Stroke volume and sympathetic responses to lower-body negative pressure reveal new insight into circulatory shock in humans*1

2004 ◽  
Author(s):  
V CONVERTINO
Keyword(s):  
Stroke Volume ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Circulatory Shock ◽  
Lower Body ◽  
Sympathetic Responses ◽  
Insight Into

scholarly journals Hormone phase influences sympathetic responses to high levels of lower body negative pressure in young healthy women

2016 ◽  
Vol 311 (5) ◽  
pp. R957-R963 ◽  
Author(s):  
Charlotte W. Usselman ◽  
Chantelle A. Nielson ◽  
Torri A. Luchyshyn ◽  
Tamara I. Gimon ◽  
Nicole S. Coverdale ◽  
...  
Keyword(s):  
Menstrual Cycle ◽  
Stroke Volume ◽  
Negative Pressure ◽  
Contraceptive Use ◽  
Lower Body Negative Pressure ◽  
Muscle Sympathetic Nerve Activity ◽  
Peripheral Resistance ◽  
Hormonal Contraceptives ◽  
Lower Body ◽  
Sympathetic Responses

We tested the hypothesis that sympathetic responses to baroreceptor unloading may be affected by circulating sex hormones. During lower body negative pressure at −30, −60, and −80 mmHg, muscle sympathetic nerve activity (MSNA), heart rate, and blood pressure were recorded in women who were taking ( n = 8) or not taking ( n = 9) hormonal contraceptives. All women were tested twice, once during the low-hormone phase (i.e., the early follicular phase of the menstrual cycle and the placebo phase of hormonal contraceptive use), and again during the high-hormone phase (i.e., the midluteal phase of the menstrual cycle and active phase of contraceptive use). During baroreceptor unloading, the reductions in stroke volume and resultant increases in MSNA and total peripheral resistance were greater in high-hormone than low-hormone phases in both groups. When normalized to the fall in stroke volume, increases in MSNA were no longer different between hormone phases. While stroke volume and sympathetic responses were similar between women taking and not taking hormonal contraceptives, mean arterial pressure was maintained during baroreceptor unloading in women not taking hormonal contraceptives but not in women using hormonal contraceptives. These data suggest that differences in sympathetic activation between hormone phases, as elicited by lower body negative pressure, are the result of hormonally mediated changes in the hemodynamic consequences of negative pressure, rather than centrally driven alterations to sympathetic regulation.

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

1990 ◽  
Vol 78 (4) ◽  
pp. 399-401 ◽  
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.

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.

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.

Hemodynamic Strategies in Blood Pressure Regulation During Orthostatic Challenge in Women

1997 ◽  
Vol 22 (4) ◽  
pp. 351-367
Author(s):  
Tania L. Culham ◽  
Gabrielle K. Savard
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Peripheral Resistance ◽  
Orthostatic Tolerance ◽  
Lower Body ◽  
Orthostatic Challenge ◽  
Carotid Baroreflex

Several studies indicate that carotid baroreflex responsiveness is a good predictor of orthostatic tolerance. Two groups of healthy women with high (HI) and low (LO) carotid baroreflex responsiveness were studied (a) to determine any differences in the level of orthostatic tolerance of the two groups, and (b) to study the hemodynamic strategies used by HI and LO responders to regulate arterial pressure during the orthostatic challenge of lower body negative pressure (LBNP). Orthostatic tolerance was similar between the two groups, whereas the hemodynamic strategies recruited to maintain blood pressure at −40 mmHg LBNP differed: HI responders exhibited greater LBNP-induced decreases in stroke volume and cardiac output, as well as a greater increase in peripheral resistance compared to LO responders (p < .05). In addition, a significant increase in plasma renin activity during LBNP was found in the HI responders only. No significant between-group differences were found in arterial and cardiopulmonary control of vascular resistance or arterial haroreflex control of heart rate during LBNP. Key words: arterial pressure, carotid baroreceptor, lower body negative pressure, orthostatic tolerance, stroke volume

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.

Attenuated cardiac baroreflex in men with presyncope evoked by lower body negative pressure

2001 ◽  
Vol 100 (3) ◽  
pp. 303-309 ◽  
Author(s):  
Duminda N. WIJEYSUNDERA ◽  
Gary C. BUTLER ◽  
Shin-ichi ANDO ◽  
Michael J. POLLARD ◽  
Peter PICTON ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Stroke Volume ◽  
Negative Pressure ◽  
Healthy Subjects ◽  
Lower Body Negative Pressure ◽  
Muscle Sympathetic Nerve Activity ◽  
Venous Pressure ◽  
Power Spectra ◽  
Lower Body ◽  
Burst Frequency

Mechanisms responsible for presyncope during lower body negative pressure (LBNP) in otherwise healthy subjects are poorly understood. Muscle sympathetic nerve activity (MSNA), blood pressure, heart rate (HR), HR power spectra, central venous pressure (CVP) and stroke volume were determined in 14 healthy men subjected to incremental LBNP. Of these, seven experienced presyncope at LBNP >-15 mmHg. Subjects who tolerated LBNP >-15 mmHg had significantly lower CVP (2.6±1.0 versus 7.2±1.2 mmHg; means±S.E.M., P < 0.02), HR (59±2 versus 66±3 beats/min, P < 0.05) and MSNA burst frequency (29.0±2.4 versus 39.0±3.5 bursts/min, P < 0.05) during supine rest. LBNP at -15 mmHg had no effect on blood pressure, but caused similar and significant reductions in stroke volume and cardiac output in both groups. Subjects who tolerated LBNP had significant reflex increases in HR, MSNA burst frequency and burst amplitude with LBNP of -15 mmHg. These responses were absent in those who experienced presyncope. The gain of the cardiac baroreflex regulation of MSNA was markedly attenuated in pre-syncopal subjects (1.2±0.6 versus 8.8±1.4 bursts/100 heart beats per mmHg; P < 0.001). Healthy subjects who experience presyncope in response to LBNP appear more dependent, when supine, upon MSNA to maintain preload, and less able to increase sympathetic vasoconstrictor discharge to skeletal muscle reflexively in response to orthostatic stimuli.

scholarly journals The Effects of Cold and Lower Body Negative Pressure on Cardiovascular Homeostasis

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
David J. Kean ◽  
Corey A. Peacock ◽  
Gabriel J. Sanders ◽  
John McDaniel ◽  
Lisa A. C. Colvin ◽  
...  
Keyword(s):  
Stroke Volume ◽  
Negative Pressure ◽  
Cerebral Oxygenation ◽  
Lower Body Negative Pressure ◽  
Recovery Period ◽  
Lower Body ◽  
Minute Exposure ◽  
Arterial Blood ◽  
Blood Pressures ◽  
Cardiovascular Variables

Purpose. The purpose of this study is to determine how cold exposure and lower body negative pressure effected cardiovascular variables.Methods. Eleven males (20.3 years ± 2.7) underwent two 20-minute exposures to LBNP. During the 2 trials, the subjects were exposed to cold air (10°C) (COLD) and to ambient temperature (23°C) (AMB). The trials consisted of a 100-minute pre-LBNP period followed by a 20-minute exposure to LBNP and then a 15-minute recovery period. Cardiovascular variables were recorded every 30 minutes using bioimpedance.Results. When LBNP was applied during the AMB trials, stroke volume immediately decreased. During the COLD trial, there was a five-minute delay before the decrease in stroke volume. Heart rate increased immediately after LBNP initiation during the AMB trials but there was a delay in the increase during the COLD trials. That same pattern was followed with mean arterial blood pressures. Cerebral oxygenation was significantly lower throughout the COLD trial as compared to the AMB trials. Six subjects reported symptoms of syncope or presyncope during the AMB trials but there were no reports of symptoms during the COLD trials.Conclusion. From analysis of this data, cold improved the subject’s tolerance to LBNP.

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