Lower Body Negative Pressure Test Research Articles

The change in Baroreflex Regulation of Heart Rhythm after “Dry” Immersion Appears during Orthostasis, but not Lower Body Negative Pressure Test

The ratio of low-frequency (LF, ~0.1 Hz) waves of RR interval duration (RRI) and systolic blood pressure (SAP) reflects the cardiac baroreflex sensitivity (BRS). Gravitational unloading (GU) may alter BRS during the passive orthostatic test (HUT) and lower body negative pressure (LBNP) test. Both effects cause blood redistribution to the lower body, but HUT is accompanied by greater unloading of sinocarotid baroreceptors than LBNP and activation of the vestibulosympathetic reflex but GU effects on BRS in these tests have not been directly compared previously. In this study we tested the hypothesis that the effect of “dry” immersion (DI, on-ground model of GU) on BRS in the same subjects will be more pronounced during HUT than during LBNP, which causes a comparable decrease in stroke volume. Nine healthy men participated in two test sessions (before and after 7-day DI) consisting of five 3-min HUT (65°) and five 3-min LBNP (–35 mmHg) with averaging the parameters in each test. Wavelet analysis was used to determine the amplitude of the RRI and SAP waves in the range of 0.05–0.13 Hz. The amplitude of LF waves of SAP increased in both tests, after DI - more significantly in HUT. The amplitude of LF RRI waves decreased in the two tests; the degree of decrease did not differ between tests and did not change under the influence of DI. The α-coefficient (the ratio of the amplitudes of RRI and SAP LF waves) decreased equally in the two tests before DI, but after DI, the degree of α-coefficient reduction increased in HUT test but did not change in LBNP test. Thus, the effect of DI on BRS is evident in HUT, but not in LBNP, which may be explained by the more pronounced influence of HUT on the mechanisms of neural control of heart rhythm.

The Change in Baroreflex Regulation of Heart Rhythm after “Dry” Immersion Appears during Orthostasis, but not Lower Body Negative Pressure Test

The Change in Baroreflex Regulation of Heart Rhythm after “Dry” Immersion Appears during Orthostasis, but not Lower Body Negative Pressure Test

Diverse effects of seven-day dry immersion on hemodynamic responses in head-up tilt and lower body negative pressure tests

Head-up tilt (HUT) and lower body negative pressure (LBNP) tests are commonly used to assess orthostatic tolerance after space flight. Due to the mechanistic difference between the effects of these tests, they can provide different patterning of post-flight alterations, but this has not been proven directly, to our knowledge. Dry immersion (DI) is a ground-based experimental model which reproduces the effects of microgravity on the cardiovascular system. The aim of this work was to compare the effects of 7-day DI on hemodynamic responses to HUT and LBNP in 9 young men. HUT (65°, 3 min) and LBNP (Chibis suit, −35 mm Hg, 3 min) tests were carried out 3 days before DI, on the 7th day of DI and on the 3rd day of recovery. ECG (to calculate heart rate, HR), arterial pressure (AP), and stroke volume (SV) were continuously recorded. The tests were repeated 5 times and the data for all repetitions were averaged. Before DI, HUT and LBNP similarly decreased SV, a measure of orthostatic test. On the 7th day of DI, the decrease of SV as well as the increases of HR and mean AP were observed in supine position. DI similarly increased SV and HR responses in HUT and LBNP tests, but the effect on mean AP response was observed in HUT test and absent in LBNB test. All indicators recovered on post-immersion day 3. Therefore, 7-day DI weakens autonomic AP control only in HUT test, presumably, due to inappropriate increase of lower body vascular resistance.

A Comparison of Haemodynamic Responses between Head-Up Tilt and Lower Body Negative Pressure.

Orthostatic intolerance (OI), a disorder of the autonomic nervous system, it is the development of symptoms when standing upright which are relieved when reclining. Head-up tilt (HUT) table test is a common test for assessing orthostatic tolerance. However, HUT is limited with low sensitivity and specificity. Another approach to stimulate the changing direction and value of the gravity field vector is the lower body negative pressure (LBNP) chamber. The aims of the study is to evaluate the physiological responses of healthy subjects on HUT and LBNP, and examine the relations of two tests. A total of 19 subjects were recruited. A validated wearable device, Sotera Visi Mobile was use to collect physiological signals simultaneously throughout the experiment procedures. Each subject went through a baseline supine rest, 70o of HUT test, another round of baseline supine rest, followed by activation of LBNP test. Three level of suction were applied, i.e. -30 mmHg, -40 mmHg, and -50 mmHg. In this pilot study, healthy subjects showed significantly increased of heart rate, and decreased of systolic blood pressure and diastolic blood pressure, in both HUT and LBNP tests. Although both tests are capable of stimulating a decreased blood volume in the central circulation, but the physiological responses behaved differently and shown only very week correlation. This suggesting that a combination of LBNP test with HUT test might work the best in orthostatic intolerance assessment.

Low-dose morphine reduces tolerance to central hypovolemia in healthy adults without affecting muscle sympathetic outflow.

Hemorrhage is a leading cause of preventable battlefield and civilian trauma deaths. Low-dose (i.e., an analgesic dose) morphine is recommended for use in the prehospital (i.e., field) setting. Morphine administration reduces hemorrhagic tolerance in rodents. However, it is unknown whether morphine impairs autonomic cardiovascular regulation and consequently reduces hemorrhagic tolerance in humans. Thus, the purpose of this study was to test the hypothesis that low-dose morphine reduces hemorrhagic tolerance in conscious humans. Thirty adults (15 women/15 men; 29 ± 6 yr; 26 ± 4 kg·m-2, means ± SD) completed this randomized, crossover, double-blinded, placebo-controlled trial. One minute after intravenous administration of morphine (5 mg) or placebo (saline), we used a presyncopal limited progressive lower-body negative pressure (LBNP) protocol to determine hemorrhagic tolerance. Hemorrhagic tolerance was quantified as a cumulative stress index (mmHg·min), which was compared between trials using a Wilcoxon matched-pairs signed-rank test. We also compared muscle sympathetic nerve activity (MSNA; microneurography) and beat-to-beat blood pressure (photoplethysmography) during the LBNP test using mixed-effects analyses [time (LBNP stage) × trial]. Median LBNP tolerance was lower during morphine trials (placebo: 692 [473-997] vs. morphine: 385 [251-728] mmHg·min, P < 0.001, CI: -394 to -128). Systolic blood pressure was 8 mmHg lower during moderate central hypovolemia during morphine trials (post hoc P = 0.02; time: P < 0.001, trial: P = 0.13, interaction: P = 0.006). MSNA burst frequency responses were not different between trials (time: P < 0.001, trial: P = 0.80, interaction: P = 0.51). These data demonstrate that low-dose morphine reduces hemorrhagic tolerance in conscious humans. Thus, morphine is not an ideal analgesic for a hemorrhaging individual in the prehospital setting.NEW & NOTEWORTHY In this randomized, crossover, placebo-controlled trial, we found that tolerance to simulated hemorrhage was lower after low-dose morphine administration. Such reductions in hemorrhagic tolerance were observed without differences in MSNA burst frequency responses between morphine and placebo trials. These data, the first to be obtained in conscious humans, demonstrate that low-dose morphine reduces hemorrhagic tolerance. Thus, morphine is not an ideal analgesic for a hemorrhaging individual in the prehospital setting.

Low-dose fentanyl does not alter muscle sympathetic nerve activity, blood pressure, or tolerance during progressive central hypovolemia.

Hemorrhage is a leading cause of battlefield and civilian trauma deaths. Several pain medications, including fentanyl, are recommended for use in the prehospital (i.e., field setting) for a hemorrhaging solider. However, it is unknown whether fentanyl impairs arterial blood pressure (BP) regulation, which would compromise hemorrhagic tolerance. Thus, the purpose of this study was to test the hypothesis that an analgesic dose of fentanyl impairs hemorrhagic tolerance in conscious humans. Twenty-eight volunteers (13 females) participated in this double-blinded, randomized, placebo-controlled trial. We conducted a presyncopal limited progressive lower body negative pressure test (LBNP; a validated model to simulate hemorrhage) following intravenous administration of fentanyl (75 µg) or placebo (saline). We quantified tolerance as a cumulative stress index (mmHg·min), which was compared between trials using a paired, two-tailed t test. We also compared muscle sympathetic nerve activity (MSNA; microneurography) and beat-to-beat BP (photoplethysmography) during the LBNP test using a mixed effects model [time (LBNP stage) × trial]. LBNP tolerance was not different between trials (fentanyl: 647 ± 386 vs. placebo: 676 ± 295 mmHg·min, P = 0.61, Cohen's d = 0.08). Increases in MSNA burst frequency (time: P < 0.01, trial: P = 0.29, interaction: P = 0.94) and reductions in mean BP (time: P < 0.01, trial: P = 0.50, interaction: P = 0.16) during LBNP were not different between trials. These data, the first to be obtained in conscious humans, demonstrate that administration of an analgesic dose of fentanyl does not alter MSNA or BP during profound central hypovolemia, nor does it impair tolerance to this simulated hemorrhagic insult.

Endothelium dependent vasodilation is not enhanced in healthy women with varying degrees of orthostatic intolerance

The purpose of this study was to determine if the vasodilator capacity of the popliteal artery in women was augmented or the vasoconstrictor capacity in the lower extremity was attenuated in women with orthostatic intolerance. Orthostatic tolerance was assessed using a graded lower body negative pressure test and cumulative stress index (CSI). Popliteal artery diameter and velocity (Doppler ultrasound) was measured in 13 orthostatically tolerant and 7 orthostatically intolerant (OT: CSI range, -633 to -1875 mmHg; OI: CSI range, -80 to -552 mmHg·min; P = 0.015) women after 5 min of distal calf occlusion (FMD), 3 min of cold pressor test (CPT), and 5 min of distal calf occlusion combined with CPT (FMD+CPT). Peak popliteal diameter, measured during FMD+CPT was not different from peak popliteal diameter during FMD. Popliteal FMD, normalized to the shear stimulus, was not different between OT and OI women or between FMD and FMD+CPT. Despite similar vasoconstrictor responses to CPT, assessed by the reduction in peak popliteal artery conductance (OT: -11.0±15.6%; OI: -9.1±23.8%), the magnitude of change in peak popliteal conductance actually increased during FMD+CPT and was similar in OT vs. OI women (OT: 5.8±31.5%; OI: 47.2±60.1%). In conclusion, endothelium dependent vasodilation of the popliteal artery at rest is not enhanced in healthy women with varying degrees of orthostatic intolerance. The increase in popliteal vascular conductance during the combined stimulus (FMD+CPT) may suggest inhibition of sympathetic vasoconstriction via nitric oxide mediated vasodilation (or other dilators) and/or differential control of sympathetic activation in the arms and legs.

Heart Rate Variability Analysis During Lower Body Negative Pressure Test Induced Central Hypovolemia

Abstract In clinical patient monitoring scenarios, the detection of hemorrhage is still a major problem. Traditional vital signs like heart rate and blood pressure are insensitive to blood loss due to compensatory mechanisms in the body that can sustain these parameters until shortly before cardiovascular collapse. These compensatory mechanisms during blood loss are primarily driven by the autonomic nervous system. Heart rate variability analysis is a viable tool in the quantitative analysis of the autonomic nervous system and shows promising results in the context of hypovolemia detection. In order to investigate if HRV parameters suitably reflect a mild to moderate blood volume reduction, we conducted a lower body negative pressure test study with 30 volunteering participants thereby simulating progressive central hypovolemia. Here, HRV parameters from the time domain (mean HR, SDNN, RMSSD, rSDRM, pNN50), the frequency domain (VLF, LF, HF, LF/HF), non-linear HRV parameters (SD1, SD2, SD1/SD2, SampEn, ApEn) and the respiratory rate (RR) were collected. The changes of the evaluated parameters as a consequence of the reduced blood volume were statistically evaluated. A statistically significant deviation from their baseline values could be found for RMSSD, rSDRM, pNN50, HF, LF/HF, SD1 and SD1/SD2 at a chamber pressures starting at −30 mmHg. Therefore, we support the proposition that heart rate variability analysis can help in detecting otherwise occult hypovolemia.

Evaluation of Pulse Arrival Times during Lower Body Negative Pressure Test for the Non-Invasive Detection of Hypovolemia.

The early detection of occult bleeding is a difficult problem for clinicians because physiological variables such as heart rate and blood pressure that are measured with standard patient monitoring equipment are insensitive to blood loss. In this study, the pulse arrival time (PAT) was investigated as an easily recorded, non-invasive indicator of hypovolemia. A lower body negative pressure (LBNP) study with a stepwise increase of negative pressure was conducted to induce central hypovolemia in a study population of 30 subjects. PAT values were extracted from simultaneous recordings of the electrocardiogram (ECG) and photoplethysmographic (PPG) recordings both from the index finger and from within the outer ear canal. Stroke volume (SV) was recorded as a reference measure by transthoracic echocardiography. An inter- and intra-individual correlation analysis between changes in SV and the PAT measurements was performed. Furthermore, it was assessed if PAT measurements can indicate a diminished SV in this scenario. It could be demonstrated that the measured PAT values are significantly increased at the lowest LBNP pressure level. A very strong intra-individual correlation (ρ ≥ 0.8) and a moderate inter-individual correlation (ρ ≥ 0.5) between PAT and SV measurements were found. Thus, PAT measurements could be a viable tool to monitor patient specific volemic trends. Further research is needed to investigate if PAT information can be utilized for a more robust inter-subject quantification of the degree of hypovolemia.

Cold water submersion attenuates post-submersion aerobic performance and orthostatic tolerance irrespective of partial rehydration with water

This study examined the independent effects of cold-water submersion and a rehydration strategy on an aerobic endurance performance and orthostatic tolerance following a four-hour dive in cold water (10°C). Nine male subjects completed a control (CON) performance and lower-body negative pressure test (LBNP) and two water immersion visits with either no rehydration (NR) or a post-immersion rehydration (RH) with 1 L of water. Following submersion, subjects ran to exhaustion and submitted to LBNP. Core body temperature declined during submersion and remained reduced from baseline until the run (P ⟨ 0.001) and was not different between NR and RH (P = 0.13). Total urine output during submersion was not different between groups (1.69 ± 0.49 (NR), 1.75 ± 0.52 (RH) L; P = 0.74) eliciting a body mass reduction of -2.2 ± 0.3 and -0.8 ±; 0.3% (P ⟨ 0.01), respectively. Run duration was not different (547 ± 141 (NR), 566 ± 152 (RH) s; P = 0.79); however, both NR and RH run duration was shorter compared to CON (722 ± 170 s; P = 0.04). Cumulative stress index was suppressed in NR (534 ± 163 mmHg*min) and RH (591 ± 129 mmHg*min) compared to CON (707 ± 170 mmHg*min, P V#8804; 0.03), with no differences between submersion trials (P = 0.23). Compared to a non-submersed state, run duration and orthostatic tolerance was reduced following a four-hour cold-water submersion. Rehydration with 1 L of water following submersion did not offer a performance advantage over no rehydration.

Cardiac pacemaker channel (HCN4) inhibition and atrial arrhythmogenesis after releasing cardiac sympathetic activation

Clinical trials and studies with ivabradine implicate cardiac pacemaker channels (HCN4) in the pathogenesis of atrial arrhythmias. Because acute changes in cardiac autonomic tone predispose to atrial arrhythmias, we studied humans in whom profound cardiac sympathetic activation was rapidly relieved to test influences of HCN4 inhibition with ivabradine on atrial arrhythmias. We tested 19 healthy participants with ivabradine, metoprolol, or placebo in a double blind, randomized, cross-over fashion on top of selective norepinephrine reuptake inhibition with reboxetine. Subjects underwent combined head up tilt plus lower body negative pressure testing followed by rapid return to the supine position. In the current secondary analysis with predefined endpoints before data unblinding, continuous finger blood pressure and ECG recordings were analyzed by two experienced cardiac electrophysiologists and a physician, blinded for treatment assignment. The total atrial premature activity (referred to as atrial events) at baseline did not differ between treatments. After backwards tilting, atrial events were significantly higher with ivabradine compared with metoprolol or with placebo. Unlike beta-adrenoreceptor blockade, HCN4 inhibition while lowering heart rate does not protect from atrial arrhythmias under conditions of experimental cardiac sympathetic activation. The model in addition to providing insight in the role of HCN4 in human atrial arrhythmogenesis may have utility in gauging potential atrial pro-arrhythmic drug properties.

Effect of Hyperhydration on the Cardiovascular Responses to an LBNP Presyncopal Challenge

PURPOSETo determine the effects of hyperhydration on heart rate, blood pressure, leg blood volume and forearm blood flow during a lower body negative challenge to presyncope.METHODSNine subjects (Age = 20.2 ± 1.3 yrs, Weight = 75.3 ± 21.1 kgs) participated in two graded LBNP (Lower Body Negative Pressure) tests to pre‐syncope while forearm blood flow (FBF), heart rate (HR), blood pressure (BP), and leg blood volume were measured. Each subject was tested in a control trial (with no fluid ingestion), and after consumption of a hypervolemia‐inducing beverage (NaCl solution of 4.9g per kg of body weight in 10mL of grape flavored Propel). Treatment order was randomized for all subjects. A cumulative stress index (CSI) was subsequently calculated (minutes completed x box pressure) to assess changes in orthostatic tolerance between the control and fluid ingestion LBNP. For all trials in the LBNP chamber, subjects were tested at LBNP levels of −20 mmHg, −40 mmHg, and −60 mmHg for three minutes at each trial, and then an additional increase of −10 mmHg every three minutes until pre‐syncopal symptoms appeared. Forearm blood flow was measured using venous occlusion plethysmography. Near‐infrared spectroscopy (Portamon, Artinis, Inc.) in the right calf muscle was used to determine lower leg blood volume.RESULTSThere were no significant differences in CSI between the hyperhydration (619.8 ± 55.2mmHg.min) and control conditions (640.0 ± 70.3 mmHg.min). Furthermore, the change in forearm blood flow, lower leg blood volume, and heart rate during the LBNP hyperhydration trial were not different from the control trial.CONCLUSIONIngestion of a hypervolemia‐inducing beverage did not alter orthostatic tolerance or the cardiovascular responses to an orthostatic challenge. This suggests that either a larger volume of fluid or a fluid with a different composition needs to be ingested to improve orthostatic tolerance.

The Interaction Between Heart Systole and Cerebral Circulation During Lower Body Negative Pressure Test.

The time constant (τ[s]) estimates how fast the arterial part of the cerebrovascular bed fills with blood volume during the cardiac cycle, whereas a product of τ and heart rate (HR) (τ*HR[%]) assesses how this period of arterial filling is related to an entire heart cycle. In this study we aimed to investigate cerebral hemodynamics using τ and τ*HR during a progressive lower body negative pressure (LBNP) test.Transcranial Doppler cerebral blood flow velocity (CBFV), Finapres arterial blood pressure (ABP), and HR, along with end-tidal CO2, were simultaneously recorded in 38 healthy volunteers during an LBNP test. The τ was estimated using mathematical transformation of ABP and CBFV pulse waveforms. After a gradual shortening of τ from baseline (0.20 ± 0.06 s) to maximal LBNP before the onset of presyncope (0.15 ± 0.05 s), we observed a significant increase in τ at presyncope (0.24 ± 0.15 s; p = 0.0001). In the course of LBNP, the τ*HR did not significantly change from baseline (25.6 ± 5.7 % vs 26.6 ± 8.9 %, p = n.s.) except for presyncope, when it increased to 40.4 ± 21.1 % (p < 0.000001). Because the time needed to fill the arterial part of the cerebrovascular bed with blood is prolonged during presyncope, an increased part of the heart cycle seems to be spent on the cerebral blood supply.

Human venous hemodynamics in microgravity and prediction of orthostatic tolerance in flight

The paper presents the results of investigating the lower limbs venous status in cosmonauts (n = 13) with the use of occlusion plethysmography in 6-month missions to the Russian segment of the International space station (ISS). An interrelation of shifts in venous capacitance, compliance and filling with orthostatic tolerance (OT) in the lower body negative pressure test (LBNP) was stated. OT predictability by the leg vein status in the course of space flight was demonstrated. The objective changes of veins predictive of OT reduction were identified. There are 3 levels of changes in venous capacitance, compliance and filling that prognosticate respective reductions in LBNP tolerance and were attested in 91% of the in-flight LBNP testing.

Effect of Localized Exercise on Blood Volume and Orthostatic Tolerance

Previous studies have documented connections between orthostatic intolerance and changes in whole-body blood volume after exercise. However, few studies have looked at whether localized exercise has a direct influence on blood volume in the exercised limb and how that might influence orthostatic tolerance. PURPOSE: To determine the effects of localized exercise on blood volume within the gastrocnemius muscle and orthostatic tolerance. METHODS: Nine subjects (Age = 20.2 ± 1.3 yrs, Weight = 75.3 ± 21.1 kgs) participated in three graded LBNP (Lower Body Negative Pressure) tests to pre-syncope while forearm blood flow (FBF), heart rate (HR), blood pressure (BP), and leg blood volume were measured. Near-Infrared Spectroscopy (Portamon, Artinis, Inc.) in the right calf muscle was used to determine lower leg blood volume. Near-Infrared Spectroscopy measures continuous changes in blood volume by measuring the change in oxygenated (O2Hb) and deoxygenated (Hhb) hemoglobin concentration to determine total hemoglobin (tHb) concentrations Each subject was tested in a control trial (with no exercise), after exercise in the left leg (contralateral) of the exercise, and in the right leg (ipsilateral) of the exercise in a randomized order. Exercise trials were performed using an isokinetic dynamometer (Cybex Norm, Cybex Inc.) immediately before the LBNP testing. Subjects performed three sets of 30 plantar flexions with a 30 second rest period between sets. Cumulative stress index (CSI) was subsequently calculated (minutes completed x box pressure) to assess changes in orthostatic tolerance between the control and exercise conditions. RESULTS: CSI significantly decreased (p<0.05) after exercise in both the right and left leg trials (Right = 452.9 ± 51.8 mmHg.min; Left = 556.2±58.3mmHg.min) compared to control values (Control = 640.0 ± 70.3 mmHg.min) suggesting reduced orthostatic tolerance with leg exercise. Furthermore, during LBNP blood volume in the right leg (measured) was similar (P<0.05) after right and left leg exercise ( Right 0 = -4.2 ± 2.2, -70 mmHg = -16.0 ± 3.4; Left 0 = -2.7 ± 1.0, -70 mmHg 24.4 ± 4.0) CONCLUSION: Localized exercise in the lower leg significantly reduced orthostatic tolerance. However, it appears as if blood volume in the exercised leg is similar to blood volume in the non-exercised leg, suggesting no direct influence of localized exercise on venous compliance and LBNP tolerance.

The heart cannot pump blood that it does not receive.

The heart cannot pump blood that it does not receive.

Normothermic central hypovolemia tolerance reflects hyperthermic tolerance

To test the hypothesis that those who are highly tolerant to lower body negative pressure (LBNP) while normothermic are also highly tolerant to this challenge while hyperthermic. Sixty pairs of normothermic and hyperthermic LBNP tests to pre-syncope were evaluated. LBNP tolerance was quantified via the cumulative stress index (CSI), which is calculated as the sum of the product of the LBNP level and the duration of each level until test termination (i.e., 20mmHg×3min+30mmHg×3min, etc.). CSI was compared between normothermic and hyperthermic trials. Internal and skin temperatures, heart rate, and arterial pressure were measured throughout. Hyperthermia reduced (P<0.001) CSI from 997±437 to 303±213mmHgmin. There was a positive correlation between normothermic and hyperthermic LBNP tolerance (R (2)=0.38; P<0.001). As a secondary analysis, the 20 trials with the highest LBNP tolerance while normothermic were identified (indicated as the HIGH group; CSI 1,467±356mmHgmin), as were the 20 trials with the lowest normothermic tolerance (indicated as the LOW group; CSI 565±166mmHgmin; P<0.001 between groups). While hyperthermia unanimously reduced CSI in both HIGH and LOW groups, in this hyperthermic condition CSI was ~threefold higher in the HIGH group (474±226mmHgmin) relative to the LOW group (160±115mmHgmin; P<0.001). LBNP tolerance while hyperthermic is related to normothermic tolerance and, associated with this finding, those who have a high LBNP tolerance while normothermic remain relatively tolerant when hyperthermic.

Time dynamics of cerebral blood flow during LBNP (1183.11)

Background: The time constant (τ) estimates how fast the arterial part of cerebral vascular bed is filled with blood volume during the cardiac systole. We have demonstrated previously that τ provides new insights into time dynamics in different cardiovascular diseases and during CO2 challenge in normal subjects. In this study we aimed to investigate time dynamics of cerebral blood flow using τ during progressive lower body negative pressure (LBNP) test.Material and Methods:Simultaneous recordings of TCD cerebral blood flow velocity (CBFV) in MCA, Finapres arterial blood pressure (ABP) and heart rate (HR) along with end‐tidal CO2 (EtCO2) were performed in 38 healthy volunteers (26 ± 4 years) during LBNP test. τ and τ*HR [beat] were estimated during lower body negative pressure ‐ using mathematical transformation of ABP and CBFV pulse waveforms. The analysis of variance (ANOVA) with Bonferroni post‐hoc test were used to compare the differences in hemodynamic variables between the stages of LBNP test. The level of significance was set as 0.05.Key Results / Statistics: From baseline to maximal LBNP before the onset of presyncope the gradual shortening of τ by 74±6% (mean ±95%CI) of baseline was observed with no further decrease in τ at presyncope (76±8%) ‐ see figure 1. The τ*HR did not change significantly in the course of LBNP up to the presyncope when it increased by 119±11% of baseline (p&lt;0.0013). At presyncope reduction in ABP was by 90±5% of baseline, in CBFV by 77±3% of baseline, and in EtCO2 by 81±5% of baseline whereas HR increased by 162±9% of baseline.Conclusion: The time constant Tau sheds light onto a new aspect of the pathophysiology of presyncope. Although the heart systole contributes an increasing part to the cerebral circulation the failure of cerebral circulation cannot be prevented. Tau*HR indicates a significant downslow of the cerebral circulation during LBNP just before the occurrence of presyncopal complaints.

Prediction of human orthostatic tolerance by changes in arterial and venous hemodynamics in the microgravity environment

The authors intentionally present exclusively the results of their recent studies of arterial and venous hemodynamics as predictors of human orthostatic tolerance (OT) during space flight and on return to Earth. There is a sufficient demonstration of the in-flight OT predictability by arterial hemodynamic reactions to LBNP and venous hemodynamic changes in response to the lower extremities occlusion. Three levels of cerebral blood flow deficits in the course of the lower body negative pressure test (LBNP) performed in microgravity were first defined. The authors offer quantitative arguments for the dependence of cerebral flow deficit on the degree of LBNP tolerance degradation. Patterns of arterial hemodynamics during LBNP were used successfully to diagnose the actual orthostatic tolerance and also to follow its trend as flight extended, which attests to the predictability of OT change in an individual cosmonaut on space flight. Occlusion plethysmography of legs revealed three levels of response of the most informative venous parameters (capacity, distensibility and rate of filling) correlating with severity of OT degradation.

Lower Body Negative Pressure–Induced Vagal Reaction: Role for the Osmopressor Response?

Water ingestion elicits an osmopressor response in patients with impaired baroreflexes. In young, healthy subjects, water elicits sympathetic vasoconstriction. This study investigated the effect of water on the lower body negative pressure (LBNP)-induced vasovagal reaction and also analyzed its effect on the change of regional cerebral blood flow during LBNP. Twelve young healthy subjects underwent LBNP (40 mm Hg) tolerance testing for 45 minutes or until presyncopal symptoms occurred. Subjects received either LBNP or no LBNP with or without prior water ingestion. The severity of vasovagal reaction was determined by participant self-report rating of orthostatic symptoms during the LBNP test. Changes of regional cerebral blood flow (rCBF) between LBNP and water ingestion with LBNP groups were assessed using statistical parametrical mapping analyses. Water ingestion attenuated the severity of symptomatic scores during LBNP (P = 0.004). Water ingestion increased Total peripheral vascular resistance (P < 0.001) and attenuated the blood pressure drop (P < 0.001) at the cessation of study. LBNP decreased rCBF over the left superior prefrontal gyrus, limbic-parahippocampal gyrus, left sublobar-caudate body, and hypothalamus (P < 0.001). Water increased rCBF significantly over the right frontal lobe, including the inferior and medial prefrontal gyrus, subcallosal, and sublobar insula, during LBNP stimulation (P < 0.001). Water ingestion strongly reduces symptomatic burden of the vasovagal reaction induced by LBNP stimulation. The cortical activation of limbic and prefrontal cortex likely indicates the involvement of osmopressor response in central autonomic cardiovascular physiology. The central cortical activation of osmopressor response might provide insight into the mechanisms by which water ingestion reduces the vasovagal reaction.