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PubMed1986

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↗
PubMed1992

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↗
PubMed2005

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↗
PubMed1996

Effects of facial cooling on elderly and young subjects: interactions with breath-holding and lower body negative pressure.

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.

Adult↗
PubMed2002

[Effects of simulated microgravity on cardiovascular function and counter effect of lower body negative pressure].

Studies on effect of simulated microgravity on cardiovascular function and counter effect of lower body negative pressure (LBNP) in recent years were summarized. The mechanism of simulated microgravity induced orthostatic intolerance may involve the reduction of cardiovascular function and cerebral blood flow, and endocrine changes. The significance of mathematical model in the study of mechanism of microgravity induced orthostatic intolerance was also discussed. The counter effect of LBNP was emphasized.

Bed Rest↗
PubMed1998

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↗
PubMed1992

Cardiovascular response to lower body negative pressure before, during, and after ten days head-down tilt bedrest.

The haemodynamic response to lower body negative pressure (LBNP) was studied in 6 test subjects before (baseline), during, and after (recovery) ten days of 6 degrees head-down bedrest. The LBNP protocol consisted of a 35 min control period, application of a staircase differential pressure profile (15 min at -15 mmHg; 5 min at -30 mmHg; 15 min at -40 mmHg), and a 10 min post-stress observation period. Cardiac output was measured by a foreign gas rebreathing technique. Finger plethysmographic arterial blood pressure (BP), ECG, and heart rate (HR), lower limb crossectional area, and the electrical impedance of three body segments were recorded continuously. As expected, HDT caused a decrease in plasma volume and total body fluid volume. Resting CO at the end of HDT was 16% below the baseline level and similar to CO in the upright position before HDT. Stroke volume (SV) was also reduced, but there were no significant changes in control HR or BP. Absolute changes in CO and SV during LBNP were similar at baseline and during HDT, but the relative changes were larger during HDT. HR and vasoconstriction responses were enhanced, but presyncope occurred in two subjects. Reduced cardiac filling with decreased stroke volume at rest is the apparent primary cause of the altered LBNP response during HDT.

Adult↗
PubMed1998

Effects of a sympathetic activation by a lower body negative pressure on glucose and lipid metabolism.

The effects of a sympathetic activation elicited by a lower body negative pressure (LBNP) (at -15 mmHg for 75 min) were assessed in 7 healthy subjects on two occasions: (i) in post-absorptive conditions, and (ii) during glucose infusion (22.2 mumol kg-1 min-1). LBNP increased plasma norepinephrine concentration and heart rate. It did not alter whole-body glucose metabolism (measured with [6,6-2H]glucose) and glycerol turnover (measured with [1,1,2,3,3-2H]glycerol). Interstitial glycerol concentrations were monitored with microdialysis in subcutaneous adipose tissue and in skeletal muscle. LBNP increased dialysate glycerol concentrations in muscle by 16% (P < 0.03) but not in adipose tissue in post-absorptive conditions, and by 37% in adipose tissue (P < 0.05) but not in muscle during glucose infusion. These results indicate that an LBNP-induced sympathetic activation (i) does not increase endogenous glucose production, and (ii) induces only a slight stimulation of lipolysis in adipose tissue during glucose infusion.

Adolescent↗
PubMed1994

Changes in blood and plasma composition with lower body negative pressure on the ground and in space in one subject.

In one cosmonaut, we investigated lower body negative pressure (LBNP)-induced capillary fluid shifts which we hypothesized would be changed by microgravity (micrograms) adaptation. Sound pulse velocity (SV) was determined in whole blood and plasma samples, using a new method that could detect 0.1% protein concentration changes. Experiments were performed 3 months preflight (supine), during space flight (6th day in orbit), and postflight (supine; 4th day after landing). Antecubital blood was taken at the beginning (3 min: time a) and after shut-down (+2 min: time b) of 40 min LBNP (-15/-30/-35 mm Hg for 15/15/10 min, respectively), since in control experiments with multiple sampling on Earth, the largest difference (increase) between blood and plasma SV was observed between a and b. Our cosmonaut had a 1.6 m/s increase in blood sound pulse velocity (BSV) preflight and a 4.0 m/s increase postflight, whereas BSV stayed unchanged in flight. Plasma sound pulse velocity (PSV) increased 1.2 m/s preflight and 1.7 m/s postflight, whereas PSV did not rise (-0.4 m/s) in flight. This would indicate profoundly altered LBNP-induced fluid dynamics in flight, compared to control (1-g) conditions. On the 4th day postflight, blood and plasma sound velocity increased more with LBNP than preflight, indicating greater hemoconcentration than under control conditions. In summary, the data suggest: 1) altered fluid shifts between blood and interstitial compartments during LBNP with 6 d adaptation to microgravity; and 2) increased hemoconcentration during LBNP early after a 10-d spaceflight.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2003

Assessment of cerebrovascular and cardiovascular responses to lower body negative pressure as a test of cerebral autoregulation.

The aim of this study was to determine whether lower body negative pressure (LBNP), combined with noninvasive methods of assessing changes in systemic and cerebral vascular resistance, is suitable as a method for assessing cerebral autoregulation. In 13 subjects we continuously assessed heart rate, blood pressure, cerebral blood flow velocity (CBFV) and cardiac output during graded levels of LBNP from 0 to -50 mm Hg. With increasing levels of LBNP, cardiac output declined significantly (to 55.8+/-4.5% of baseline value) but there was no overall change in mean arterial pressure. CBFV also fell at higher levels of LBNP (to 81.4+/-3.2% of baseline) but the percentage CBFV change was significantly less than that in cardiac output (P<0.01). The maximum increase in cerebrovascular resistance (pulsatility ratio) was significantly less than that in total peripheral resistance (17+/-6% vs. 105+/-16%, P<0.01). Spectral analysis showed that the power of low-frequency oscillations in mean arterial pressure, but not CBFV, increased significantly at the -50 mm Hg level of LBNP. These results show that, even during high levels of orthostatic stress, cerebral autoregulation is preserved and continues to protect the cerebral circulation from changes in the systemic circulation. Furthermore, assessment of cardiovascular and cerebrovascular parameters during LBNP may provide a useful clinical test of cerebral autoregulation.

Adult↗
PubMed1979

Lower body negative pressure: a method to differentiate vasodilators in the intact rat.

1. In rats lower body negative pressure induced venous pooling in a reproducible manner. The response to LBNP in the pentobarbitone-anaesthetized rat appeared not to be influenced by the autonomic nervous system. 2. The hypotensive effect of arterial vasodilators was diminished at 5 mmHg LBNP, compared with effects at 3 mmHg, whereas the hypotensive effect of venous vasodilators was not changed at 5 mmHg LBNP, compared with that at 3 mmHg LBNP. 3. In the pithed rat dihydroergotamine caused venoconstriction. In the phenobarbitone-anaesthetized rat the hypotensive effect of venous vasodilators was decreased significantly by pretreatment with this drug, whereas it did not influence the hypotensive effect of arterial vasodilators. 4. Thus venodilatation by LBNP and venoconstriction by dihydroergotamine provide a method for differentiating arterial and venous sites of action of vasodilators in intact rats.

Animals↗
PubMed2003

Cardiovascular and autonomic responses to lower body negative pressure: do not explain gender differences in orthostatic tolerance.

This study tested the hypotheses that differences in the adrenergic, central venous pressure (CVP), cardiovascular, or baroreflex responses to lower body negative pressure (LBNP) or differences in body size would be associated with gender differences in orthostatic tolerance. Subjects (24 females, 22 males) underwent graded LBNP to -100 mmHg or presyncope. At rest, the males had higher SV (+ 21 ml x beat(-1)), cardiac output (+ 1.65 L x min(-1)), systolic blood pressure (+ 29 mmHg) and mean arterial pressure (+ 8 mmHg; all P < 0.05). Neither the CVP responses to LBNP to -60 mmHg, the deltaforearm vascular conductance/deltaCVP with LBNP to -20 mmHg nor the deltaheart rate/deltaCVP with LBNP of -30 to -60 mmHg differed between genders. LBNP tolerance was lower for the females than males (276 +/- 12 vs 337 +/- 14 mmHg x min; LBNP tolerance index; P < 0.01) and, of the resting data, only gender was associated with LBNP tolerance (R(2) = 20 %). Use of gender, the maximal change in HR with LBNP and the change in HR from 0 to -40 mmHg in a regression equation could explain 75 % of the variability in orthostatic tolerance. No cardiovascular parameter differed between genders in the two minutes preceding presyncope. In the last completed stage and at test termination, [epinephrine] and [norepinephrine] were higher in the men. These data suggest that the CVP, cardiovascular and baroreflex responses to graded LBNP are similar in men and women despite marked differences in LBNP tolerance. Differences in body size do not explain the gender difference although differences in the adrenergic responses at maximal LBNP may play a role.

Adult↗
PubMed1994

Use of lower body negative pressure to assess changes in heart rate response to orthostatic-like stress during 17 weeks of bed rest.

This study examined the heart rate response to lower body negative pressure (LBNP) during 17 weeks of horizontal bed rest to estimate the development and duration of orthostatic instability elicited by this model for space flight. Based on data from Skylab, the authors hypothesized that orthostatic (LBNP) instability would appear during the first 3 to 4 weeks, and would then remain constant for the duration of bed rest. Heart rates of four healthy adult male subjects were monitored at rest and during LBNP for 1 week of ambulatory control, 17 weeks of horizontal bed rest, and 5 weeks of recovery. The LBNP protocol consisted of 10 minutes of control (atmospheric pressure) and 5 minutes each at 5, 10, 20, 30, 40, and 50 mm Hg decompression, followed by a 10-minute recovery period; this protocol was repeated weekly to document the progressive changes in heart rate response to LBNP. Lower body negative pressure was terminated early if symptoms compatible with the onset of syncope occurred. Throughout the study, heart rate was unchanged at 5, 10, and 20 mm Hg, but it increased at 30, 40, and 50 mm Hg LBNP. During the pre-bed rest period, peak heart rate was 97 +/- 10 beats/min (mean +/- SE), occurring at 50 mm Hg for all four subjects. After 3 days of bed rest, all monitored heart rate responses, including values after release of LBNP, were only slightly elevated (NS) above pre-bed rest level. Peak heart rate was 118 +/- 21 beats/min at 50 mm Hg decompression (NS; N = 3).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Effects of histamine H2-receptor blockade on the cardiovascular reflex response to lower-body negative pressure in man.

The role of histamine H2-receptors in cardiovascular control is unknown. In seven healthy volunteers, we studied how histamine H2-receptor blockade affected the reflex response to hypovolaemia induced by lower-body negative pressure (LBNP). In placebo-treated individuals, LBNP down to -40 mmHg did not change systolic pressure but increased diastolic pressure, heart rate, forearm vascular resistance, plasma noradrenaline concentration and plasma renin activity. After pretreatment with ranitidine, a specific histamine H2-receptor antagonist, the diastolic pressure rise no longer sufficed to maintain a constant systolic pressure during LBNP. Ranitidine pretreatment also attenuated the heart rate response and the rise in plasma renin activity induced by LBNP, but did not significantly change the reflex forearm vasoconstriction or the forearm plasma noradrenaline response. The results suggest that histamine H2-receptor blockade attenuates the reflex vasoconstrictor response to lower-body negative pressure. The mechanism behind this effect remains unknown, but the data do not support the idea that the effect is exerted in the skeletal muscle vascular bed.

Adult↗
PubMed1994

Resistance training increases lower body negative pressure tolerance.

This study investigated whether whole body resistance training would increase tolerance to lower body negative pressure (LBNP). Twelve males (age = 19.6 +/- 0.4 yr; mean +/- SD) underwent an acute, 12-wk program of upper and lower body resistance training (ART). Pre- and posttraining, the ART group and a control group (CON; N = 8; age = 25.4 +/- 2.4 yr) underwent LBNP tolerance tests and neck pressure-suction testing. Additionally, a group of chronically resistance-trained individuals (CRT group; N = 5; age = 22.4 +/- 0.9 yr) were tested. LBNP tolerance was increased in the ART group after training and the CRT group exhibited a significantly higher LBNP tolerance than the other groups. The ART group exhibited a decreased leg circumference change at the same absolute negative pressure at which tolerance occurred pretraining. This indicated a decreased fluid pooling after ART. The CRT group exhibited a "flattened" hypotensive portion of the carotid sinus-heart rate baroreflex curve, but this appeared to be due to the increased neck muscle mass of the subjects. We conclude that whole body ART increases LBNP tolerance possibly mediated through alterations in vascular compliance. CRT results in even greater LBNP tolerance with the responsible mediating mechanisms unclear.

Adult↗
PubMed1992

The cerebral hemodynamics of normotensive hypovolemia during lower-body negative pressure.

Although severe hypovolemia can lead to hypotension and neurological decline, many patients with neurosurgical disorders experience a significant hypovolemia while autonomic compensatory mechanisms maintain a normal blood pressure. To assess the effects of normotensive hypovolemia upon cerebral hemodynamics, transcranial Doppler ultrasound monitoring of 13 healthy volunteers was performed during graded lower-body negative pressure of up to -50 mm Hg, an accepted laboratory model for reproducing the physiological effects of hypovolemia. Middle cerebral artery flow velocity declined by 16% +/- 4% (mean +/- standard error of the mean) and the ratio between transcranial Doppler ultrasound pulsatility and systemic pulsatility rose 22% +/- 8%, suggesting cerebral small-vessel vasoconstriction in response to the sympathetic activation unmasked by lower-body negative pressure. This vasoconstriction may interfere with the autoregulatory response to a sudden fall in blood pressure, and may explain the common observation of neurological deficit during hypovolemia even with a normal blood pressure.

Adult↗
PubMed1995

Relationship between atrial natriuretic peptide (ANP), renin (PRA), aldosterone (PAC), hemodynamic responses to lower body negative pressure (LBNP) and +Gz tolerance.

The redistribution of a certain thoracic blood volume to the lower parts of the body and decrease of the venous return of blood to the heart during lower body negative pressure leads to the central hypovolemia and the deactivation of cardiopulmonary and arterial baroreceptors. Many compensatory mechanisms are involved during central hypovolemia, which is also reflected by the changes in the secretion of different vasoactive hormones. Due to this fact the LBNP stimulus is widely used for the investigation of regulatory (compensatory) mechanisms in cardiovascular system providing deeper understanding of orthostatic reaction. Recently several papers were published on application of this experimental model for +Gz acceleration tolerance assessment. The purpose of this study was evaluate the possible dependence between the changes of ANP secretion, renin-angiotensin-aldosterone system activity, the changes of some hemodynamic parameters during the model of gravitational stress i.e. LBNP exposure and +Gz acceleration tolerance.

Adaptation, Physiological↗
PubMed1996

Pelvic blood pooling of men and women during lower body negative pressure.

INTRODUCTION: The objective of this study was to investigate possible gender differences in the hemodynamic responses of the lower body during lower body negative pressure (LBNP). METHODS: In this study, 17 women (mean age = 56 yrs) and 15 men (mean age = 55 yrs) underwent a 15 min exposure to -50 mm Hg LBNP. A Beckman (BR-100) Impedance Plethysmograph was used to measure each subject's leg and pelvic blood flow and pooling during the LBNP test. RESULTS: The women had an 83% greater increase in blood volume in the pelvic region than men as a result of the LBNP exposure. Women and men had similar increases in leg blood volume as a result of the 15 min exposure to -50 mm Hg. There was no significant gender difference in the decreased amount of blood flow to the leg or pelvic regions by the end of -50 mm Hg LBNP. CONCLUSIONS: These results demonstrate that women have greater blood pooling in the pelvic region compared to men when exposed to -50 mm Hg LBNP. These results should be considered when designing life-support equipment for men and women pilots and astronauts, especially the designing of anti-G and Space Shuttle re-entry garments.

Aged↗