Sustained increases in sympathetic outflow during prolonged lower body negative pressure in humans

The purpose of this study was to determine whether prolonged unloading of cardiopulmonary baroreceptors with lower body negative pressure (LBNP) causes constant increases in sympathetic outflow to skeletal muscles. Eight healthy subjects underwent a 20-min control period followed by 20 min of 15-mmHg LBNP. This pressure was selected because it did not cause any significant change in mean arterial blood pressure (sphygmomanometry) or heart rate, suggesting that the cardiopulmonary baroreceptors were selectively unloaded and the activity of the arterial baroreceptors was unchanged. Muscle sympathetic nerve activity in the peroneal nerve (MSNA, microneurography) increased from an average of 21.8 +/- 1.7 bursts/min over the last 5 min of control to 29.0 +/- 2.9 bursts/min during the 1st min of LBNP (P less than 0.05 LBNP vs. control). The increase in MSNA observed during the 1st min was sustained throughout LBNP. Forelimb blood flow (plethysmography) decreased abruptly at the onset of the LBNP from a control value of 4.3 +/- 0.5 ml.min-1.100 ml-1 to 2.5 +/- 0.2 at the 1st min; the flow then increased and remained significantly above this value, but below the control value, throughout LBNP. Similar blood flow findings were obtained in additional studies, when the hand circulation was excluded during the flow measurements. Forearm skin blood flow (laser Doppler) also decreased abruptly at the onset of LBNP and was followed by partial recovery, but these changes were too small to account for all the increases in limb blood flow over the course of LBNP.(ABSTRACT TRUNCATED AT 250 WORDS)

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Regional vascular responses to prolonged lower body negative pressure in normal subjects

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1989.257.1.h219 ◽

1989 ◽

Vol 257 (1) ◽

pp. H219-H225 ◽

Cited By ~ 16

Author(s):

A. T. Hirsch ◽

D. J. Levenson ◽

S. S. Cutler ◽

V. J. Dzau ◽

M. A. Creager

Keyword(s):

Blood Flow ◽

Plasma Renin Activity ◽

Glomerular Filtration ◽

Negative Pressure ◽

Lower Body Negative Pressure ◽

Plasma Renin ◽

Normal Subjects ◽

Plasma Norepinephrine ◽

Lower Body ◽

Cardiopulmonary Baroreceptors

The purpose of this study was to determine the effects of sustained unloading of baroreceptors in humans. The regional hemodynamic responses to lower body negative pressure (LBNP) were determined in 20 normal subjects. LBNP at -10 mmHg for 1 h decreased central venous pressure (CVP) without affecting blood pressure or heart rate, suggesting that only cardiopulmonary baroreceptors were unloaded. Forearm blood flow (FBF) and splanchnic blood flow (SBF) both decreased. Renal blood flow (RBF) did not change, but glomerular filtration rate (GFR) increased. Plasma renin activity rose slightly, whereas plasma norepinephrine levels did not change. Peak LBNP (either -20 or -40 mmHg for 1 h) caused a further decline in CVP and narrowed pulse pressure, thus unloading both arterial and cardiopulmonary baroreceptors. FBF returned to base-line values and SBF decreased further. RBF fell and the GFR remained increased. Plasma renin activity increased further, and plasma norepinephrine level rose. Thus the forearm and splanchnic circulations are sensitive to sustained unloading of cardiopulmonary baroreceptors; renal vasoconstriction occurs with additional unloading of arterial baroreceptors. Renin-angiotensin system activation during LBNP may be pertinent to the preservation of glomerular filtration.

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Divergent roles of plasma osmolality and the baroreflex on sweating and skin blood flow

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00411.2011 ◽

2012 ◽

Vol 302 (5) ◽

pp. R634-R642 ◽

Cited By ~ 24

Author(s):

Aaron G. Lynn ◽

Daniel Gagnon ◽

Konrad Binder ◽

Robert C. Boushel ◽

Glen P. Kenny

Keyword(s):

Blood Flow ◽

Heat Stress ◽

Core Temperature ◽

Skin Blood Flow ◽

Negative Pressure ◽

Lower Body Negative Pressure ◽

Plasma Osmolality ◽

Whole Body ◽

Lower Body ◽

Change In Mean

Plasma hyperosmolality and baroreceptor unloading have been shown to independently influence the heat loss responses of sweating and cutaneous vasodilation. However, their combined effects remain unresolved. On four separate occasions, eight males were passively heated with a liquid-conditioned suit to 1.0°C above baseline core temperature during a resting isosmotic state (infusion of 0.9% NaCl saline) with (LBNP) and without (CON) application of lower-body negative pressure (−40 cmH2O) and during a hyperosmotic state (infusion of 3.0% NaCl saline) with (LBNP + HYP) and without (HYP) application of lower-body negative pressure. Forearm sweat rate (ventilated capsule) and skin blood flow (laser-Doppler), as well as core (esophageal) and mean skin temperatures, were measured continuously. Plasma osmolality increased by ∼10 mosmol/kgH2O during HYP and HYP + LBNP conditions, whereas it remained unchanged during CON and LBNP ( P ≤ 0.05). The change in mean body temperature (0.8 × core temperature + 0.2 × mean skin temperature) at the onset threshold for increases in cutaneous vascular conductance (CVC) was significantly greater during LBNP (0.56 ± 0.24°C) and HYP (0.69 ± 0.36°C) conditions compared with CON (0.28 ± 0.23°C, P ≤ 0.05). Additionally, the onset threshold for CVC during LBNP + HYP (0.88 ± 0.33°C) was significantly greater than CON and LBNP conditions ( P ≤ 0.05). In contrast, onset thresholds for sweating were not different during LBNP (0.50 ± 0.18°C) compared with CON (0.46 ± 0.26°C, P = 0.950) but were elevated ( P ≤ 0.05) similarly during HYP (0.91 ± 0.37°C) and LBNP + HYP (0.94 ± 0.40°C). Our findings show an additive effect of hyperosmolality and baroreceptor unloading on the onset threshold for increases in CVC during whole body heat stress. In contrast, the onset threshold for sweating during heat stress was only elevated by hyperosmolality with no effect of the baroreflex.

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Onset of mild lower body negative pressure induces transient change in mean arterial pressure in humans

European Journal of Applied Physiology ◽

10.1007/s00421-002-0630-4 ◽

2002 ◽

Vol 87 (3) ◽

pp. 251-256 ◽

Cited By ~ 9

Author(s):

Jonny Hisdal ◽

Karin Toska ◽

Torun Flatebø ◽

Lars Walløe

Keyword(s):

Mean Arterial Pressure ◽

Arterial Pressure ◽

Negative Pressure ◽

Lower Body Negative Pressure ◽

Lower Body ◽

Transient Change ◽

Change In Mean

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Bradykinin has no acute effect on the response of forearm blood flow to sympathetic stimulation in man

Clinical Science ◽

10.1042/cs0780399 ◽

1990 ◽

Vol 78 (4) ◽

pp. 399-401 ◽

Cited By ~ 2

Author(s):

M. J. Cullen ◽

J. R. Cockcroft ◽

D. J. Webb

Keyword(s):

Blood Flow ◽

Angiotensin Ii ◽

Negative Pressure ◽

Enzyme Inhibitor ◽

Lower Body Negative Pressure ◽

Acute Effect ◽

Acute Administration ◽

Lower Body ◽

Resistance Vessels ◽

Sympathetic Responses

1. Six healthy male subjects received 0.9% (w/v) NaCl (saline) followed by incremental doses of bradykinin (1, 3 and 10 pmol/min), via the left brachial artery. Blood flow and the response of blood flow to lower-body negative pressure were measured in both forearms during infusion of saline and each dose of bradykinin. 2. Bradykinin produced a moderate and dose-dependent increase in blood flow in the infused, but not the non-infused, forearm. Lower-body negative pressure produced an approximately 15–20% reduction in blood flow in both forearms, and this response was unaffected by local infusion of bradykinin. 3. Bradykinin, in contrast to angiotensin II, had no acute effect on peripheral sympathetic responses to lower-body negative pressure. We conclude that, in forearm resistance vessels in man, withdrawal of angiotensin II, rather than accumulation of bradykinin, is likely to account for the attenuation of peripheral sympathetic responses after acute administration of a converting-enzyme inhibitor.

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

Journal of Neurophysiology ◽

10.1152/jn.2001.86.2.559 ◽

2001 ◽

Vol 86 (2) ◽

pp. 559-564 ◽

Cited By ~ 21

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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Evidence for unloading arterial baroreceptors during low levels of lower body negative pressure in humans

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00184.2008 ◽

2009 ◽

Vol 296 (2) ◽

pp. H480-H488 ◽

Cited By ~ 26

Author(s):

Qi Fu ◽

Shigeki Shibata ◽

Jeffrey L. Hastings ◽

Anand Prasad ◽

M. Dean Palmer ◽

...

Keyword(s):

Steady State ◽

Stroke Volume ◽

Negative Pressure ◽

Lower Body Negative Pressure ◽

Right Atrial ◽

Lower Body ◽

Arterial Baroreflex ◽

Arterial Baroreceptors ◽

Low Levels ◽

Cardiopulmonary Baroreceptors

Low levels (i.e., ≤20 mmHg) of lower body negative pressure (LBNP) have been utilized to unload “selectively” cardiopulmonary baroreceptors in humans, since steady-state mean arterial pressure and heart rate (HR) have been found unchanged at such levels. However, transient reductions in blood pressure (BP), followed by reflex compensation, may occur without detection, which could unload arterial baroreceptors. The purposes of this study were to test the hypothesis that the arterial baroreflex is engaged even during low levels of LBNP and to determine the time course of changes in hemodynamics. Fourteen healthy individuals (age range 20–54 yr) were studied. BP (Portapres and Suntech), HR (ECG), pulmonary capillary wedge pressure (PCWP) or pulmonary artery diastolic pressure (PDP) and right atrial pressure (RAP) (Swan-Ganz catheter) and hemodynamics (Modelflow) were recorded continuously at baseline and −15- and −30-mmHg LBNP for 6 min each. Application of −15-mmHg LBNP resulted in rapid and sustained falls in RAP and PCWP or PDP, progressive decreases in cardiac output and stroke volume, followed subsequently by transient reductions in both systolic and diastolic BP, which were then restored through the arterial baroreflex feedback mechanism after ∼15 heartbeats. Additional studies were performed in five subjects using even lower levels of LBNP, and this transient reduction in BP was observed in three at −5- and in all at −10-mmHg LBNP. The delay for left ventricular stroke volume to fall at −15-mmHg LBNP was about 10 cardiac cycles. An increase in systemic vascular resistance was detectable after 20 heartbeats during −15-mmHg LBNP. Steady-state BP and HR remained unchanged during mild LBNP. However, BP decreased, while HR increased, at −30-mmHg LBNP. These results suggest that arterial baroreceptors are consistently unloaded during low levels (i.e., −10 and −15 mmHg) of LBNP in humans. Thus “selective” unloading of cardiopulmonary baroreceptors cannot be presumed to occur during these levels of mild LBNP.

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Effect of acute hypoxemia on cerebral blood flow velocity control during lower body negative pressure

Physiological Reports ◽

10.14814/phy2.13594 ◽

2018 ◽

Vol 6 (4) ◽

pp. e13594 ◽

Cited By ~ 3

Author(s):

Noud van Helmond ◽

Blair D. Johnson ◽

Walter W. Holbein ◽

Humphrey G. Petersen-Jones ◽

Ronée E. Harvey ◽

...

Keyword(s):

Blood Flow ◽

Cerebral Blood Flow ◽

Flow Velocity ◽

Negative Pressure ◽

Blood Flow Velocity ◽

Cerebral Blood Flow Velocity ◽

Lower Body Negative Pressure ◽

Lower Body ◽

Velocity Control

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Comparison of two indices for forearm noradrenaline release in humans

Clinical Science ◽

10.1042/cs0990363 ◽

2000 ◽

Vol 99 (5) ◽

pp. 363-369 ◽

Cited By ~ 6

Author(s):

Gerard A. RONGEN ◽

Jacques W. M. LENDERS ◽

Paul SMITS ◽

John S. FLORAS

Keyword(s):

Blood Flow ◽

Sodium Nitroprusside ◽

Noradrenaline Release ◽

Negative Pressure ◽

Forearm Blood Flow ◽

Lower Body Negative Pressure ◽

Lower Body ◽

Release Of Noradrenaline ◽

Appearance Rate

Although there is as yet no method which measures directly the neuronal release of noradrenaline in humans in vivo, the isotope dilution technique with [3H]noradrenaline has been applied to estimate forearm neuronal noradrenaline release into plasma. Two different equations have been developed for this purpose: one to estimate the spillover of noradrenaline into the venous effluent, and a modified formula (often referred to as the appearance rate) which may reflect more closely changes in the neuronal release of noradrenaline into the synaptic cleft, particularly during interventions that alter forearm blood flow. The present study was performed to compare the effects of two interventions known to exert contrasting actions on neuronal forearm noradrenaline release and forearm blood flow. Intra-arterial infusion of sodium nitroprusside at doses without systemic effect increases forearm blood flow, but not neuronal noradrenaline release. In contrast, lower-body negative pressure at -25 mmHg causes forearm vasoconstriction by stimulating neuronal noradrenaline release. During sodium nitroprusside infusion, forearm noradrenaline spillover increased from 1.1±0.3 to 2.2±1.0 pmol·min-1·100 ml-1 (P < 0.05), whereas the forearm noradrenaline appearance rate was unchanged. Lower-body negative pressure did not affect the forearm noradrenaline spillover rate, but increased the forearm noradrenaline appearance rate from 3.4±0.4 pmol·min-1·100 ml-1 at baseline to 5.0±0.9 pmol·min-1·100 ml-1 (P < 0.05). These results indicate that the noradrenaline appearance rate provides the better approximation of changes in forearm neuronal noradrenaline release in response to stimuli which alter local blood flow.

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Differential effects of lower body negative pressure on forearm and calf blood flow

Journal of Applied Physiology ◽

10.1152/jappl.1986.61.3.994 ◽

1986 ◽

Vol 61 (3) ◽

pp. 994-998 ◽

Cited By ~ 24

Author(s):

L. K. Essandoh ◽

D. S. Houston ◽

P. M. Vanhoutte ◽

J. T. Shepherd

Keyword(s):

Blood Flow ◽

Negative Pressure ◽

Skeletal Muscles ◽

Lower Body Negative Pressure ◽

Valsalva Maneuver ◽

Lower Body ◽

Blood Flows ◽

Resistance Vessels ◽

Series Of Experiments ◽

The Right

Modest degrees of lower body negative pressure (less than 20 mmHg) cause a reflex constriction of forearm resistance vessels attributable to a decrease in activity of cardiopulmonary mechanoreceptors. In the present study, we sought to determine whether the calf vessels respond similarly. Left forearm and right calf blood flows were measured simultaneously by strain-gauge plethysmography in 10 healthy volunteers. Forearm flows decreased significantly from control during negative pressures of 10, 15, or 20 mmHg, whereas calf flows did not decrease significantly until 20 mmHg; at 10, 15, and 20 mmHg, decreases in forearm flow were significantly greater than those of the calf. Similar results were obtained in a second series of experiments in which venous pooling in the right leg during lower body negative pressure was prevented by enclosing it in a boot. At 40 mmHg, or after a Valsalva maneuver, both forearm and calf vessels constricted markedly and to the same degree. It appears that the reflex reduction in blood flow to the skeletal muscles of the limbs resulting from deactivation of the low-pressure intrathoracic mechanoreceptors is directed primarily to the arm.

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