scholarly journals Plasma hyperosmolality improves tolerance to combined heat stress and central hypovolemia in humans

2017 ◽  
Vol 312 (3) ◽  
pp. R273-R280 ◽  
Author(s):  
Daniel Gagnon ◽  
Steven A. Romero ◽  
Hai Ngo ◽  
Paula Y. S. Poh ◽  
Craig G. Crandall
Keyword(s):  
Heart Rate ◽  
Heat Stress ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sympathetic Nerve Activity ◽  
Lower Body Negative Pressure ◽  
Muscle Sympathetic Nerve Activity ◽  
Plasma Osmolality ◽  
Lower Body ◽  
Nerve Activity

Heat stress profoundly impairs tolerance to central hypovolemia in humans via a number of mechanisms including heat-induced hypovolemia. However, heat stress also elevates plasma osmolality; the effects of which on tolerance to central hypovolemia remain unknown. This study examined the effect of plasma hyperosmolality on tolerance to central hypovolemia in heat-stressed humans. With the use of a counterbalanced and crossover design, 12 subjects (1 female) received intravenous infusion of either 0.9% iso-osmotic (ISO) or 3.0% hyperosmotic (HYPER) saline. Subjects were subsequently heated until core temperature increased ~1.4°C, after which all subjects underwent progressive lower-body negative pressure (LBNP) to presyncope. Plasma hyperosmolality improved LBNP tolerance (ISO: 288 ± 193 vs. HYPER: 382 ± 145 mmHg × min, P = 0.04). However, no differences in mean arterial pressure ( P = 0.10), heart rate ( P = 0.09), or muscle sympathetic nerve activity ( P = 0.60, n = 6) were observed between conditions. When individual data were assessed, LBNP tolerance improved ≥25% in eight subjects but remained unchanged in the remaining four subjects. In subjects who exhibited improved LBNP tolerance, plasma hyperosmolality resulted in elevated mean arterial pressure (ISO: 62 ± 10 vs. HYPER: 72 ± 9 mmHg, P < 0.01) and a greater increase in heart rate (ISO: +12 ± 24 vs. HYPER: +23 ± 17 beats/min, P = 0.05) before presyncope. No differences in these variables were observed between conditions in subjects that did not improve LBNP tolerance (all P ≥ 0.55). These results suggest that plasma hyperosmolality improves tolerance to central hypovolemia during heat stress in most, but not all, individuals.

Cardiovascular and neurohormonal effects of intravenous adrenomedullin in conscious rabbits

1995 ◽  
Vol 269 (5) ◽  
pp. R1289-R1293 ◽  
Author(s):  
M. Fukuhara ◽  
T. Tsuchihashi ◽  
I. Abe ◽  
M. Fujishima
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Conscious Rabbits ◽  
Renal Sympathetic

Adrenomedullin is a vasodilative peptide and shows slight homology with calcitonin gene-related peptide. In the present study, we investigated the effects of adrenomedullin on cardiovascular and neurohormonal responses in 13 conscious rabbits. The animals were chronically instrumented with bipolar electrodes on the left renal sympathetic nerve. Intravenous administration of human adrenomedullin (10, 100, 1,000, and 3,000 pmol/kg, n = 6) caused a dose-dependent reduction in mean arterial pressure (0 +/- 2, -1 +/- 2, -19 +/- 2, and -29 +/- 4 mmHg, respectively) concomitant with increases in heart rate, renal sympathetic nerve activity, plasma renin activity, and plasma norepinephrine. The significant reduction in mean arterial pressure induced by 1,000 pmol/kg of adrenomedullin occurred within 1 min after injection and lasted for 15 min (n = 7). In contrast, the significant increases in heart rate and renal sympathetic nerve activity lasted for more than 50 min. When mean arterial pressure was decreased by 15 mmHg by adrenomedullin, the increases in heart rate and renal sympathetic nerve activity were 53 +/- 8 beats/min and 78 +/- 13%, respectively, which were significantly smaller than those induced by intravenous injection of sodium nitroprusside (102 +/- 14 beats/min and 155 +/- 34%, respectively). These results suggest that intravenous adrenomedullin exerts a hypotensive action that is associated with the attenuated reflex-mediated sympathetic activation.

Modulation of control of muscle sympathetic nerve activity during orthostatic stress in humans

2004 ◽  
Vol 287 (5) ◽  
pp. H2147-H2153 ◽  
Author(s):  
Masashi Ichinose ◽  
Mitsuru Saito ◽  
Takeshi Ogawa ◽  
Keiji Hayashi ◽  
Narihiko Kondo ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Lower Body Negative Pressure ◽  
Muscle Sympathetic Nerve Activity ◽  
Total Activity ◽  
Orthostatic Stress ◽  
Lower Body ◽  
Arterial Baroreflex ◽  
Nerve Activity ◽  
Burst Strength

We tested the hypothesis that orthostatic stress would modulate the arterial baroreflex (ABR)-mediated beat-by-beat control of muscle sympathetic nerve activity (MSNA) in humans. In 12 healthy subjects, ABR control of MSNA (burst incidence, burst strength, and total activity) was evaluated by analysis of the relation between beat-by-beat spontaneous variations in diastolic blood pressure (DAP) and MSNA during supine rest (CON) and at two levels of lower body negative pressure (LBNP: −15 and −35 mmHg). At −15 mmHg LBNP, the relation between burst incidence (bursts per 100 heartbeats) and DAP showed an upward shift from that observed during CON, but the further shift seen at −35 mmHg LBNP was only marginal. The relation between burst strength and DAP was shifted upward at −15 mmHg LBNP (vs. CON) and further shifted upward at −35 mmHg LBNP. At −15 mmHg LBNP, the relation between total activity and DAP was shifted upward from that obtained during CON and further shifted upward at −35 mmHg LBNP. These results suggest that ABR control of MSNA is modulated during orthostatic stress and that the modulation is different between a mild (nonhypotensive) and a moderate (hypotensive) level of orthostatic stress.

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.

Vestibulosympathetic reflex during mental stress

2002 ◽  
Vol 93 (4) ◽  
pp. 1260-1264 ◽  
Author(s):  
Jason R. Carter ◽  
Chester A. Ray ◽  
William H. Cooke
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Neural Activity ◽  
Mental Stress ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Neural Activation ◽  
Nerve Activity ◽  
Vestibulosympathetic Reflex ◽  
Mental Stimulation

Increases in sympathetic neural activity occur independently with either vestibular or mental stimulation, but it is unknown whether sympathetic activation is additive or inhibitive when both stressors are combined. The purpose of the present study was to investigate the combined effects of vestibular and mental stimulation on sympathetic neural activation and arterial pressure in humans. Muscle sympathetic nerve activity (MSNA), arterial pressure, and heart rate were recorded in 10 healthy volunteers in the prone position during 1) head-down rotation (HDR), 2) mental stress (MS; using arithmetic), and 3) combined HDR and MS. HDR significantly ( P< 0.05) increased MSNA (9 ± 2 to 13 ± 2 bursts/min). MS significantly increased MSNA (8 ± 2 to 13 ± 2 bursts/min) and mean arterial pressure (87 ± 2 to 101 ± 2 mmHg). Combined HDR and MS significantly increased MSNA (9 ± 1 to 16 ± 2 bursts/min) and mean arterial pressure (89 ± 2 to 100 ± 3 mmHg). Increases in MSNA (7 ± 1 bursts/min) during the combination trial were not different from the algebraic sum of each trial performed alone (8 ± 2 bursts/min). We conclude that the interaction for MSNA and arterial pressure is additive during combined vestibular and mental stimulation. Therefore, vestibular- and stress-mediated increases of MSNA appear to occur independently in humans.

scholarly journals Countdown before voluntary exercise induces muscle vasodilation with baroreflex-mediated decrease in muscle sympathetic nerve activity in humans

2020 ◽  
Vol 128 (5) ◽  
pp. 1196-1206
Author(s):  
Kazumasa Manabe ◽  
Shizue Masuki ◽  
Yu Ogawa ◽  
Koji Uchida ◽  
Yoshi-ichiro Kamijo ◽  
...  
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Sympathetic Nerve Activity ◽  
Consumption Rate ◽  
Cerebral Blood Flow Velocity ◽  
Muscle Sympathetic Nerve Activity ◽  
Voluntary Exercise ◽  
Thigh Muscle ◽  
Nerve Activity ◽  
Increase Oxygen Consumption

Prospective cardiovascular adjustment occurs before starting voluntary exercise, increasing heart rate and arterial pressure followed by muscle vasodilation; however, the precise mechanisms and significance for this vasodilation remain unknown. We found that during the countdown before starting exercise cerebral blood flow velocity increased, followed by increases in heart rate and arterial pressure, which suppressed MSNA through baroreflex, resulting in thigh muscle vasodilation to increase oxygen consumption rate, which might make it easier to start exercise.

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.

Diastolic pressure determines autonomic responses to pressure perturbation in humans

1989 ◽  
Vol 66 (2) ◽  
pp. 800-807 ◽  
Author(s):  
J. S. Sanders ◽  
D. W. Ferguson
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Sympathetic Nerve Activity ◽  
Diastolic Pressure ◽  
Human Subjects ◽  
Muscle Sympathetic Nerve Activity ◽  
Venous Pressure ◽  
Central Venous ◽  
Nerve Activity ◽  
Normal Human

Arterial baroreceptors reflexly regulate sympathetic and heart rate responses to alteration of blood pressure. The primary mechanical determinant of arterial baroreceptor activity in humans remains unclear. We examined the influence of systolic, diastolic, pulse, and mean arterial pressures on efferent muscle sympathetic nerve activity (MSNA, microneurography) and heart rate responses during perturbation of arterial pressure in 10 normal human subjects [age 25 +/- 2 (SE) yr]. We directly measured arterial pressure, heart rate, and MSNA during intravenous vasodilator infusion (nitroprusside, 6 +/- 1 micrograms.kg-1.min-1, n = 6; or hydralazine, 16 +/- 2 mg, n = 4) while central venous pressure was held constant by simultaneous volume expansion. Changes in arterial pressures were compared with changes in heart rate and MSNA over 3-min periods of vasodilator infusion during which we observed increases in systolic and pulse pressures with simultaneous decreases in mean and diastolic pressures. During vasodilator infusion, there were increases in systolic (124.2 +/- 2.1 to 131.7 +/- 2.9 Torr, P less than 0.001) and pulse pressures (57.0 +/- 2.2 to 72.7 +/- 2.7 Torr, P less than 0.001) although mean arterial pressure fell (88.0 +/- 2.6 to 80.4 +/- 2.7 Torr, P less than 0.001) because of decreases in diastolic pressure (67.2 +/- 3.0 to 59.0 +/- 2.7 Torr, P less than 0.001). The changes in arterial pressures were accompanied by simultaneous increases in heart rate (66.4 +/- 3.0 to 92.6 +/- 4.8 beats/min, P less than 0.001) and MSNA (327 +/- 59 to 936 +/- 171 U, P less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Whole body heat stress attenuates baroreflex control of muscle sympathetic nerve activity during postexercise muscle ischemia

2009 ◽  
Vol 106 (4) ◽  
pp. 1125-1131 ◽  
Author(s):  
Jian Cui ◽  
Manabu Shibasaki ◽  
Scott L. Davis ◽  
David A. Low ◽  
David M. Keller ◽  
...  
Keyword(s):  
Heart Rate ◽  
Heat Stress ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Whole Body ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Whole Body Heat Stress ◽  
Body Heat

Both whole body heat stress and stimulation of muscle metabolic receptors activate muscle sympathetic nerve activity (MSNA) through nonbaroreflex pathways. In addition to stimulating muscle metaboreceptors, exercise has the potential to increase internal temperature. Although we and others report that passive whole body heating does not alter the gain of the arterial baroreflex, it is unknown whether increased body temperature, often accompanying exercise, affects baroreflex function when muscle metaboreceptors are stimulated. This project tested the hypothesis that whole body heating alters the gain of baroreflex control of muscle sympathetic nerve activity (MSNA) and heart rate during muscle metaboreceptor stimulation engaged via postexercise muscle ischemia (PEMI). MSNA, blood pressure (BP, Finometer), and heart rate were recorded from 11 healthy volunteers. The volunteers performed isometric handgrip exercise until fatigue, followed by 2.5 min of PEMI. During PEMI, BP was acutely reduced and then raised pharmacologically using the modified Oxford technique. This protocol was repeated two to three times when volunteers were normothermic, and again during heat stress (increase core temperature ∼ 0.7°C) conditions. The slope of the relationship between MSNA and BP during PEMI was less negative (i.e., decreased baroreflex gain) during whole body heating when compared with the normothermic condition (−4.34 ± 0.40 to −3.57 ± 0.31 units·beat−1·mmHg−1, respectively; P = 0.015). The gain of baroreflex control of heart rate during PEMI was also decreased during whole body heating ( P < 0.001). These findings indicate that whole body heat stress reduces baroreflex control of MSNA and heart rate during muscle metaboreceptor stimulation.

Spectral analysis of heart rate, arterial pressure, and muscle sympathetic nerve activity in normal humans

1998 ◽  
Vol 274 (4) ◽  
pp. H1211-H1217 ◽  
Author(s):  
Akio Nakata ◽  
Shigeo Takata ◽  
Toyoshi Yuasa ◽  
Atsuhiro Shimakura ◽  
Michiro Maruyama ◽  
...  
Keyword(s):  
Heart Rate ◽  
Spectral Analysis ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Autoregressive Model ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Model Fitting ◽  
Power Spectral Analysis ◽  
Nerve Activity

We investigated the frequency components of fluctuations in heart rate, arterial pressure, respiration, and muscle sympathetic nerve activity (MSNA) in 11 healthy women using an autoregressive model and examined the relation among variables using Akaike’s relative power contribution analysis with multivariate autoregressive model fitting. Power spectral analysis of MSNA revealed two peaks, with low-frequency (LF) and high-frequency (HF) components. The LF component of MSNA was a major determinant of the LF component of arterial pressure and R-R interval variability (0.70 ± 0.07 and 0.18 ± 0.05, respectively). The effect of the LF component of MSNA on arterial pressure showed no change in response to propranolol but was diminished (0.35 ± 0.08) by phentolamine ( P < 0.02). The effect of the LF component of MSNA on R-R interval was not altered by pharmacological sympathetic nerve blockade. The HF component of MSNA did not influence other variables but was influenced by R-R interval, arterial pressure, and respiration. These findings indicate that the LF component of MSNA reflects autonomic oscillations, whereas the HF component is passive and influenced by other cardiovascular variables.

Effects of intravenous infusions of angiotensin II on muscle sympathetic nerve activity in humans

1991 ◽  
Vol 261 (3) ◽  
pp. R690-R696 ◽  
Author(s):  
T. Matsukawa ◽  
E. Gotoh ◽  
K. Minamisawa ◽  
M. Kihara ◽  
S. Ueda ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Sympathetic Outflow ◽  
Ang Ii ◽  
Nerve Activity ◽  
Intravenous Infusions

The effect of angiotensin II (ANG II) on the sympathetic outflow was examined in normal humans. The mean arterial pressure and muscle sympathetic nerve activity (MSNA) were measured before and during intravenous infusions of phenylephrine (0.5 and 1.0 micrograms.kg-1.min-1) or ANG II (5, 10, and 20 ng.kg-1.min-1) for 15 min at 30-min intervals. The baroreflex slope for the relationship between the increases in mean arterial pressure and the reductions in MSNA was significantly less acute during the infusions of ANG II than during the infusions of phenylephrine. When nitroprusside was infused simultaneously to maintain central venous pressure at the basal level, MSNA significantly increased during the infusions of ANG II (5 ng.kg-1.min-1 for 15 min) but not during the infusions of phenylephrine (1.0 micrograms.kg-1.min-1 for 15 min), with accompanying attenuation of the elevation in arterial pressure induced by these pressor agents. These findings suggest that ANG II stimulates the sympathetic outflow without mediating baroreceptor reflexes in humans.

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