Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Lower Body Negative Pressure”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 127 records · Page 7Linked to original sources
PubMed2003

Influence of glucose and insulin on transcapillary fluid absorption from the arm during lower body negative pressure in man.

This study examined the influence of insulin and glucose on the transcapillary fluid absorption during lower body negative pressure (LBNP) in humans. Ten healthy males [23 (1) years] were exposed to LBNP of 45 cmH(2)O on two occasions: (1) before and during a hyperinsulinaemic clamp (HI) and (2) before and during a hyperglycaemic clamp (HG). Transcapillary fluid absorption and blood flow were recorded with volumetric technique. Forearm blood flow increased during HI from 2.3 (0.3) ml (100 ml)(-1) min(-1) to 3.3 (0.5) ml (100 ml)(-1) min(-1) ( P<0.05). The haemodynamic response to LBNP was similar during HI and HG compared with control LBNP. Transcapillary fluid absorption during LBNP increased during HG from 0.044 (0.007) ml (100 ml)(-1) min(-1) to 0.059 (0.009) ml (100 ml)(-1) min(-1 )( P<0.01), whereas it was unchanged during HI. In conclusion, hyperglycaemia augments transcapillary fluid absorption from skeletal muscle and skin during LBNP whereas hyperinsulinaemia has no such effect. This indicates that in human hyperglycaemia contributes to plasma volume restitution during hypovolaemic circulatory stress.

Absorption↗
PubMed1989

Ten weeks of aerobic training do not affect lower body negative pressure responses.

Based mostly on cross-sectional data, it has been suggested that aerobic training may decrease lower body negative pressure (LBNP) tolerance through a hypothesized attenuation in both high- and low-pressure baroreflex gain. An experimental group (EXP) of eight male subjects [22.1 +/- 1.4 (SD) yr] underwent a 10-wk treadmill and cycle ergometer training program, which resulted in a 21% increase in maximal O2 uptake (VO2 max), 45.7 +/- 1.5 vs. 55.2 +/- 1.7 (SE) ml.kg-1.min-1; P less than 0.05]. A control group, (CON; n = 7; 27.3 +/- 5.7 yr), which did not undergo training, had no significant changes in VO2 max (49.4 +/- 3.3 vs. 48.8 +/- 3.2 ml.kg-1.min-1). Before and after training the EXP and CON groups participated in LBNP tolerance tests (terminated at presyncope) and neck pressure-suction testing (to describe the carotid sinus-heart rate baroreflex). LBNP tolerance, as defined by three different indexes, and carotid sinus-heart rate baroreflex gain were not altered in either group after training. Furthermore, there were no changes in LBNP heart rate, blood pressure, leg circumference, forearm blood flow, or forearm vascular resistance responses at any level of LBNP challenge after training. In conclusion, 10 wk of aerobic training did not change LBNP tolerance or alter the reflex cardiovascular compensatory mechanisms activated during LBNP.

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↗
PubMed1976

The involvement of noradrenergic nerves in the cardiovascular reflex responses to lower body negative pressure in the anaesthetised rabbit.

1. Resting cardiovascular status and the reflex responses to lower body negative pressure (LBNP) were examined in control rabbits and in rabbits sympathectomised with 6-hydroxydopamine (6-OHDA). 2. Resting systemic arterial pressure and total peripheral resistance were significantly higher in control than in 6-OHDA treated animals. 3. Control animals responded to LBNP at -25 mm Hg with a peripheral vasoconstriction and tachycardia. These responses were absent in 6-OHDA-treated animals. 4. Control animals responded to LBNP at -70 mm Hg with a peripheral vasoconstriction and a bradycardia followed by a tachycardia. There was no significant change in heart rate in response to this stimulus in 6-OHDA-treated animals, although a slight vasoconstriction was seen. 5. Bethanidine blocked the tachycardia and vasoconstriction seen in response to LBNP in control and 6-OHDA-treated rabbits. Under these conditions there was no significant difference between the total peripheral resistance of the control and treated animals. 6. The results indicated that neither the maintenance of the resting systemic arterial pressure nor the reflexes elicited by LBNP in control or in chronically sympathectomised rabbits involved hormonal mechanisms, but LBNP was maintained for 1 min only. These findings are discussed in the context of previous observations.

Animals↗
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↗
PubMedDate not supplied

Forced expiratory flow-volume curves during the application of lower-body negative pressure.

Ten normal subjects were studied during supine rest and quiet standing, and when exposed, supine, to lower-body negative pressure (LBNP) of 30, 40 and 50 mmHg, each for a period of 7 min, in random order. Their partial and complete flow-volume curves, heart rate and blood pressure were recorded during the last 3 min in each condition. The expected reflex cardiovascular responses to the decrease in central blood volume during standing and during LBNP were seen. The forced vital capacity was somewhat greater during standing and during LBNP than while supine. The airflow variables measured from the flow-volume curve-except MEF25% (partial)--were significantly increased during progressive LBNP but did not reach the raised values found when the posture changed from supine to standing. The observations suggest that besides the redistribution of the central blood volume to the periphery, other factors must contribute to the increase in airflows during standing.

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↗
PubMed1996

Exercise training mode affects the hemodynamic responses to lower body negative pressure in women.

To determine if different exercise modes used to improve cardiovascular fitness result in differing cardiovascular responses to lower body negative pressure (LBNP) in exercise-trained women, seven chronically exercising female runners (RUN) and 11 swimmers (SWIM) of similar fitness levels maximal oxygen uptake, [VO(2max), mean (SEM) = 50 (2) and 45 (2) ml*kg(-1)*min(-1), respectively; P > 0.05] underwent serial exposures to LBNP at pressures of 0, -1.3, -2.7 and -5.3 kPa (referenced to ambient barometric pressure). Forearm vascular resistance (venous occlusion plethysmography) increased with LBNP but did not differ between groups at any level of LBNP. At 0 and - 1.3 kPa, the total peripheral resistance index (TPRI; impedance cardiography) was significantly (P <0.05) higher in RUN than SWIM [1.118(0.028) vs 0.787 (0.040) at 0 kPa and 1.245 (0.100) vs 0.840 (0.040) 2 kPa*l* min(-1)*m(-2) at -1.3kPa]. At an LBNP of -2.7kPa, stroke index (SI) was significantly higher in SWIM than RUN [57.8(4.6) vs 41.9 (4.0) ml*beat(-1)*m(-2)] while TPRI remained greater in RUN than SWIM. At -5.3 kPa, SWIM exhibited a higher cardiac index [3.232 (0.209) vs 2.447 (0.189) l*min(-1)*m(-2)] and SI [49.4 (4.4) vs 31.0 (4.5) ml *beat(-1)*m(-2)] but reduced heart rate [71(3) vs 83(5) beats . min(-1)] and TPRI [0.968 (0.043) vs 1.655 (0.128) kPa*1*min(-1)* m(-2)]. Mean arterial pressure declined significantly at an LBNP of -5.3 kPa in both groups; pulse pressure was lower (P <0.05) in RUN than SWIM at LBNP values of -2.7 and -5.3 kPa. These data suggest that: (1) female runners experience a greater increase in systemic vasoconstriction even though female swimmers can better maintain their cardiac index at high levels of LBNP, and (2) training mode appears to affect the pulse pressure responses to LBNP in exercise-trained women.

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↗
PubMed1998

Presyncope during progressive hypovolaemia simulated by lower body negative pressure is not prevented by high-dose naloxone.

BACKGROUND: The haemodynamic response to progressive hypovolaemia, whether simulated by lower body negative pressure (LBNP) or head-up tilt, or induced by haemorrhage or haemodialysis, has a typical biphasic pattern: a first, sympathoexcitatory, phase of vasoconstriction, tachycardia, and stable blood pressure, and a second, sympathoinhibitory, phase of vasodilatation, bradycardia, and hypotension. The opioid system is involved in this response, since animal studies showed that opioid antagonism by naloxone can attenuate hypovolaemic hypotension. In humans, this finding could not be confirmed. We hypothesized that this could result from inadequate dosing. METHODS: Six healthy subjects underwent LBNP at -45 mmHg until presyncope before and after administration of naloxone 2 mg/kg. During the study, blood pressure, heart rate, vascular resistance, cardiac output, and plasma beta-endorphin were measured. RESULTS: LBNP caused an immediate increase in vasoconstriction and heart rate, resulting in stable blood pressure. After 12 +/- 3.5 min, vasodilatory hypotension followed, accompanied by a modest increase in plasma beta-endorphin. Naloxone did not alter the first or the second phase of the circulatory response, and tolerance to LBNP even tended to decrease (hypotension after 7.5 +/- 2.0 min, NS). Pre-LBNP plasma beta-endorphin as well as hypotensive levels were increased after naloxone. CONCLUSIONS: Our results suggest that naloxone, in a sufficient dose to interfere with the opioid system, does not influence the circulatory response to simulated hypovolaemia in humans is not influenced by naloxone. Given the mechanistic resemblance of LBNP hypotension to dialysis-induced hypotension, we propose that high-dose naloxone is not useful to treat the latter form of hypotension.

Adult↗
PubMed1990

Cerebral tissue oxygen status and psychomotor performance during lower body negative pressure (LBNP).

Cerebral oxygen sufficiency was studied noninvasively, using multiwavelength near-infrared spectrophotometry, in eight subjects exposed to lower body negative pressure (LBNP) of up to -90 mm Hg to induce presyncopal symptoms and signs. LBNP caused only small changes in the forebrain measures until the last 60 s of the exposures, whereupon oxyhemoglobin (HbO2) and oxidised cytochrome c oxidase fell, reduced hemoglobin (Hb) rose slightly, and the tissue blood volume (HbO2 + Hb) fell. In subjects showing presyncope, these changes anticipated the onset of a terminal bradycardia by some 20 s and may provide the trigger for cardiovascular decompensation, while the cessation of LBNP led to an overshoot in cerebral blood volume suggestive of a reactive hyperemia. Psychomotor testing showed a significant slowing of reaction time with LBNP, but only for the easiest component of a complex task, while saccadic latencies were found to be shortened following LBNP exposure.

Adult↗
PubMed1999

Reliability and precision of a new thoracic electrical bioimpedance monitor in a lower body negative pressure model.

OBJECTIVE: To evaluate the reliability and precision of measurement in a new thoracic electrical bioimpedance (TEB) monitor. DESIGN: Prospective clinical trial using healthy volunteers. SETTING: Military tertiary care teaching hospital. SUBJECTS: Seventy-five healthy adult volunteers taking no medications. INTERVENTIONS: Induction of severe preload reduction using a standardized lower-body negative pressure protocol. Measurement of hemodynamic variables using a TEB monitor before, during, and immediately after application of negative pressure. MEASUREMENTS AND RESULTS: Seventy-five subjects were enrolled and completed the study. Pulse, blood pressure, stroke index, cardiac index, systolic time ratios (STR), and index of contractility were obtained on all subjects undergoing monitoring with the lower body negative pressure (LBNP) device. Hemodynamic measurements were recorded at 15-sec intervals during incremental application of 0, -10, -20, -40, and -60 mm Hg pressure for 10 mins at each pressure. Maximal tolerated LBNP produced reductions in cardiac, stroke, and contractility indices of 50%, 65%, and 45%, respectively. Pulse and STRs increased 44% and 113%, respectively. The precision of measurement (mean +/- 2 SD) for TEB-derived cardiac and stroke index was 16% and 10%, respectively. Repeatability of measurement was assessed by measuring hemodynamic changes after the abrupt cessation of maximal LBNP. There were significant increases in stroke index (p < .001) and decreases in STRs (p < .001) and pulse (p < .001) 3 mins after LBNP. There was no significant difference between initial and post-LBNP cardiac index (p > .05). Regression equations were applied to scattergram plots of stroke index vs. STRs and index of contractility vs. body mass. The use of these plots allowed elimination of values that appeared to be spurious (stroke index vs. STRs) and also raised the question whether the Sramek-Bemstein equation (stroke volume = left ventricular ejection time x volume of electrically participating tissue x dZ/dt/Zo) fully explained all the factors affecting the TEB waveform. CONCLUSIONS: This new monitor appears to overcome many of the signal processing problems encountered with previous devices. The results clearly demonstrate that accurate and reliable measurement of bioimpedance waveforms is possible and suggest that the monitor is capable of generating precise hemodynamic data across a wide spectrum of hemodynamic alterations. However, the evidence also indicates that new algorithms may be needed to more fully explain the multiple factors affecting this waveform.

Adolescent↗
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↗
PubMed2005

Effects of age and fitness on tolerance to lower body negative pressure.

BACKGROUND: The purpose of this investigation was to determine the effects of age and fitness on tolerance to maximal lower body negative pressure (LBNP). METHODS: Ten older fit (OF) [73.9 +/- 2 years; 39.0 +/- 2 ml.kg(-1).min(-1) (age and estimated VO(2)peak, respectively)], 10 older unfit (OU) (70.9 +/- 1 years; 27.1 +/- 2 ml.kg(-1).min(-1)), 10 young fit (YF) (22.6 +/- 0.5 years; 57.1 +/- 2 ml.kg(-1).min(-1)), and 10 young unfit (YU) (23.1 +/- 1 years; 41.1 +/- 2 ml.kg(-1).min(-1)) participants underwent graded LBNP of -10 mmHg every 4 minutes to either presyncope or -100 mmHg. RESULTS: Compared to the other groups, YF had an earlier increase in heart rate (-40 mmHg vs the last stage; YF vs OF, OU, and YU, respectively) and decline in stroke volume (-20 mmHg vs -40 mmHg; YF vs OF, OU, and YU, respectively). OU had a higher resting mean arterial pressure; this difference was maintained until the last stage. OF had an earlier decline in total peripheral conductance than the other groups (-20 mmHg vs -40 mmHg). Tolerance to maximal LBNP did not differ among the groups. CONCLUSIONS: Despite differences in the responses to submaximal LBNP, neither age nor cardiovascular fitness affect tolerance to maximal LBNP.

Adult↗
PubMed1979

Lower body negative pressure box for +Gz simulation in the upright seated position.

The cost of purchasing and operating a human centrifuge is substantial. Lower body negative pressure (LBNP) is considered an acceptable experimental substitute for the +Gz stress of the centrifuge. Since civil aviation pilots are usually subjected to +Gz stress in an upright seated position, an upright seated version of the supine LBNP box was developed. In this version, a negative pressure of -40 torr is considered the equivalent of a 2 +Gz stress. This box has successfully withstood a test pressure of -120 torr. Pedal ergometry within the box is easily accomplished. The box was anthropometrically engineered to accommodate a human height range of 160-195 cm. Locating the box within an altitude chamber allows the application of LBNP at any level of chamber altitude. The total cost of fabrication is approximately $500.

Aerospace Medicine↗
PubMed2002

The repeatability of cerebral autoregulation assessment using sinusoidal lower body negative pressure.

A forced periodic variation in blood pressure produces a similar variation in cerebral blood velocity. The amplitudes and phases of the pressure and velocity waveforms are indicative of the dynamic response of the cerebral autoregulation. The phase of the velocity leads the pressure; the greater the phase difference the faster the autoregulation response. Various techniques have been employed to oscillate arterial blood pressure but measurement reproducibility has been poor. The purpose of this study was to assess the reproducibility of phase measurements when sinusoidal lower body negative pressure is used to vary blood pressure. Five healthy volunteers were assessed at two vacuum levels on each of eight visits. For each measurement a 12 s sinusoidal cycle was maintained for 5 min. The Fourier components of blood pressure and the middle cerebral artery velocity were determined at the oscillation frequency. The phase of velocity consistently led the pressure. The mean phase difference was 42+/-13 degrees for the stronger vacuum and 36+/-42 degrees for the weaker vacuum. The variation given is the within-subjects standard deviation estimated from a one-way analysis of variance. Sinusoidal lower body negative pressure is a useful stimulus for investigating autoregulation; it has advantages over other methods. High vacuums show good reproducibility but are too uncomfortable for patient use.

Adult↗
PubMed2005

Cortical regions associated with autonomic cardiovascular regulation during lower body negative pressure in humans.

The purpose of the present study was to determine the cortical structures involved with integrated baroreceptor-mediated modulation of autonomic cardiovascular function in conscious humans independent of changes in arterial blood pressure. We assessed the brain regions associated with lower body negative pressure (LBNP)-induced baroreflex control using functional magnetic resonance imaging with blood oxygen level-dependent (BOLD) contrast in eight healthy male volunteer subjects. The levels of LBNP administered were 5, 15 and 35 mmHg. Heart rate (HR; representing the cardiovascular response) and LBNP (representing the baroreceptor activation level) were simultaneously monitored during the scanning period. In addition, estimated central venous pressure (CVP), arterial blood pressure (ABP) and muscle sympathetic nerve activity were recorded on a separate session. Random effects analyses (SPM2) were used to evaluate significant (P < 0.05) BOLD signal changes that correlated separately with both LBNP and HR (15- and 35-mmHg versus 5-mmHg LBNP). Compared to baseline, steady-state LBNP at 15 and 35 mmHg decreased CVP (from 7 +/- 1 to 5 +/- 1 and 4 +/- 1 mmHg, respectively) and increased MSNA (from 12 +/- 1 to 23 +/- 3 and 36 +/- 4 bursts min(-1), respectively, both P < 0.05 versus baseline). Furthermore, steady-state LBNP elevated HR from 54 +/- 2 beats min(-1) at baseline to 64 +/- 2 beats min(-1) at 35-mmHg suction. Both mean arterial and pulse pressure were not different between rest and any level of LBNP. Cortical regions demonstrating increased activity that correlated with higher HR and greater LBNP included the right superior posterior insula, frontoparietal cortex and the left cerebellum. Conversely, using the identical statistical paradigm, bilateral anterior insular cortices, the right anterior cingulate, orbitofrontal cortex, amygdala, midbrain and mediodorsal nucleus of the thalamus showed decreased neural activation. These data corroborate previous investigations highlighting the involved roles of the insula, anterior cingulate cortex and amygdala in central autonomic cardiovascular control. In addition, we have provided the first evidence for the identification of the cortical network involved specifically with baroreflex-mediated autonomic cardiovascular function in conscious humans.

Adult↗
PubMed1992

Probing heart rate and blood pressure control mechanisms during graded levels of lower body negative pressure (LBNP).

Following space flight or head down tilt bed rest, cardiovascular deconditioning is often observed as a failure to maintain arterial blood pressure with symptoms of presyncope or syncope. LBNP can be used as a stressor of the cardiovascular system to observe the regulatory process. We have recently developed a new method to study cardiovascular control. Coarse graining spectral analysis (CGSA), allows simultaneous extraction of the harmonic components to evaluate sympathetic and parasympathetic nervous activities, and of the underlying complexity of the physiological response as given by the slope (beta) or fractal dimension (DF). The recognition that system complexity plays a major role in maintenance of cardiovascular stability is a relatively new concept. It was the purpose of the present study to examine the underlying complexity of heart rate and systolic blood pressure (SBP) variablities as indicated by the DF and power spectral analysis. Eight healthy men completed a test protocol of 20 min supine rest followed sequentially by 10 min at -5, -15, -25, -40, and -50 mmHg LBNP, and 10 min supine recovery. At rest, DF of R-R interval was 3.57 (beta = 1.56 +/- 0.12). There was a progressive decline in DF with LBNP, until at -50 mmHg, DF decreased to 1.2 (beta = 2.66 +/- 0.09). The DF for SBP was 1.3 (beta = 2.1 +/- 0.18) at rest, and was not significantly changed during LBNP. In the mid- and high-frequency ranges of the spectra, there was a moderately high degree of coherence between the variability in R-R interval and SBP. These findings indicate that short term SBP has a relatively low and unchanged complexity compared to heart rate. The changes in DF of heart rate variability were marked with increasing levels of LBNP. The results of this, and our previous study, indicate that a decline of DF to a critical level (near 1.4) is associated with orthostatic hypotension. These data show the utility of simple, non-invasive methods of data collection in conjunction with sophisticated data analysis techniques to point to possible mechanisms of orthostatic hypotension.

Adult↗