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.

Reflex sympathetic activation in humans is accompanied by inhibition of gastric HCO3- secretion

1988 ◽  
Vol 255 (6) ◽  
pp. G752-G758 ◽  
Author(s):  
H. Sjovall ◽  
H. Forssell ◽  
J. Haggendal ◽  
L. Olbe
Keyword(s):  
Heart Rate ◽  
Vascular Resistance ◽  
Pulse Pressure ◽  
Negative Pressure ◽  
Sympathetic Activity ◽  
Plasma Catecholamine ◽  
Series Of Experiments ◽  
Plasma Catecholamine Concentrations ◽  
Peripheral Sympathetic Activity ◽  
Forearm Vascular Resistance

The study was performed to determine whether the sympathetic nervous system contributes to the reflex control of gastric HCO3- secretion in humans. Gastric HCO3- secretion was registered by a computerized technique based on measurements of pH and PCO2 in gastric effluent. To minimize formation of CO2 in the stomach, subjects were pretreated with the H2-receptor blocker ranitidine. Compensations were made for HCO3- of nongastric origin. As indicators of cardiovascular sympathetic activity, we measured heart rate, forearm vascular resistance, and plasma catecholamine concentrations. In one series of experiments, peripheral sympathetic activity was enhanced by the application of a negative pressure around the lower part of the body (lower body negative pressure, LBNP), at a rate sufficient to induce a slight decrease in systemic arterial pressure. In another series of experiments, peripheral sympathetic activity was inhibited by elevation of the legs, a procedure that simulates volume loading by redistributing blood volume toward the central circulation. LBNP at -20 mmHg decreased systolic pressure and pulse pressure and significantly increased heart rate, forearm vascular resistance, and plasma catecholamine levels. All these effects were observed in the first 15-min period of LBNP and were well maintained throughout the 45-min observation period. LBNP also inhibited basal gastric HCO3- secretion rate in seven of eight individuals, but this response was slower in onset with a latency of at least 15 min. Elevation of the legs increased pulse pressure and decreased forearm vascular resistance. Catecholamines were not measured in these experiments. Gastric HCO3- secretion tended to increase, but the magnitude of the response was highly variable.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Rodent cardiovascular responses to baroreceptor unloading: Effect of plane of anaesthesia

2011 ◽  
Vol 36 (3) ◽  
pp. 376-381 ◽  
Author(s):  
Charlotte W. Usselman ◽  
Louis Mattar ◽  
Jasna Twynstra ◽  
Ian Welch ◽  
J. Kevin Shoemaker
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Cardiovascular Responses ◽  
Cardiovascular Control ◽  
Noxious Stimulation ◽  
Lower Body

The objective of this study was to determine whether a plane of urethane–α-chloralose anaesthesia that suppresses motor reflexes would affect baroreflex cardiovascular control relative to a plane of anaesthesia that leaves motor reflexes intact. Adult male Sprague–Dawley rats were anaesthetized to either a light (motor reflexes intact) or deep (motor reflexes suppressed) plane of anaesthesia. Animals were exposed to graded (–2 to –10 mm Hg) lower body negative pressure while heart rate, vascular resistance, and mean arterial pressure were assessed. No between-group differences were observed in baseline hemodynamics. Graded lower body negative pressure progressively increased heart rate (p < 0.01) and vascular resistance (p < 0.001) and reduced mean arterial pressure (p < 0.001) similarly in light and deep planes of anaesthesia. Therefore, the deep plane of anaesthesia was not associated with a degradation of the autonomic response to baroreceptor unloading beyond that observed at the light plane. These data support the use of urethane–α-chloralose anaesthesia in studies examining reflex cardiovascular control concomitant with some degree of noxious stimulation.

Reflex responses to regional venous pooling during lower body negative pressure in humans

1998 ◽  
Vol 84 (2) ◽  
pp. 454-458 ◽  
Author(s):  
John R. Halliwill ◽  
Lori A. Lawler ◽  
Tamara J. Eickhoff ◽  
Michael J. Joyner ◽  
Sharon L. Mulvagh
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Lower Body ◽  
Reflex Responses ◽  
Venous Pooling ◽  
Vasoconstrictor Response

Halliwill, John R., Lori A. Lawler, Tamara J. Eickhoff, Michael J. Joyner, and Sharon L. Mulvagh. Reflex responses to regional venous pooling during lower body negative pressure in humans. J. Appl. Physiol. 84(2): 454–458, 1998.—Lower body negative pressure is frequently used to simulate orthostasis. Prior data suggest that venous pooling in abdominal or pelvic regions may have major hemodynamic consequences. Therefore, we developed a simple paradigm for assessing regional contributions to venous pooling during lower body negative pressure. Sixteen healthy men and women underwent graded lower body negative pressure protocols to 60 mmHg while wearing medical antishock trousers to prevent venous pooling under three randomized conditions: 1) no trouser inflation (control), 2) only the trouser legs inflated, and 3) the trouser legs and abdominopelvic region inflated. Without trouser inflation, heart rate increased 28 ± 4 beats/min, mean arterial pressure fell −3 ± 2 mmHg, and forearm vascular resistance increased 51 ± 9 units at 60 mmHg lower body negative pressure. With inflation of either the trouser legs or the trouser legs and abdominopelvic region, heart rate and mean arterial pressure did not change during lower body negative pressure. By contrast, although the forearm vasoconstrictor response to lower body negative pressure was attenuated by inflation of the trouser legs (Δforearm vascular resistance 33 ± 10 units, P < 0.05 vs. control), attenuation was greater with the inflation of the trouser legs and abdominopelvic region (Δforearm vascular resistance 16 ± 5 units, P < 0.05 vs. control and trouser legs-only inflation). Thus the hemodynamic consequences of pooling in the abdominal and pelvic regions during lower body negative pressure appear to be less than in the legs in healthy individuals.

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.

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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