scholarly journals Hemodynamic response during lower body negative pressure: role of volume status.

1998 ◽  
Vol 9 (1) ◽  
pp. 105-113 ◽  
Author(s):  
G Ligtenberg ◽  
P J Blankestijn ◽  
H A Koomans
Keyword(s):  
Heart Rate ◽  
Cardiac Index ◽  
Blood Volume ◽  
Pulse Pressure ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Peripheral Resistance ◽  
Hemodynamic Response ◽  
Volume Status ◽  
Lower Body

Sudden dialysis-related hypotension is characterized by paradoxical vasodilation, suggestive of sympathoinhibition. A similar hypotensive reaction can be evoked by lower body negative pressure (LBNP), which thus allows the study of the numerous factors involved in dialysis hypotension separately. This article examines the influence of changes in volume status on the hemodynamic response to LBNP (45 mmHg up to the iliac crest, maximum 60 min) in 12 healthy subjects. LBNP caused a decrease in cardiac index and pulse pressure, and an increase in heart rate and total peripheral resistance, most of which developed within the first 3 min of LBNP. Six subjects developed sudden hypotension characterized by vasodilation after 9 +/- 4 min of LBNP. After saline expansion (25 ml/kg), which increased blood volume by approximately 8%, five subjects endured LBNP for the full 60 min. However, after 60 min of LBNP, the circulatory parameters suggested a similar critical situation as that observed before presyncope in their first experiment. The other six subjects endured the full 60 min of LBNP. After furosemide-induced volume reduction associated with 1.6 +/- 0.2 kg weight loss and approximately 7% blood volume reduction, five of them developed vasodilatory presyncope after 17 +/- 5 min of LBNP. Comparison of presyncopal and nonpresyncopal experiments within subjects, as well as between subjects, showed that the early (3 min) response to LBNP was different: Despite similar decreases in cardiac index, the values for systolic pressure, pulse pressure, peripheral resistance, and stroke volume were lower, and the heart rate was higher in the experiments ending in presyncope. It is concluded that the volume status is a determinant of the tolerance to LBNP, probably by affecting the vasoconstrictive response. By inference, this study suggests that the vasoconstrictive response to the hemodynamic stress of hemodialysis is also influenced by the volume status.

scholarly journals Differential Effects of Low- and High-Intensity Lower Body Negative Pressure on Noradrenaline and Adrenaline Kinetics in Humans

1996 ◽  
Vol 90 (5) ◽  
pp. 337-343 ◽  
Author(s):  
Marie-Cecile Jacobs ◽  
David S. Goldstein ◽  
Jacques J. Willemsen ◽  
Paul Smits ◽  
Theo Thien ◽  
...  
Keyword(s):  
Heart Rate ◽  
Vascular Resistance ◽  
Pulse Pressure ◽  
Negative Pressure ◽  
High Intensity ◽  
Lower Body Negative Pressure ◽  
Lower Body ◽  
Total Body ◽  
Noradrenaline And Adrenaline ◽  
Forearm Vascular Resistance

1. Lower body negative pressure provides a means to examine neurocirculatory reflexive responses to decreases in venous return to the heart. We assessed whether the pattern of catecholaminergic responses to lower body negative pressure depends on the intensity of the stimulus (−15 versus −40 mmHg). 2. In 14 healthy subjects, responses of forearm blood flow and noradrenaline spillover and of total body noradrenaline and adrenaline spillover were assessed during infusion of [3H]noradrenaline and [3H]adrenaline during −15 and −40 mmHg of lower body negxative pressure. 3. During lower body negative pressure at −15 mmHg, heart rate and pulse pressure did not change, but forearm vascular resistance increased by 25–50%. Forearm noradrenaline spillover increased by about 50%, from 0.63 ± 0.16 to 0.94 ± 0.23 pmol min−1 100 ml−1 (P<0.05). Total body noradrenaline spillover did not change, and total body adrenaline spillover increased significantly by about 30%. Clearances of noradrenaline and adrenaline were unchanged. 4. During lower body negative pressure at −40 mmHg, heart rate increased and pulse pressure decreased. Forearm vascular resistance increased by about 100%, and forearm noradrenaline spillover increased by 80%, from 0.73 ± 0.19 to 1.32 ± 0.36 pmol min−1 100 ml−1 (P<0.05). Total body noradrenaline spillover increased by 30%, and total body adrenaline spillover increased by about 50%. Clearances of both noradrenaline and adrenaline decreased. 5. The results are consistent with the view that selective deactivation of cardiopulmonary baroreceptors during low-intensity lower body negative pressure increases sympathoneural traffic to forearm skeletal muscle and increases adrenomedullary secretion without a concomitant generalized increase in sympathoneural outflows. Concurrent deactivation of cardiopulmonary and arterial baroreceptors during high-intensity lower body negative pressure evokes a more generalized increase in sympathoneural activity, accompanied by further increased adrenomedullary secretion and decreased plasma clearances of noradrenaline and adrenaline. The findings support differential increases in skeletal sympathoneural and adrenomedullary outflows during orthostasis, with more generalized sympathoneural responses to systemic hypotension.

Association of sex and age with responses to lower-body negative pressure

1988 ◽  
Vol 65 (4) ◽  
pp. 1752-1756 ◽  
Author(s):  
M. A. Frey ◽  
G. W. Hoffler
Keyword(s):  
Heart Rate ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Peripheral Resistance ◽  
Older Men ◽  
Lower Body ◽  
Fluid Shift ◽  
Arterial Blood ◽  
Age Related ◽  
Older Subjects

Responses of 21 women and 29 men (29-56 yr of age) to -50 Torr lower body negative pressure (LBNP) were examined for differences due to sex or age. Responses to LBNP were normal, including fluid shift from thorax to lower body, increased heart rate and peripheral resistance, and decreased stroke volume, cardiac output, and Heather index of ventricular function. Mean arterial blood pressure did not change. Comparison of responses of the women to responses of an age-matched subset of the men (n = 26) indicated the men had larger relative increases in calf circumference and greater increases in peripheral resistance during LBNP than the women, whereas the women experienced greater increases in thoracic impedance and heart rate. Analyses of responses of the 29 men for age-related differences indicated older subjects had greater increases in peripheral resistance and less heart rate elevation in response to LBNP (P less than 0.05 for all differences, except sex-related heart rate difference, where P less than 0.10). Based on these data and the data of other investigators, we hypothesize the age-related circulatory differences in response to LBNP are due to a reduction in vagal response and a switch to predominant sympathetic nervous system influence in older men. We cannot exclude the possibility that diminished responsiveness in the afferent arm of the baroreceptor reflex also plays a role in the attenuated heart rate response of older men to LBNP.

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.

Arterial pulse pressure and vasopressin release in humans during lower body negative pressure

1993 ◽  
Vol 264 (5) ◽  
pp. R1024-R1030 ◽  
Author(s):  
P. Norsk ◽  
P. Ellegaard ◽  
R. Videbaek ◽  
C. Stadeager ◽  
F. Jessen ◽  
...  
Keyword(s):  
Pulse Pressure ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Venous Pressure ◽  
Plasma Norepinephrine ◽  
Lower Body ◽  
Arterial Pulse ◽  
Vasopressin Release ◽  
Arterial Pulse Pressure ◽  
Arterial Plasma

The hypothesis was tested that narrowing of arterial pulse pressure (PP) is a determinant of arginine vasopressin (AVP) release in humans. Six normal males completed a two-step lower body negative pressure (LBNP) protocol of -20 and -50 mmHg, respectively, for 10 min each. None of these subjects experienced presyncopal symptoms. Arterial plasma AVP and plasma renin activity (PRA) (at 2-min intervals) only increased subsequent to a decrease in PP (invasive brachial arterial measurements) and stroke volume (ultrasound Doppler technique, n = 4). Simultaneously, mean arterial pressure did not change. A selective decrease in central venous pressure and left atrial diameter (echocardiography, n = 4) at LBNP of -20 mmHg did not affect AVP or PRA, whereas arterial plasma norepinephrine increased (n = 4). During LBNP, significant (P < 0.05) intraindividual linear correlations were observed between log(AVP) and PP in four of the subjects with r values from -0.75 to -0.99 and between log(PRA) and PP in all six subjects with r values from -0.89 to -0.98. In conclusion, these results are in compliance with the hypothesis that narrowing of PP in humans during central hypovolemia is a determinant of AVP and renin release.

scholarly journals Continuous Monitoring of Changes in Blood Volume and Limb Volume During Lower Body Negative Pressure

2007 ◽  
Vol 29 (3) ◽  
pp. 235-245
Author(s):  
Fumio YAMAZAKI ◽  
Keizo SHIRAKI ◽  
Yutaka ENDO ◽  
Sueko SAGAWA
Keyword(s):  
Blood Volume ◽  
Negative Pressure ◽  
Continuous Monitoring ◽  
Lower Body Negative Pressure ◽  
Lower Body ◽  
Limb Volume

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)

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.

Cardiovascular responses to lower body negative pressure in trained and untrained older men

1992 ◽  
Vol 73 (6) ◽  
pp. 2693-2700 ◽  
Author(s):  
S. Fortney ◽  
C. Tankersley ◽  
J. T. Lightfoot ◽  
D. Drinkwater ◽  
J. Clulow ◽  
...  
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Older Men ◽  
Volume Index ◽  
Lower Body ◽  
Vo2 Max ◽  
Cardiac Volumes

To determine whether aerobic conditioning alters the orthostatic responses of older subjects, cardiovascular performance was monitored during graded lower body negative pressure in nine highly trained male senior athletes (A) aged 59–73 yr [maximum O2 uptake (VO2 max) = 52.4 +/- 1.7 ml.kg-1 x min-1] and nine age-matched control subjects (C) (VO2 max = 31.0 +/- 2.9 ml.kg-1 x min-1). Cardiac volumes were determined from gated blood pool scintigrams by use of 99mTc-labeled erythrocytes. During lower body negative pressure (0 to -50 mmHg), left ventricular end-diastolic and end-systolic volume indexes and stroke volume index decreased in both groups while heart rate increased. The decreases in cardiac volumes and mean arterial pressure and the increase in heart rate between 0 and -50 mmHg were significantly less in A than in C. For example, end-diastolic volume index decreased by 32 +/- 4 ml in C vs. 14 +/- 2 ml in A (P < 0.01), mean arterial pressure declined 7 +/- 5 mmHg in C and increased by 5 +/- 3 mmHg in A (P < 0.05), and heart rate increased 13 +/- 3 beats/min in C and 7 +/- 1 beats/min in A (P < 0.05). These data suggest that increased VO2 max among older men is associated with improved orthostatic responses.

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