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Repeatability and protocol comparability of presyncopal symptom limited lower body negative pressure exposures.

Data on repeatability and comparability of different presyncopal symptom-limited lower body negative pressure (PSL-LBNP) exposure protocols, while scarce, are critical to the interpretation of studies using PSL-LBNP methods. To investigate if PSL-LBNP tolerance, heart rate, and blood pressure were repeatable, 11 subjects were exposed to 4 PSL-LBNP tests; each test occurring at the same time of day, separated by at least 72 h, and using the same protocol. No significant differences were found in either the heart rate or blood pressure responses to the PSL-LBNP or the tolerance indices (cumulative stress index; maximum negative pressure tolerated; and duration of negative pressure exposure). To study the comparability of different PSL-LBNP protocols, nine subjects were exposed randomly to five PSL-LBNP tests using protocols that varied in stage duration but not pressure profile. The protocols had 1-, 3-, 5-, 7-, or 9-min stage durations. These PSL-LBNP exposures were conducted at the same time of day and separated by at least 72 h. While no differences were noted in either the response pattern or magnitude of heart rate or blood pressure to the differing protocols, the cumulative stress index and the duration of negative pressure exposure varied proportionally with the length of the stage durations. With the exception of the 1-min protocol, the maximum negative pressure tolerated did not vary regardless of the protocol used.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Endocrine response to acute changes of brain blood flow due to lower body negative pressure in man.

The decrease of brain flow due to lower body negative pressure (LBNP) was used to study the role of cerebral glucopenia in the activation of anterior pituitary function in 10 young healthy men. During LBNP with a maximum negative pressure of--50 mm Hg the changes in heart rate, blood pressure cerebral blood flow (with the aid of rheoencephalography) and electrocardiogram were recorded and the levels of hGH, ACTH, hPRL, insulin and cortisol were measured with the aid of radioimmunoassay. During the first investigation an infusion of 20% glucose (1 g per min for first 30 min and 0.5 g per min for next 30 min) was used, while during the second investigation (one week later) the infusion of saline was applied. It was found that the infusion of glucose prevented the increase of hGH which was observed only during the infusion of saline. No differences in the level of ACTH, cortisol and hPRL were observed between the investigations with glucose and saline infusion. The increased level of insulin was related to the level of glucose during the infusion, while no changes were found during saline infusion. It was suggested that the increase of hGH level during LBNP resulted from glucopenia in cerebral tissue.

Adrenocorticotropic Hormone↗

Lower body negative pressure as a tool for research in aerospace physiology and military medicine.

Lower body negative pressure (LBNP) has been extensively used for decades in aerospace physiological research as a tool to investigate cardiovascular mechanisms that are associated with or underlie performance in aerospace and military environments. In comparison with clinical stand and tilt tests, LBNP represents a relatively safe methodology for inducing highly reproducible hemodynamic responses during exposure to footward fluid shifts similar to those experienced under orthostatic challenge. By maintaining an orthostatic challenge in a supine posture, removal of leg support (muscle pump) and head motion (vestibular stimuli) during LBNP provides the capability to isolate cardiovascular mechanisms that regulate blood pressure. LBNP can be used for physiological measurements, clinical diagnoses and investigational research comparisons of subject populations and alterations in physiological status. The applications of LBNP to the study of blood pressure regulation in spaceflight, groundbased simulations of low gravity, and hemorrhage have provided unique insights and understanding for development of countermeasures based on physiological mechanisms underlying the operational problems.

Aerospace Medicine↗

Effect of lower body negative pressure on cerebral circulation.

This experiment was performed to study the effects of lower body negative pressure (LBNP) on cerebral circulation. Cerebral hemodynamics were monitored continuously and noninvasively in eight subjects at 30 mmHg of LBNP for 25 minutes by following items: 1) the carotid Doppler flowmeter which measures the carotid blood flow, 2) the transcranial Doppler sonography which measures the flow velocity of the middle cerebral artery, 3) the near infrared spectrophotometer which measures the oxygenated and deoxygenated hemoglobin in the brain. The mean flow velocity of the middle cerebral artery and the blood flow of the common carotid artery significantly decreased during LBNP, even though the mean arterial blood pressure was well maintained. The oxygenated hemoglobin was significantly increased during LBNP, while the deoxygenated hemoglobin was not changed significantly. Our results suggest that exposure to moderate LBNP (30 mmHg) decreased the cerebral blood flow with the vasodilation on the arterial side of the brain.

Adult↗

Leg mass and lower body negative pressure tolerance in men and women.

To explore the hypothesis that lower body muscle mass correlates with orthostatic tolerance, 18 healthy volunteers (age 18-48 yr; 10 men, 8 women) underwent a graded lower body negative pressure (LBNP) protocol consisting of six, 5-min stages of suction up to 60 mmHg in 10-mmHg increments. Forearm blood flow, heart rate, and blood pressure were measured, and forearm vascular resistance was calculated. Leg muscle mass was assessed by dual-energy X-ray absorptiometry. All subjects received standard intravenous hydration for at least 8 h before the study. Six men and four women completed all stages of LBNP. Four men and four women developed presyncopal symptoms, including marked bradycardia and/or hypotension, at LBNP levels of 30 mmHg (n = 2;1 man, 1 woman), 40 mmHg (n = 2;1 man, 1 woman), and 50 mmHg (n = 4;2 men, 2 women). The presyncopal subjects had leg muscle masses ranging from 19.5 to 25.2 kg in men and from 11.7 to 16.6 kg in women. In subjects who completed all stages of LBNP, leg muscle mass ranged from 17.5 to 24.1 kg in men and from 10.4 to 18.0 kg in women. Leg muscle mass did not differ between presyncopal subjects and those who completed the protocol. Furthermore, there were no differences in the hemodynamic responses to LBNP between subjects with low vs. high leg mass. These data suggest that leg muscle mass is not a critical determinant of LBNP tolerance in otherwise healthy men and women.

Absorptiometry, Photon↗

Cardiovascular responses to lower body negative pressure in endurance and static exercise-trained men.

The cardiovascular responses to lower body negative pressure (LBNP) (to -50 torr) were examined in 8 sedentary control (UT), 8 endurance-trained (ET), and 8 weight-trained (WT) human subjects. The results were used to compare and contrast the blood pressure control system of the three subject groups. The primary differences in response included a more effective maintenance of blood pressure, by reason of greater stroke volume and cardiac indices of the WT subjects during LBNP (P less than 0.05). Peripheral vascular resistances were not different (P greater than 0.05) throughout LBN P between the three groups. Therefore, the improved blood pressure maintenance of the WT subjects was attributed to a cardiac effect. The ET subjects were less effective in maintaining blood pressure than UT or WT subjects. This finding was apparently due to an attenuated baroreflex sensitivity, as evidenced by a significantly (P less than 0.05) lower delta heart rate/delta systemic blood pressure ratio, 0.99 for ET vs 1.51 and 1.38 or the UT and WT groups respectively, calculated from the responses observed from 0 to -50 torr of LBNP.

Adult↗

Norepinephrine kinetics and cardiac output during nonhypotensive lower body negative pressure.

Recently we have shown that arterial norepinephrine (NE) concentration increases significantly during lower body negative pressure (LBNP) of -15 mmHg. Interestingly, the increase was found to be related predominantly to a decrease in arterial NE clearance. We postulated that this reduction in clearance would be related to a reduction in cardiac output. Accordingly, we measured both cardiac output (2-dimensional echocardiographic/Doppler technique) and arterial NE kinetics ([3H]NE continuous infusion radiotracer technique) during LBNP of -15 mmHg. These measures of cardiac output and arterial NE spillover and clearance were obtained in 12 normal subjects at baseline, 5 and 10 min (Early) and 25 and 30 min (Late) of LBNP. We found that arterial NE concentration increased significantly, by 25% Early and 22% Late (P = 0.001). Spillover, however, did not change (P = 0.258), whereas clearance decreased by 12% Early and 19% Late (P = 0.014), and cardiac output decreased by 15% Early and 19% Late (P = 0.001). These reductions in clearance and cardiac output correlated significantly (r = 0.61, P = 0.001). No correlation was noted between spillover and cardiac output (r = 0.027, P = 0.874). We conclude that the increases in arterial NE concentration during nonhypotensive LBNP are predominantly due to decreased cardiac output with resultant decreases in systemic clearance of NE. These findings suggest that the ability to clear NE from the circulation is linked to the level of cardiac output and that low cardiac output states by themselves may lead to an elevation in arterial plasma NE concentrations.

Adult↗

Heart rate variability during head down tilt and lower body negative pressure in the Russian Tschibis.

The cardiovascular function in space seems to be normal. However, abnormalities of cardiovascular responses have been found during lower body negative pressure suction in space. The etiology of the cardiovascular deconditioning in space is still unknown. A previous study showed, that short periods of head down tilt (HDT-6 degrees) induce changes in the spectral pattern of heart rate variabilty (HRV) and an increase in the sympathethic activation caused by orthostatic stress. The aim of this study was to test following hypotheses: 1. The dynamic of heart rate variability is different in the head down tilt and supine positions. 2. The application of lower body negative pressure (LBNP) during head down tilt induces similar heart rate variability patterns like the standing position. 3. After short term head down tilt the cardiovascular response to lower body negative pressure stressor is altered.

Adult↗

Femoral flow response to lower body negative pressure: an orthostatic tolerance test.

UNLABELLED: The objective was to check, during a lower body negative pressure (LBNP) test, new vascular parameters for the detection of orthostatic intolerance induced by head-down-tilt (HDT) and spaceflight. METHODS: The lower-limb volume flow and vascular resistance were evaluated by Doppler ultrasound. The HDT population consisted of two groups: control [6 subjects resting in a HDT (-6 degrees) position for 28 d] and countermeasure (6 subjects also in HDT for 28 d, but with repeated LBNP and exercise). The LBNP orthostatic test (four steps: -20, -30, -40, -50 mm Hg, of 3 min each) was performed before, during, and after the HDT. For the 14-d spaceflight (Antares) the cosmonaut underwent the LBNP test (10 min at -25 mm Hg and 10 min at -45 mm Hg), at preflight (3 times), inflight (day 11), and postflight (twice). RESULTS: HDT--As the LBNP pressure decreased, the femoral blood flow decreased and the lower-limb vascular resistances increased in both HDT groups. In the control group the femoral flow was less reduced, at each of the 4 levels of depressure (p < 0.01). The amplitude of the leg vascular resistances was reduced at -40 mm Hg, and at -50 mm Hg, on HDT day 15 in both groups (before LBNP, after 1 week's exercise for the countermeasure group), and on post-HDT day 1 (p < 0.01) only in the control group. The femoral vascular resistance response had completely recovered in the countermeasure group on post-HDT day 1. During the post-HDT tilt table test, all 6 controls had a drop in blood pressure of 20 mm Hg (4 subjects) or 10 mm Hg (2 subjects); 3 had pre-syncopal symptoms. The HDT countermeasure subjects had neither any clinical signs of orthostatic intolerance nor any blood pressure drop. 14d-Spaceflight--During the flight, the cosmonaut did not use any countermeasures (exercise, LBNP). On flight day +11, and on postflight day 3, the femoral vascular resistance response to LBNP was decreased as observed in the control group on HDT day +15 and post HDT. On postflight day 7, the femoral response had completely recovered. The middle cerebral flow response to the various pre-, in-, and postflight LBNP tests consisted of a slight decrease of the cerebral flow together with resistances of comparable amplitude (-10 to -20%) to those measured during the same LBNP test in the HDT control group. CONCLUSION: The femoral hemodynamics are much more disturbed than the cerebral ones in vascular deconditioning. The assessment of the lower limb vascular reactivity will be of interest in predicting orthostatic intolerance, and checking the efficiency of counter-measures.

Cardiovascular Deconditioning↗

[Assessment of cerebral autoregulation using transcranial Doppler sonography under lower body negative pressure].

A novel technique for transcranial Doppler sonographic assessment of cerebral autoregulation was tried out in 20 healthy volunteers, ten of them right-handed and ten left-handed. A fall in arterial blood pressure was produced through lower body negative pressure (LBNP) of -50 mmHg during 1 min. The Doppler shift signal of both middle cerebral arteries was recorded simultaneously and analyzed digitally to obtain mean Doppler shift frequency and Doppler signal power. Their product, as an index of volume flow, was calculated on-line. By positioning and coupling of the transducers and keeping the position of the head stable throughout the test, spurious readings due to the effects of gravity or head movement were excluded. With an average fall of mean arterial blood pressure of 10.3 +/- 7.7 mmHg, the TCD flow index as averaged over the entire period of LBNP was 103.6 +/- 19.5% of the value measured under atmospheric pressure, demonstrating a physiological autoregulation. In the right-handed subjects the flow index during LBNP was significantly higher on the right than on the left side. In only one of the ten right-handed individuals the side difference was reversed, while this was the case in five of the ten left-handed subjects.

Adult↗

Progressive withdrawal of muscle nerve sympathetic activity preceding vaso-vagal syncope during lower-body negative pressure.

We report the observation of a vaso-vagal syncope (VVS) occurring during lower body negative pressure in a young male volunteer. Recording of the peripheral blood flow, blood pressure and muscular sympathetic nerve activity revealed first a progressive withdrawal of muscle nerve sympathetic activity with redistribution of blood flow before the onset of the VVS.

Adult↗

Development of lower body negative pressure as a countermeasure for orthostatic intolerance.

Exposure to prolonged (1-4 hr) lower body negative pressure (LBNP) is a countermeasure against postflight orthostatic intolerance which is used in the Soviet space program and planned for use in the American space program. LBNP in combination with fluid-loading is believed to act by promoting a transient positive fluid balance resulting in an increase in vascular, as well as extravascular fluid. Inflight LBNP also may provide beneficial orthostatic effects by restoring baroreceptor reflex functions and/or lower body venous compliance. Current research efforts at the Johnson Space Center are directed towards increasing the effectiveness and efficiency of the LBNP and saline countermeasure. A promising avenue may involve combining pharmacologic agents, such as inhaled anti-diuretic hormone, or mineralocorticoids, with mechanical stimuli such as LBNP.

Humans↗

Association of sex and age with responses to lower-body negative pressure.

Responses of 21 women and 29 men (29-56 yr of age) to -50 Torr lower body negative pressure (LBNP) were examined for differences due to sex or age. Responses to LBNP were normal, including fluid shift from thorax to lower body, increased heart rate and peripheral resistance, and decreased stroke volume, cardiac output, and Heather index of ventricular function. Mean arterial blood pressure did not change. Comparison of responses of the women to responses of an age-matched subset of the men (n = 26) indicated the men had larger relative increases in calf circumference and greater increases in peripheral resistance during LBNP than the women, whereas the women experienced greater increases in thoracic impedance and heart rate. Analyses of responses of the 29 men for age-related differences indicated older subjects had greater increases in peripheral resistance and less heart rate elevation in response to LBNP (P less than 0.05 for all differences, except sex-related heart rate difference, where P less than 0.10). Based on these data and the data of other investigators, we hypothesize the age-related circulatory differences in response to LBNP are due to a reduction in vagal response and a switch to predominant sympathetic nervous system influence in older men. We cannot exclude the possibility that diminished responsiveness in the afferent arm of the baroreceptor reflex also plays a role in the attenuated heart rate response of older men to LBNP.

Adult↗

Effect of acute hypoxia on vascular responsiveness in man. I. Responsiveness to lower body negative pressure and ice on the forehead. II. Responses to norepinephrine and angiotensin. 3. Effect of hypoxia and hypocapnia.

An effect of hypoxemia on vascular responsiveness and blood pressure regulation has not been demonstrated in man. The response of forearm resistance vessels to several vasoconstrictor stimuli was compared during normoxia and acute hypoxia. Forearm vasoconstrictor responses to lower body negative pressure and to the application of ice to the forehead, which are neurogenic stimuli, were decreased during acute hypoxia. Lower body negative pressure caused a decrease in mean arterial pressure during hypoxia, but not during normoxia. Because norepinephrine is the neurotransmitter released during reflex vasoconstriction, we considered the possibility that decreased responsiveness to norepinephrine might be one mechanism for diminished responses to lower body negative pressure and ice on the forehead during hypoxia. Hypoxia decreased the response of forearm resistance vessels to infusions of norepinephrine and angiotensin into the brachial artery. In addition, the effectiveness of intravenous infusions of norepinephrine in elevating mean arterial pressure was decreased during hypoxia. Since exposure to acute hypoxia stimulates hyperventilation and hypocapnia, experiments were done to determine the contribution of hypocapnia during hypoxia to the decreased vasoconstriction. The results indicate that hypocapnia may diminish the vascular response to some stimuli, but the reduction in oxygen appears to be the primary mechanism for decreased vasoconstrictor responses during acute hypoxia.

Adult↗

Cardiovascular dynamics associated with tolerance to lower body negative pressure.

The purpose of this investigation was to identify cardiovascular responses associated with tolerance to lower body negative pressure (LBNP). In this study, 18 men, ages 29-51 years, were categorized as high (HT) or low (LT) LBNP tolerant based on a graded presyncopal-limited LBNP exposure criterion of -60 mm Hg relative to ambient pressure. Groups were matched for physical characteristics and preLBNP cardiovascular measurements, with the exceptions of greater (p less than 0.05) end-diastolic volume and cardiac output in the HT group. During peak LBNP, cardiac output was similar (NS) in both groups, although the HT group displayed a greater heart rate (p less than 0.05). In both groups, venous return appeared to limit cardiac output resulting in decreased arterial pressure. Tolerance to LBNP did not appear solely dependent on the absolute amount of blood pooled in the legs since the HT group demonstrated a greater (p less than 0.05) peak LBNP-induced increase in midthigh-leg volume. Greater tolerance to LBNP was associated with a larger preLBNP cardiac output reserve and higher compensatory increases in heart rate and peripheral resistance.

Adult↗

Cardiovascular responses to lower body negative pressure in trained and untrained older men.

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.

Aged↗

Comparison of cardiovascular responses between lower body negative pressure and head-up tilt.

To investigate local blood-flow regulation during orthostatic maneuvers, 10 healthy subjects were exposed to -20 and -40 mmHg lower body negative pressure (LBNP; each for 3 min) and to 60 degrees head-up tilt (HUT; for 5 min). Measurements were made of blood flow in the brachial (BF(brachial)) and femoral arteries (BF(femoral)) (both by the ultrasound Doppler method), heart rate (HR), mean arterial pressure (MAP), cardiac stroke volume (SV; by echocardiography), and left ventricular end-diastolic volume (LVEDV; by echocardiography). Comparable central cardiovascular responses (changes in LVEDV, SV, and MAP) were seen during LBNP and HUT. During -20 mmHg LBNP, -40 mmHg LBNP, and HUT, the following results were observed: 1) BF(brachial) decreased by 51, 57, and 41%, and BF(femoral) decreased by 40, 53, and 62%, respectively, 2) vascular resistance increased in the upper limb by 110, 147, and 85%, and in the lower limb by 76, 153, and 250%, respectively. The increases in vascular resistance were not different between the upper and lower limbs during LBNP. However, during HUT, the increase in the lower limb was much greater than that in the upper limb. These results suggest that, during orthostatic stimulation, the vascular responses in the limbs due to the cardiopulmonary and arterial baroreflexes can be strongly modulated by local mechanisms (presumably induced by gravitational effects).

Adaptation, Physiological↗

The renal sympathetic and renin-angiotensin response to lower body negative pressure in well-compensated cirrhosis.

BACKGROUND & AIMS: Certain antinatriuretic hormonal systems may be involved in the subclinical sodium handling abnormality in preascitic cirrhosis. The aims of this study were to determine the following in preascitic cirrhosis: (1) basal activity of the renal sympathetic and renin-angiotensin systems and (2) the relationship between the response of these systems to lower body negative pressure and sodium excretion. METHODS: Seven preascitic cirrhotic patients and 9 age- and sex-matched controls were studied on a 150 mmol sodium per day diet. Systemic and renal hemodynamics, renal neurohormonal secretion rates, and sodium excretion were assessed before, during increasing levels of, and after lower body negative pressure, each for 30 minutes. RESULTS: Both groups responded with a significant decrease in central venous pressure (P < 0.01) that remained higher in the cirrhotics than in the controls throughout the study. Cirrhotics showed significant increases compared with controls in renal renin and angiotensin II secretion rates at -20 mm Hg of lower body negative pressure, which was associated with significant renal sodium retention (96 +/- 17 micromol/min vs. 218 +/- 21 micromol/min at baseline, P < 0.05), but there was no change in renal sympathetic activity. CONCLUSIONS: In preascitic cirrhosis, sodium retention occurs in response to lower body negative pressure, which was associated with increased renal renin-angiotensin activity. Stimulation of the intrarenal renin-angiotensin system may be the initial renal pathophysiological change causing sodium retention in cirrhosis.

Adaptation, Physiological↗