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.

Aortic baroreflex control of heart rate after 15 days of simulated microgravity exposure

1994 ◽  
Vol 77 (5) ◽  
pp. 2134-2139 ◽  
Author(s):  
C. G. Crandall ◽  
K. A. Engelke ◽  
V. A. Convertino ◽  
P. B. Raven
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Negative Pressure ◽  
Simulated Microgravity ◽  
Lower Body Negative Pressure ◽  
Lower Body ◽  
Baroreflex Control ◽  
Neck Pressure ◽  
Change In Mean

To determine the effects of simulated microgravity on aortic baroreflex control of heart rate, we exposed seven male subjects (mean age 38 +/- 3 yr) to 15 days of bed rest in the 6 degrees head-down position. The sensitivity of the aortic-cardiac baroreflex was determined during a steady-state phenylephrine-induced increase in mean arterial pressure combined with lower body negative pressure to counteract central venous pressure increases and neck pressure to offset the increased carotid sinus transmural pressure. The aortic-cardiac baroreflex gain was assessed by determining the ratio of the change in heart rate to the change in mean arterial pressure between baseline conditions and aortic baroreceptor-isolated conditions (i.e., phenylephrine + lower body negative pressure + neck pressure stage). Fifteen days of head-down tilt increased the gain of the aortic-cardiac baroreflex (from 0.45 +/- 0.07 to 0.84 +/- 0.18 beats.min-1.mmHg-1; P = 0.03). Reductions in blood volume and/or maximal aerobic capacity may represent the underlying mechanism(s) responsible for increased aortic baroreflex responsiveness after exposure to a ground-based analogue of microgravity.

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.

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.

Ten weeks of aerobic training do not affect lower body negative pressure responses

1989 ◽  
Vol 67 (2) ◽  
pp. 894-901 ◽  
Author(s):  
J. T. Lightfoot ◽  
R. P. Claytor ◽  
D. J. Torok ◽  
T. W. Journell ◽  
S. M. Fortney
Keyword(s):  
Heart Rate ◽  
Negative Pressure ◽  
Aerobic Training ◽  
Carotid Sinus ◽  
Lower Body Negative Pressure ◽  
Control Group ◽  
Lower Body ◽  
Vo2 Max ◽  
Compensatory Mechanisms ◽  
Neck Pressure

Based mostly on cross-sectional data, it has been suggested that aerobic training may decrease lower body negative pressure (LBNP) tolerance through a hypothesized attenuation in both high- and low-pressure baroreflex gain. An experimental group (EXP) of eight male subjects [22.1 +/- 1.4 (SD) yr] underwent a 10-wk treadmill and cycle ergometer training program, which resulted in a 21% increase in maximal O2 uptake (VO2 max), 45.7 +/- 1.5 vs. 55.2 +/- 1.7 (SE) ml.kg-1.min-1; P less than 0.05]. A control group, (CON; n = 7; 27.3 +/- 5.7 yr), which did not undergo training, had no significant changes in VO2 max (49.4 +/- 3.3 vs. 48.8 +/- 3.2 ml.kg-1.min-1). Before and after training the EXP and CON groups participated in LBNP tolerance tests (terminated at presyncope) and neck pressure-suction testing (to describe the carotid sinus-heart rate baroreflex). LBNP tolerance, as defined by three different indexes, and carotid sinus-heart rate baroreflex gain were not altered in either group after training. Furthermore, there were no changes in LBNP heart rate, blood pressure, leg circumference, forearm blood flow, or forearm vascular resistance responses at any level of LBNP challenge after training. In conclusion, 10 wk of aerobic training did not change LBNP tolerance or alter the reflex cardiovascular compensatory mechanisms activated during 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.

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

2009 ◽  
Vol 296 (2) ◽  
pp. H480-H488 ◽  
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.

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.

Effect of temperature and baroreceptor stimulation on reflex venomotor responses

1984 ◽  
Vol 57 (5) ◽  
pp. 1384-1392 ◽  
Author(s):  
A. Tripathi ◽  
X. Shi ◽  
C. B. Wenger ◽  
E. R. Nadel
Keyword(s):  
Heart Rate ◽  
Lower Body Negative Pressure ◽  
Venous Pressure ◽  
Effect Of Temperature ◽  
Lower Body ◽  
Venous Capacitance ◽  
Ambient Temperatures ◽  
Wide Range ◽  
Baroreceptor Stimulation ◽  
Venous Volume

To investigate the interaction of thermal reflexes and baroreflexes in the control of the peripheral veins, we studied in supine humans the effects of lower body negative pressure (LBNP) and neck suction (NS) on forearm veins at ambient temperatures (Ta) of 18, 28, and 37 degrees C. Forearm venous volume (FVV)-venous pressure (FVP) relations (forearm venous capacitance) on six subjects showed an increase from 18 through 28 to 37 degrees C (P less than 0.001). Heart rate increased (P less than 0.001) and forearm venous capacitance decreased (P less than 0.001) in proportion to the level of LBNP applied from 20 to 50 Torr at all Ta. At 50 Torr LBNP, FVV at 30 cmH2O, FVP decreased from control values of 2.5, 3.8, and 4.4 to 1.6, 2.7, and 3.4 ml/100 ml at 18, 28, and 37 degrees C, respectively. We also studied venomotor responses using the occluded limb technique. Although LBNP caused venoconstriction, NS applied either alone or during LBNP produced no change in venomotor tone. Therefore we concluded that carotid baroreceptors play little role in reflex venomotor adjustments. Since changes in mean arterial and pulse pressures during LBNP did not account for the observed venomotor responses, we concluded that low-pressure baroreceptors initiate significant venoconstrictor reflexes over a wide range of Ta.

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