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Summary of lower body negative pressure experiments during space flight.

This paper summarizes the lower body negative pressure experiments performed in space, beginning with the experiments conducted on Skylab, because this program provided the most cardiovascular physiology data for United States space flight. Data obtained during studies of lower body negative pressure for use as a countermeasure after months of Russian space flight are also presented. Lower body negative pressure experiments conducted aboard Space Shuttle flights provide data about the deadaptation response of the cardiovascular system to orthostatic stress occurring during periods of zero gravity, and about protection against postflight orthostatic intolerance. Data obtained using Russian and American lower body negative pressure devices indicate that, when a crew member stands, as opposed to being supported by a seat or saddle as in the American device, there may be a slight detrimental effect in terms of the cardiovascular response to this orthostatic stress. Comparison of heart rate and blood pressure response to entry and landing of the Shuttle indicate that, although lower body negative pressure is a different stress and is applied in a different manner, the maximum heart rates during lower body negative pressure are reached at approximately the same point that the maximum heart rates are reached during entry and landing. Thus, the use of a lower body negative pressure stress in flight is a fairly good predictor of the cardiovascular response to the actual entry and landing of the Shuttle.

Blood Pressure↗

Influence of lower body negative pressure upon arginine vasopressin release.

Lower body negative pressure (9-12 kPa) was applied to ten normal subjects. Large increases in plasma arginine vasopression concentration occurred only in subjects that experienced syncopal symptoms and developed hypotension. Blood samples obtained from the superior vena cava at 1/2 min intervals during application of negative pressure showed that maximal plasma vasopressin concentrations occurred with hypotension. Chromatography of the presyncopal plasma on Sephadex G-25 gave a large peak which eluted in the position of synthetic arginine vasopressin.

Adult↗

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

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.

Adult↗

Cardiorespiratory response to lower body negative pressure.

The cardiovascular effects of supine lower body negative pressure (LBNP, 0 mm Hg, -8 mm Hg, -15 mm Hg, -25 mm Hg, -35 mm Hg, and -45 mm Hg) were studied in humans (n = 10). The LBNP's were applied in a random order (three per session) for 20 min, with 15 min between each LBNP. Leg blood flow, cardiac output (Q), stroke volume (SV) and estimated lung blood volume were significantly reduced at -15 mm Hg. Increasing LBNP to -35 mm Hg did not result in further changes. When the LBNP was increased to -45 mm Hg, Q and SV were lower than comparable values at -15 mm Hg. Heart rate was unchanged up to -25 mm Hg, after which it increased proportionally to the LBNP. Systolic blood pressure was maintained throughout. Diastolic blood pressure was unchanged below -45 mm Hg, but was significantly elevated at -45 mm Hg. Mean arterial pressure was maintained up to LBNP's of -35 mm Hg by increased vascular resistance, in spite of reduced thoracic blood volume, as indicated by reduced central venous pressure and Q. Greater levels of LBNP were outside the physiological adjustment range and blood pressure dropped progressively.

Adult↗

Cardiovascular response to graded lower body negative pressure in young and elderly man.

Lower body negative pressure (LBNP) reduces central venous pressure (CVP) and cardiac output. The elderly are reported to have a limited capacity to increase cardiac output by increasing heart rate (HR), are especially dependent on end diastolic volume to maintain stroke volume and therefore should be especially vulnerable to LBNP. The present study compared the effects of LBNP in the young and old. Stroke volume was assessed non-invasively as stroke distance (SD) by aortovelography. Two groups of healthy male volunteers were studied: eight young (29.7 +/- 2.0 years, mean +/- S.E.M.) and nine old (70.1 +/- 0.9 years). LBNP was applied progressively at 17.5, 35 and 50 mmHg in 20 min steps, with measurements taken during each steady state. There were similar, significant, falls in CVP in both groups. SD fell significantly in both groups from respective control values of 24.8 +/- 1.6 and 16.6 +/- 0.9 cm to 12.5 +/- 1.3 and 8.9 +/- 0.4 cm at a LBNP of 50 mmHg. Although SD in the elderly was significantly lower than in the young, the LBNP-induced changes were not different between groups. Both groups produced similar significant increases in vascular resistance, HR, plasma vasopressin (AVP) and noradrenaline. Mean arterial blood pressure (MBP) and plasma adrenaline did not change significantly. Therefore healthy old men respond to LBNP in a similar manner to the young, although MBP and SD are regulated around different baselines in the two groups.

Adult↗

Cardiovascular responses to lower body negative pressure in normal subjects and in patients with diabetes mellitus.

The cardiovascular responses of non-diabetic and diabetic subjects to lower body negative pressure at 1.3, 2.7, and 5.3 kPa (10, 20, and 40 mmHg) were measured. The diabetics fell into two groups--those showing little change in systolic blood pressure with lower body negative pressure at 5.3 kPa (40 mmHg) and those showing falls greater than 2.7 kPa (20 mmHg). The patterns of response in the former group of diabetics and in the non-diabetics were similar. The diabetics who showed a fall in systolic blood pressure with lower body negative pressure nonetheless responded with a forearm vasoconstriction indicating that the vasomotor dysfunction was localised to some other vascular bed. In one subject forearm vasodilatation occurred with lower body negative pressure at 5.3 kPa (40 mmHg) although his response to milder levels of lower body negative pressure appeared normal. It is suggested that the integrity of vasomotor reflexes is most reliably tested by exposure to stepped increases in lower body negative pressure.

Adolescent↗

[Effects of self-generated LBNP training on cardiovascular function and lower body negative pressure (LBNP) tolerance].

OBJECTIVE: To explore the changes of cardiac function and lower body negative pressure tolerance after self-generated Lower Body Negative Pressure device training and provide experimental evidences for its appliance. METHOD: Twelve healthy male subjects were randomly divided into two groups, and received training on two conditions for entirely closing the valve or opening to -30 mmHg of peak LBNP separately. The group A was trained for five days and three minutes per day. Heartfunction, HUT and tolerance of LBNP were measured in pre-training, 3 d and post-training. The group B was trained for ten days and five minutes each day. All the measurements that was the same as in group A were made. RESULT: Heart function of group A decreased and tolerance of LBNP increased significantly (P<0.05). In group B, heart function increased significantly after 8 days training, so did tolerance of LBNP. CONCLUSION: It suggested that lower body negative pressure tolerance could be improved by self-generated Lower Body Negative Pressure device training. The changes of cardiac function, however, were based on the project of training.

Adaptation, Physiological↗

Cerebral artery blood flow velocity changes following rapid release of lower body negative pressure.

BACKGROUND: Circulatory changes occur during exposure to Lower Body Negative Pressure (LBNP). These changes may have some similarities to exposure to moderately and slowly increased G-loads in a relaxed subject without anti-G suit. HYPOTHESIS: Changes will also occur in cerebral blood circulation during a rapid release of LBNP. METHODS: Transcranial Doppler ultrasound (TCD) was used to measure middle cerebral artery blood flow velocity (CBFV) in 14 human subjects following rapid release of a ramped lower body negative pressure (LBNP) (0.33 mm Hg.s) to presyncope (mean peak negative pressure of -124 mm Hg). RESULTS: The mean CBFV decreased to an average of 60% (p < 0.05) of the baseline value at peak LBNP. Mean CBFV was still decreased to 65% and 84% of the baseline value (p < 0.05) at the third heart beat and 30 s, respectively, after pressure release. The systolic CBFV decreased similarly to 57% (p < 0.05) of baseline during peak LBNP, and was still 63% (p < 0.05) at the third heart beat after pressure release. Heart rate increased by a mean of 51% (p < 0.001) and systolic heart level blood pressure decreased by 28% (p < 0.001) during peak negative pressure. Both heart rate and blood pressure returned to baseline levels within 30 s after pressure release. CONCLUSIONS: Following a presyncopal LBNP, the CBFV is not fully restored up to 30 s after the release of the negative pressure. This delayed returning of cerebral circulation following orthostatic stress may have some similarities to what occurs after the release of a gradual onset G-load in a relaxed subject without anti-G suit.

Adult↗

Cardiovascular responses to application of lower body negative pressure of male volunteers in seated position.

Lower body negative pressure (LBNP) has been used to evaluate orthostatic tolerance and for studying the effects of +Gz induced physiological strain and hence has great practical significance in aerospace medicine. Cardiovascular responses in man on application to LBNP (-40 mmHg) in seated (upright) position in a specially designed LBNP chamber have been studied in eight normal healthy male volunteers between the age group of 25-36 yrs. They were subjected to -40 mmHg negative pressure in steps of -10 mmHg for a duration of 5 min each. The total duration of the experiment was 20 min. Heart rate (HR), blood pressure (BP) Cardiac output (CO) were measured and mean blood pressure (MBP) and total peripheral resistance (TPR) were computed. The results indicate a significant increase in HR (P < 0.01), SV (P < 0.01). Studies on limited number of subjects on application to LBNP (40 mmHg) in supine position have also been carried out and compared with the physiological strain induced in subjects in seated position. Study of HR, SV, CO, responses of the subjects on exposure to LBNP in seated position elicit similar response in subjects exposed to +Gz stress as reported by other workers. It is concluded that LBNP technique can be used to study the effects of +Gz induced physiological strain in man.

Adult↗

Lower body negative pressure: a test of cardiovascular autonomic function.

Lower body negative pressure (LBNP) may provide an alternative test of cardiovascular autonomic function for patients unable to perform the Valsalva maneuver (VM). LBNP at -40 mmHg for 30 s was compared to the VM at 40 mmHg for 15 s with heart rate and blood pressure measured continuously in three age groups: 10-25 years; 26-40 years; and 41-55 years. Heart rate and blood pressure responses were comparable, with moderately diminished changes in blood pressure and heart rate in the LBNP test. When heart response to LBNP was converted to a ratio similar to that calculated for the VM, a high degree of correlation was found (R(2) = 0.5711). The LBNP test shows promise as an alternative test of cardiovascular autonomic function based on studies in normal subjects. The less marked changes may relate to the more passive nature of the applied stress. Future work should improve the device's accessibility and establish values for patients with autonomic disorders.

Adolescent↗

Effect of a central redistribution of fluid volume on response to lower-body negative pressure.

We studied cardiovascular responses to lower-body negative pressure (LBNP) following 1 hour (h) of 6 degrees head-down tilt to determine whether a redistribution of blood volume toward the central circulation modifies the subsequent response to orthostatic stress. Responses of 12 men, ages 30-39 years, were evaluated by electrocardiography, impedance cardiography, sphygmomanometry, and measurement of calf circumference. During the LBNP that followed head-down tilt--as compared with control LBNP (no preceding head-down tilt)--subjects had smaller stroke volume and cardiac output, greater total peripheral resistance, and less calf enlargement. These differences reflect differences in the variables immediately preceding LBNP. Magnitudes of the responses from pre-LBNP to each pressure stage of the LBNP procedure did not differ between protocols. Mean and diastolic arterial pressures were slightly elevated after LBNP-control, but they fell slightly during LBNP post-tilt. These cardiovascular responses to simulated gravitational stress following head-down tilt may reflect the manner in which adaptation to microgravity affects subsequent responses to orthostatic stress on return to Earth.

Adult↗

[Oxygen status and regional blood flow in the gingival mucosa as affected by lower body negative pressure].

Five test subjects were exposed to lower body negative pressure (LBNP). During exposure their regional circulation and oxygen balance of the gingival mucosa were measured and electrocardiography and kinetocardiography were performed to calculate parameters of the left heart function. The study showed a distinct correlation between LBNP tolerance and the level of compensatory reactions of the gingival mucosa blood flow and the cardiovascular system as a whole. The subjects with a high LBNP tolerance showed well pronounced regional compensatory reactions of the gingival mucosa that were not accompanied by significant changes in the left heart function. The subjects with a moderate tolerance exhibited either weak or no regional compensatory reactions of the gingival mucosa and significant changes in the left heart function.

Adult↗

Effects of gender on the autonomic modulation of the cardiovascular responses to lower body negative pressure.

BACKGROUND: The cardiovascular responses to submaximal lower body negative pressure (LBNP) appear to differ between genders, but the underlying mechanisms are uncertain. HYPOTHESIS: These differences are due to differences in the autonomic modulation of the cardiovascular system. METHODS: There were 14 women and 13 men who underwent LBNP to -50 mmHg in 10 mmHg increments of 6 min each. Heart rate (HR), stroke volume (SV), BP, forearm blood flow and R-R interval data were acquired. Spectral analysis of the R-R interval data was used to assess autonomic modulation with the low frequency component (LF) set at 0.04 to 0.15 Hz and the high frequency component (HF) at 0.15 to 0.4 Hz. RESULTS: The responses to LBNP to -40 mmHg did not differ between groups. LBNP of -50 mmHg evoked greater HR increases in the women than the men (7.2 +/- 1.0 vs. 3.8 +/- 1.1 bpm; p < 0.05), while SV, cardiac output and total peripheral conductance decreased more (-15 +/- 2 vs. -8 +/- 2 ml x beat(-1); -0.668 +/- 0.131 vs. -0.1778 +/- 0.124 L x min(-1); -0.009 +/- 0.002 vs. -0.004 +/- 0.001 units; p < 0.05). Normalized HF, an indicator of the vagal influence on HR variability, declined below rest at -40 mmHg while the LF/HF ratio, an indicator of sympathetic neural modulation of HR variability, increased above rest at -40 mmHg. These responses did not differ significantly between groups. CONCLUSIONS: These results suggest that gender differences in the cardiovascular responses to LBNP are not due to gross differences in modulation of the autonomic nervous systems.

Adult↗

[Development of self-generating lower body negative pressure device].

OBJECTIVE: To develop a kind of self-generating lower body negative pressure device. METHOD: The device consists of a flexible bellows, reinforced by several steel rings and sealed by gasproof adhesive plaster. An adjustable valve, a one-way flap valve, shoulder straps and handles are incorporated on the top of the bellows. The user's lower body was contained in the bellows. As the user's legs were extended, the bellows was elongated and the air pressure in it decreased. RESULT: Negative pressures of -58, -46, -38 and -26 mm-Hg respectively was created with the adjustable inlet valve completely closed, one-quarter open, half open, or fully open. CONCLUSION: This self-generating lower body negative pressure device combines exercise and LBNP into one thing and is safe and easy to use. It might be used in preventing cardiovascular deconditioning during spaceflight or for anti-G training of pilots.

Aerospace Medicine↗

Differential effects of lower body negative pressure on forearm and calf blood flow.

Modest degrees of lower body negative pressure (less than 20 mmHg) cause a reflex constriction of forearm resistance vessels attributable to a decrease in activity of cardiopulmonary mechanoreceptors. In the present study, we sought to determine whether the calf vessels respond similarly. Left forearm and right calf blood flows were measured simultaneously by strain-gauge plethysmography in 10 healthy volunteers. Forearm flows decreased significantly from control during negative pressures of 10, 15, or 20 mmHg, whereas calf flows did not decrease significantly until 20 mmHg; at 10, 15, and 20 mmHg, decreases in forearm flow were significantly greater than those of the calf. Similar results were obtained in a second series of experiments in which venous pooling in the right leg during lower body negative pressure was prevented by enclosing it in a boot. At 40 mmHg, or after a Valsalva maneuver, both forearm and calf vessels constricted markedly and to the same degree. It appears that the reflex reduction in blood flow to the skeletal muscles of the limbs resulting from deactivation of the low-pressure intrathoracic mechanoreceptors is directed primarily to the arm.

Adult↗

Carotid arterial haemodynamics after mild degrees of lower-body negative pressure in man.

1. Pulsatile changes in the diameter of the common carotid artery were studied transcutaneously using an echo-tracking technique in 15 normal subjects: eight subjects before and during application of graded lower-body negative pressure from -5 to -15 mmHg, and seven subjects before and during weight-bearing head-up tilt at 30 and 60 degrees. 2. In concomitant studies of changes in forearm vascular resistance, it was seen that mild lower-body negative pressure produced deactivation of cardiopulmonary receptors without changes in systemic blood pressure or heart rate. 3. After lower-body negative pressure, a significant decrease in carotid arterial diastolic diameter [from 0.662 +/- 0.028 to 0.624 +/- 0.033 cm (lower-body negative pressure -10 mmHg) and 0.640 +/- 0.030 cm lower-body negative pressure -15 mmHg), P < 0.001 and < 0.05] was observed. 4. After head-up tilt, carotid arterial diameter was also significantly decreased at 30 and 60 degrees, whereas a significant increase in heart rate occurred only at 60 degrees and mean blood pressure did not change. 5. The study provides evidence that the geometry of the arterial wall is substantially modified by non-invasive manoeuvres such as head-up tilting and lower-body negative pressure. The latter is assumed to selectively deactivate human cardiopulmonary receptors, but the present data suggest that local changes may also influence carotid baroreceptors.

Adult↗

Lower body negative pressure as a model to study progression to acute hemorrhagic shock in humans.

Hemorrhage is a leading cause of death in both civilian and battlefield trauma. Survival rates increase when victims requiring immediate intervention are correctly identified in a mass-casualty situation, but methods of prioritizing casualties based on current triage algorithms are severely limited. Development of effective procedures to predict the magnitude of hemorrhage and the likelihood for progression to hemorrhagic shock must necessarily be based on carefully controlled human experimentation, but controlled study of severe hemorrhage in humans is not possible. It may be possible to simulate hemorrhage, as many of the physiological compensations to acute hemorrhage can be mimicked in the laboratory by applying negative pressure to the lower extremities. Lower body negative pressure (LBNP) sequesters blood from the thorax into dependent regions of the pelvis and legs, effectively decreasing central blood volume in a similar fashion as acute hemorrhage. In this review, we compare physiological responses to hemorrhage and LBNP with particular emphasis on cardiovascular compensations that both share in common. Through evaluation of animal and human data, we present evidence that supports the hypothesis that LBNP, and resulting volume sequestration, is an effective technique to study physiological responses and mechanisms associated with acute hemorrhage in humans. Such experiments could lead to clinical algorithms that identify bleeding victims who will likely progress to hemorrhagic shock and require lifesaving intervention(s).

Acute Disease↗

Regulation of arterial blood pressure in humans during isometric muscle contraction and lower body negative pressure.

Previous studies have shown that the blood pressure response to isometric handgrip remains unchanged during reductions in preload induced by lower body negative pressure (LBNP). The purpose of the present study was to assess the beat-by-beat haemodynamic mechanisms allowing for precise control of mean arterial pressure (MAP). We have followed the cardiovascular variables involved in the regulation of MAP during isometric handgrip with and without additional application of LBNP during defined periods of the ongoing contraction. Sixteen subjects participated. Mean arterial blood pressure (MAP), heart rate (HR), stroke volume (SV), cardiac output (CO), blood flow velocity in the brachial artery, acral skin blood flow, as well as total (TPR) and local (LPR) peripheral resistance were continuously recorded/calculated before, during and after 2 min of handgrip both with and without concomitant LBNP. The main finding was that MAP increased at the same rate and to the same absolute level whether or not LBNP was applied. A uniform increase in MAP was observed even though the cardiovascular variables evolved differently in the periods with and without LBNP. At the onset of LBNP at -20 mmHg, there was a transient drop in MAP and a transient increase in HR, but within seconds, MAP was regulated back to the slope caused by the isometric handgrip proper. CO and SV, which were declining gradually, showed an additional marked but gradual reduction upon LBNP application. At the same time, both LPR and TPR increased markedly and continuously. In summary, the increase in MAP during isometric handgrip remained essentially unchanged by LBNP-induced alterations in preload. The increase in MAP was caused by a marked increase in peripheral resistance. This supports the concept of a central set point, continuously regulated upwards as long as the isometric handgrip persists. Furthermore, it reveals a considerable flexibility in the cardiovascular control mechanisms used to achieve the desired arterial pressure.

Adaptation, Physiological↗