditioning, male rats were studied before and after undergoing one of three treatment conditions for 9 days: 1) cage control (n = 15, CON), 2) horizontal suspension (n = 15, HOZ), and 3) head-down suspension (n = 18, HDS). Testing included lower body negative pressure administered during chloralose-urethan anesthesia and graded doses of sympathomimetic agents (norepinephrine, phenylephrine, and tyramine) administered to conscious unrestrained animals. Both HDS and HOZ were associated with a small decrease in the hypotensive response to lower body negative pressure. The HOZ group, but not the HDS group, exhibited augmented reflex tachycardia. Furthermore, both HDS and HOZ groups manifested reduced pressor responses to phenylephrine after treatment. These reductions were associated with significantly attenuated increases in mesenteric vascular resistance. However, baroreflex control of heart rate was not altered by the treatment conditions. Collectively, these results indicate that 9 days of HDS in rats does not elicit hemodynamic response patterns generally associated with cardiovascular deconditioning induced by hypogravic conditions.

Abstract 14436: Nightly Lower Body Negative Pressure Redistributes Blood Volume and Prevents Maladaptive Vascular Remodeling Induced by Microgravity

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Katrin A Dias ◽  
Christopher M Hearon ◽  
Gautam Babu ◽  
John E Marshall ◽  
James P Macnamara ◽  
...  
Keyword(s):  
Blood Volume ◽  
Negative Pressure ◽  
Vascular Remodeling ◽  
Lower Body Negative Pressure ◽  
Venous Pressure ◽  
Bed Rest ◽  
Lower Body ◽  
Long Duration ◽  
Sustained Reduction ◽  
Area And Volume

Introduction: During space flight and ground based simulations of microgravity, transmural distending pressure increases in resistance vessels above the level of the heart, causing maladaptive vascular remodeling over time. Lower body negative pressure (LBNP) mimics gravity by redistributing blood volume and reinstating hydrostatic gradients, and may preserve vascular structures above the heart while in microgravity. Methods: Ten healthy subjects (5 female, 29 ± 9 years) completed three days of supine (0°) bed rest with and without eight hours of nightly LBNP (-20mmHg) in a randomized, crossover design. Area and volume of the choroid, a highly vascularized layer of the eye sensitive to changes in hydrostatic gradients, were assessed using optical coherence tomography on the first and last day of bed rest. Central venous pressure (CVP) was measured during spontaneous breathing with a peripherally inserted central catheter. Results: CVP increased significantly from the seated to supine position (+9.1 ± 2.4mmHg, P < 0.001), leading to choroid engorgement over three days of supine bed rest (choroid area: +0.09 mm 2 95% CI 0.04 to 0.13, P = 0.0014; choroid volume: +0.37 mm 3 95% CI 0.19 to 0.55, P = 0.0011). Nightly LBNP caused a sustained reduction in supine CVP (5.7 ± 2.2mmHg to 1.2 ± 1.4mmHg, P < 0.001), indicating effective redistribution of blood volume and significantly attenuated the increase in choroid area (3.5% control vs. 0.9% LBNP, P = 0.0164) and volume (3.8% control vs. 1.8% LBNP, P = 0.0040) compared to control (Figure). Conclusions: Nightly LBNP caused caudal redistribution of blood volume that partially reinstated hydrostatic gradients and mitigated the increase in choroid area and volume by 74% and 53%, respectively. These findings illustrate that normalizing transmural distending pressures during simulated microgravity preserves vascularized structures above the level of the heart and may prevent adverse remodeling during long duration spaceflight.

Short-term variability of blood pressure: effects of lower-body negative pressure and long-duration bed rest

2012 ◽  
Vol 303 (1) ◽  
pp. R77-R85 ◽  
Author(s):  
Federico Aletti ◽  
Manuela Ferrario ◽  
Da Xu ◽  
Danielle K. Greaves ◽  
J. Kevin Shoemaker ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Venous Pressure ◽  
Bed Rest ◽  
Pressure Effects ◽  
Lower Body ◽  
Arterial Baroreflex ◽  
Long Duration ◽  
Cardiopulmonary Baroreflex

Mild lower-body negative pressure (LBNP) has been utilized to selectively unload cardiopulmonary baroreceptors, but there is evidence that arterial baroreceptors can be transiently unloaded after the onset of mild LBNP. In this paper, a black box mathematical model for the prediction of diastolic blood pressure (DBP) variability from multiple inputs (systolic blood pressure, R-R interval duration, and central venous pressure) was applied to interpret the dynamics of blood pressure maintenance under the challenge of LBNP and in long-duration, head-down bed rest (HDBR). Hemodynamic recordings from seven participants in the WISE (Women's International Space Simulation for Exploration) Study collected during an experiment of incremental LBNP (−10 mmHg, −20 mmHg, −30 mmHg) were analyzed before and on day 50 of a 60-day-long HDBR campaign. Autoregressive spectral analysis focused on low-frequency (LF, ∼0.1 Hz) oscillations of DBP, which are related to fluctuations in vascular resistance due to sympathetic and baroreflex regulation of vasomotor tone. The arterial baroreflex-related component explained 49 ± 13% of LF variability of DBP in spontaneous conditions, and 89 ± 9% ( P < 0.05) on day 50 of HDBR, while the cardiopulmonary baroreflex component explained 17 ± 9% and 12 ± 4%, respectively. The arterial baroreflex-related variability was significantly increased in bed rest also for LBNP equal to −20 and −30 mmHg. The proposed technique provided a model interpretation of the proportional effect of arterial baroreflex vs. cardiopulmonary baroreflex-mediated components of blood pressure control and showed that arterial baroreflex was the main player in the mediation of DBP variability. Data during bed rest suggested that cardiopulmonary baroreflex-related effects are blunted and that blood pressure maintenance in the presence of an orthostatic stimulus relies mostly on arterial control.

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.

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.

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