Effects of Facial Cooling on Elderly and Young Subjects: Interactions with Breath-Holding and Lower Body Negative Pressure

1996 ◽  
Vol 90 (6) ◽  
pp. 485-492 ◽  
Author(s):  
K. J. Collins ◽  
T. A. Abdel-Rahman ◽  
J. C. Easton ◽  
P. Sacco ◽  
J. Ison ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
The Elderly ◽  
Elderly Subjects ◽  
Breath Holding ◽  
Lower Body ◽  
Arterial Blood ◽  
Facial Cooling ◽  
Young Subjects

1. The effects of convective facial cooling by cold air on arterial blood pressure, heart rate and finger blood flow and on the reflex interactions between facial cooling and respiratory and orthostatic cardiac reflexes have been examined in 28 young adults (20–39 years) and 17 elderly (66–78 years) volunteer subjects. 2. During 2 min facial cooling alone, bradycardia was smaller (P < 0.001) and reduction in finger blood flow smaller (P < 0.001) in elderly subjects than in young subjects. Increases in systolic blood pressure and mean arterial pressure were similar and diastolic pressure increased only in the young subjects. Systolic blood pressure and mean arterial pressure remained elevated in the elderly 1 min after facial cooling, but subsided in the young. 3. Arterial blood pressure increased more during a 30-s breath-hold in expiration than in inspiration (P < 0.001) in both groups, and this was exaggerated by breath-hold in expiration combined with facial cooling. The bradycardia produced by facial cooling and breath-holding in expiration was more pronounced in the young subjects than in the elderly (P < 0.002). 4. Interactions between facial cooling and orthostatic reflexes induced by lower-body negative pressure showed significantly different age-related linear trends. Facial cooling diminished the hypotension induced by lower-body negative pressure in both groups. Facial cooling had a greater effect in diminishing the lower-body negative pressure-induced tachycardia in the young than in the elderly. 5. The mechanism of alteration of the facial cooling response in elderly subjects could be largely impairment of arterial baroreflexes, particularly as a result of reduced cardiac vagal activity as well as impairment of cardiopulmonary reflexes with ageing.

Angiotensin II does not contribute to rapid reflex control of arterial pressure

1991 ◽  
Vol 261 (2) ◽  
pp. R473-R477 ◽  
Author(s):  
D. R. Brown ◽  
J. D. Yingling ◽  
D. C. Randall ◽  
H. M. Aral ◽  
J. M. Evans ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Power Spectrum ◽  
Arterial Pressure ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Lower Body ◽  
Converting Enzyme ◽  
Salt Diet ◽  
Arterial Blood ◽  
Before And After

Pharmacological blockade of the renin-angiotensin converting enzyme reportedly alters the heart rate (HR) power spectrum in conscious dogs, suggesting that these hormones contribute to the short-term regulation of arterial blood pressure. We tested this possibility using four independent procedures. First, HR power spectrum was determined in seven awake dogs before and after administration of enalaprilat (300 ng/kg), a converting-enzyme inhibitor. There were no significant changes in the average amplitude for the spectral peak between 0.003 and 0.1 Hz (i.e., the "low-frequency peak"). Second, the HR power spectrum was measured in 11 awake rabbits before and after treatment with deoxycorticosterone acetate (1 mg.kg-1.day-1) and salt (0.9% saline ad libitum) for 7 days to depress plasma renin levels. There were no significant changes in the amplitude of the HR power spectrum, although mean HR decreased from 206 +/- 3 to 184 +/- 4 beats/min after treatment. In the third experiment, another group of rabbits (n = 8) was tested after 2 wk on a low-salt diet to elevate plasma angiotensin levels and then after 2 wk on a normal salt diet. Once again there were no significant effects on the HR power spectrum. Finally, tranquilized dogs (n = 9) were subjected to sinusoidally varying lower body negative pressure at selected frequencies of 0.008-0.12 Hz. Tests were conducted in the control state and after administration of an angiotensin receptor antagonist (saralasin, 1 microgram.kg-1.min-1). Lower body negative pressure-induced fluctuations in arterial blood pressure were similar in both states. We find no evidence for the role of the renin-angiotensin system in the moment-to-moment regulation of arterial pressure and HR.

Reduced spontaneous baroreflex response slope during lower body negative pressure after 28 days of head-down bed rest

1994 ◽  
Vol 77 (1) ◽  
pp. 69-77 ◽  
Author(s):  
R. L. Hughson ◽  
A. Maillet ◽  
C. Gharib ◽  
J. O. Fortrat ◽  
Y. Yamamoto ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Bed Rest ◽  
Lower Body ◽  
Short Term ◽  
Arterial Blood ◽  
Response Slope ◽  
Systolic Arterial Blood Pressure ◽  
Spontaneous Baroreflex

Effects of 28 days of continuous 6 degrees head-down tilt bed rest on spontaneous vagally mediated baroreflex response slope were evaluated from beat-by-beat relationships between R-R interval and systolic arterial blood pressure. Twelve healthy men (age 27–42 yr) were assigned to either countermeasure (CM) or no-countermeasure (no-CM) groups. CM consisted of strenuous short-term exercise once per day 6 days/wk from days 7 to 28 and lower body negative pressure (LBNP) for 15 min on days 16, 18, 20, and 22–28. Spontaneous baroreflex slope was evaluated by application of linear regression to sequences of at least three beats in which systolic blood pressure and R-R interval changed in the same direction. Measurements were made pre-, mid- (day 15), and post-bed rest at rest and during progressive LBNP tests (3 min at each of -20, -30, -40, and -50 mmHg). R-R interval decreased progressively and significantly (P < 0.0001) over duration of bed rest. Spontaneous baroreflex slope at rest in pre-bed rest was 18.5 +/- 2.1 ms/mm Hg for CM and 14.9 +/- 1.6 ms/mmHg for no-CM. There was a significant reduction in baroreflex slope as a function of bed rest, and it was further reduced during LBNP (P < 0.0001). Between CM and no-CM groups differences existed, but these were present pre-bed rest and appeared unaffected by countermeasures.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Factors mediating the pressor response to isometric muscle contraction: An experimental study in healthy volunteers during lower body negative pressure

PLoS ONE ◽  
2020 ◽  
Vol 15 (12) ◽  
pp. e0243627
Author(s):  
Niels A. Stens ◽  
Jonny Hisdal ◽  
Espen F. Bakke ◽  
Narinder Kaur ◽  
Archana Sharma ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Isometric Exercise ◽  
Peripheral Resistance ◽  
Relative Importance ◽  
Lower Body ◽  
Arterial Blood

Whilst both cardiac output (CO) and total peripheral resistance (TPR) determine mean arterial blood pressure (MAP), their relative importance in the pressor response to isometric exercise remains unclear. This study aimed to elucidate the relative importance of these two different factors by examining pressor responses during cardiopulmonary unloading leading to step-wise reductions in CO. Hemodynamics were investigated in 11 healthy individuals before, during and after two-minute isometric exercise during lower body negative pressure (LBNP; -20mmHg and -40mmHg). The blood pressure response to isometric exercise was similar during normal and reduced preload, despite a step-wise reduction in CO during LBNP (-20mmHg and -40mmHg). During -20mmHg LBNP, the decreased stroke volume, and consequently CO, was counteracted by an increased TPR, while heart rate (HR) was unaffected. HR was increased during -40 mmHg LBNP, although insufficient to maintain CO; the drop in CO was perfectly compensated by an increased TPR to maintain MAP. Likewise, transient application of LBNP (-20mmHg and -40mmHg) resulted in a short transient drop in MAP, caused by a decrease in CO, which was compensated by an increase in TPR. This study suggests that, in case of reductions of CO, changes in TPR are primarily responsible for maintaining the pressor response during isometric exercise. This highlights the relative importance of TPR compared to CO in mediating the pressor response during isometric exercise.

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.

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

1990 ◽  
Vol 68 (3) ◽  
pp. 1004-1009 ◽  
Author(s):  
M. J. Joyner ◽  
J. T. Shepherd ◽  
D. R. Seals
Keyword(s):  
Blood Flow ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Partial Recovery ◽  
Sympathetic Outflow ◽  
Lower Body ◽  
Control Value ◽  
Arterial Blood ◽  
Change In Mean ◽  
Cardiopulmonary Baroreceptors

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)

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.

Effect of ‘Autonomic Blockade’ on Cardiac β-Adrenergic Chronotropic Responsiveness in Healthy Young, Healthy Elderly and Endurance-Trained Elderly Subjects

1994 ◽  
Vol 87 (3) ◽  
pp. 297-302 ◽  
Author(s):  
G. A. Ford ◽  
O. F. W. James
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Geometric Mean ◽  
Cardiovascular Responses ◽  
The Elderly ◽  
Elderly Subjects ◽  
Healthy Elderly ◽  
Age Related ◽  
Autonomic Blockade ◽  
Young Subjects

1. Cardiac chronotropic responses to isoprenaline are reduced with ageing in man. It is unclear whether this is due to reduced cardiac β-adrenergic sensitivity or to age-associated differences in reflex cardiovascular responses to the vasodilatory effects of isoprenaline. Age-associated changes in physical activity are also reported to influence β-adrenergic sensitivity. 2. The aim of the present study was to determine the contribution of alterations in reflex changes in parasympathetic and sympathetic influences and physical fitness to the age-associated reduction in cardiac chronotropic responses to β-adrenergic agonists. 3. The effect of ‘autonomic blockade’ with atropine (40 μg/kg intravenously) and clonidine (4 μg/kg intravenously) on blood pressure, heart rate and chronotropic responses to intravenous bolus isoprenaline doses was determined in eight healthy young (mean age 21 years), nine healthy elderly (72 years) and 10 endurance-trained elderly (69 years) subjects. 4. Elderly subjects had a reduced increase in heart rate after atropine (young, 49 ± 9 beats/min; elderly, 36 ± 5 beats/min; endurance-trained elderly, 34 ± 12 beats/min; P < 0.01) and did not demonstrate the transient increase in systolic blood pressure after clonidine observed in young subjects (young, 11 ± 10 mmHg; elderly, −12 ± 16 mmHg; endurance-trained elderly, −18 ± 11 mmHg; P < 0.01). 5. Cardiac chronotropic sensitivity to isoprenaline after ‘autonomic blockade’ increased in the young but decreased in the elderly subjects. The isoprenaline dose that increased heart rate by 25 beats/min before and after autonomic blockade' was: young, before 1.6 μg, after 2.8 μg, P < 0.01 (geometric mean, paired test); elderly, before 6.9 μg, after 3.6 μg, P < 0.05; endurance-trained elderly, before 5.9 μg, after 4.0 μg, P < 0.05. Cardiac chronotropic sensitivity to isoprenaline was significantly reduced in elderly compared with young subjects before (P < 0.01) but was similar after (P = 0.09) ‘autonomic blockade’. Chronotropic sensitivity did not differ between healthy and endurance-trained elderly subjects before or after ‘autonomic blockade’. 6. The age-associated reduction in cardiac chronotropic responses to bolus isoprenaline is primarily due to an age-related reduction in the influence of reflex cardiovascular responses on heart rate and not to an age-related reduction in cardiac β-adrenergic sensitivity. Endurance training is not associated with altered β-adrenergic chronotropic sensitivity in the elderly. The transient pressor response to intravenously administered clonidine may be lost in ageing man.

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