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At least 19 records
All sourcesNASA NTRSDOE OSTI
NASA NTRS1996

Certain cardiovascular indices predict syncope in the postural tachycardia syndrome

Patients with postural tachycardia syndrome (POTS) represent a patient population with orthostatic intolerance; some are prone to syncope, others are not. The underlying neurocardiovascular mechanisms are not completely understood. The current study was undertaken to assess if certain cardiovascular indices are predictive of syncope in POTS. We compared the response to tilt-up and the Valsalva maneuver in four groups: POTS patients who fainted (POTS-f; n = 11;31 +/- 11 years): POTS patients who did not faint (POTS-nf; n = 9; 29 +/- 9 years); normal controls (NLS; n = 13; 39 +/- 11 years); patients with generalized autonomic failure with orthostatic hypotension and syncope (n = 10; 59 +/- 14 years). Beat-to-beat heart rate (HR), systolic arterial pressure, diastolic arterial pressure (DAP) and pulse pressure (PP) were monitored using Finapres. Cardiac output, stroke volume (SV) and end-diastolic volume (EDV), and calculated total peripheral resistance (TPR) were recorded using thoracic electrical bioimpedance. An autonomic reflex screen which quantitates the distribution and severity of autonomic failure was also done. With the patient supine, all POTS patients (POTS-nf; POTS-f) had increased HR (p < 0.001) and reduced SV/EDV (p < 0.001) when compared with NLS. On tilt-up, POTS-f patients were significantly different from both NLS and POTS-nf patients; the most consistent alteration was a fall instead of an increase in TPR; other changes were a greater reduction in PP, a reduction (instead of an increment) in DAP, and a different pattern of changes during the Valsalva maneuver (excessive early phase II, attenuated or absent late phase II). Our results suggest alpha-adrenergic impairment with increased pooling or hypovolemia in POTS-f patients. We conclude that it is possible to identify the mechanism of syncope in POTS patients, and perhaps other patients with orthostatic intolerance and an excessive liability to syncope.

NASA Discipline Number 14-10↗
NASA NTRS1997

Vagal and sympathetic mechanisms in patients with orthostatic vasovagal syncope

BACKGROUND: Autonomic and particularly sympathetic mechanisms play a central role in the pathophysiology of vasovagal syncope. We report direct measurements of muscle sympathetic nerve activity in patients with orthostatic vasovagal syncope. METHODS AND RESULTS: We studied 53 otherwise healthy patients with orthostatic syncope. We measured RR intervals and finger arterial pressures and in 15 patients, peroneal nerve muscle sympathetic activity before and during passive 60 degree head-up tilt, with low-dose intravenous isoproterenol if presyncope did not develop by 15 minutes. We measured baroreflex gain before tilt with regression of RR intervals or sympathetic bursts on systolic or diastolic pressures after sequential injections of nitroprusside and phenylephrine. Orthostatic vasovagal reactions occurred in 21 patients, including 7 microneurography patients. Presyncopal and nonsyncopal patients had similar baseline RR intervals, arterial pressure, and muscle sympathetic nerve activity. Vagal baroreflex responses were significantly impaired at arterial pressures below (but not above) baseline levels in presyncopal patients. Initial responses to tilt were comparable; however, during the final 200 seconds of tilt, presyncopal patients had lower RR intervals and diastolic pressures than nonsyncopal patients and gradual reduction of arterial pressure and sympathetic activity. Frank presyncope began abruptly with precipitous reduction of arterial pressure, disappearance of muscle sympathetic nerve activity, and RR interval lengthening. CONCLUSIONS: Patients with orthostatic vasovagal reactions have impaired vagal baroreflex responses to arterial pressure changes below resting levels but normal initial responses to upright tilt. Subtle vasovagal physiology begins before overt presyncope. The final trigger of human orthostatic vasovagal reactions appears to be the abrupt disappearance of muscle sympathetic nerve activity.

Non-NASA Center↗
DOE OSTI2025

Syncopated dynamical decoupling to suppress crosstalk in quantum circuits

Theoretically understanding and experimentally characterizing and modifying the underlying Hamiltonian of a quantum system is of utmost importance in achieving high-fidelity quantum gates for quantum computing. Here, in this work, we explore the use of dynamical decoupling (DD) in characterizing and suppressing undesired two-qubit couplings as well as the underlying single-qubit decoherence, both significant hurdles to achieving precise quantum control and realizing quantum computing on many hardware prototypes. Through discrete search of DD sequences, we identify sequences that protect against decoherence and selectively target unwanted two-qubit interactions of general form. On a transmon-qubit-based superconducting quantum device, we identify separate white and 1/𝑓 noise components underlying the single-qubit decoherence and a static ZZ coupling between pairs of qubits. A family of syncopated DD sequences is found and their efficiency is demonstrated in two-qubit benchmarking experiments. The syncopated decoupling technique significantly boosts performance in a realistic algorithmic quantum circuit.

97 MATHEMATICS AND COMPUTING↗
NASA NTRS1994

Microneurographic evidence of sudden sympathetic withdrawal in carotid sinus syncope; treatment with ergotamine

A proportion of patients with carotid sinus syncope (CSS) remain symptomatic even after pacemaker implantation because of persistence of a vasodepressor component. We report a patient with CSS whose syncopal episodes could be reproduced by carotid sinus massage and were due to profound hypotension associated with sudden sympathetic withdrawal, based on direct measurements of sympathetic nerve traffic. A double-blind trial with inhaled ergotamine provided significant symptomatic relief.

Non-NASA Center↗
NASA NTRS1979

Recovering the spectrum of a narrow-band process from syncopated samples

A nonuniform sampling strategy, phase quadrature sampling, in which a process of bandwith B is sampled at rate B in each of two channels where the two channels are pi/2 out of phase at frequency B is described. Phase quadrature sampling is a special case of sampling, where the phase between channels is fixed but arbitrary. A simple method for recovering the spectrum of the input process from syncopated samples is derived. The derivation indicates what values of phase between channels result in lossless sampling.

Milenkovic, P. H.↗
NASA NTRS1997

Hypovolemia in syncope and orthostatic intolerance role of the renin-angiotensin system

PURPOSE: Orthostatic intolerance is the cause of significant disability in otherwise normal patients. Orthostatic tachycardia is usually the dominant hemodynamic abnormality, but symptoms may include dizziness, visual changes, discomfort in the head or neck, poor concentration, fatigue, palpitations, tremulousness, anxiety and, in some cases, syncope. It is the most common disorder of blood pressure regulation after essential hypertension. There is a predilection for younger rather than older adults and for women more than men. Its cause is unknown; partial sympathetic denervation or hypovolemia has been proposed. METHODS AND MATERIALS: We tested the hypothesis that reduced plasma renin activity, perhaps from defects in sympathetic innervation of the kidney, could underlie a hypovolemia, giving rise to these clinical symptoms. Sixteen patients (14 female, 2 male) ranging in age from 16 to 44 years were studied. Patients were enrolled in the study if they had orthostatic intolerance, together with a raised upright plasma norepinephrine (> or = 600 pg/mL). Patients underwent a battery of autonomic tests and biochemical determinations. RESULTS: There was a strong positive correlation between the blood volume and plasma renin activity (r = 0.84, P = 0.001). The tachycardic response to upright posture correlated with the severity of the hypovolemia. There was also a correlation between the plasma renin activity measured in these patients and their concomitant plasma aldosterone level. CONCLUSIONS: Hypovolemia occurs commonly in orthostatic intolerance. It is accompanied by an inappropriately low level of plasma renin activity. The degree of abnormality of blood volume correlates closely with the degree of abnormality in plasma renin activity. Taken together, these observations suggest that reduced plasma renin activity may be an important pathophysiologic component of the syndrome of orthostatic intolerance.

Non-NASA Center↗
NASA NTRS1973

A study of ventricular contractility and other parameters possibly related to vasodepressor syncope

The effects of diminished orthostatic and exercise tolerance resulting from prolonged bedrest were studied by noninvasion methods to determine if alterations in myocardial contractility were induced by bedrest. These methods were apexcardiography, systolic time intervals, and echocardiography. It is concluded that bedrest causes detrimental alterations in the contractile state of the myocardium which accounts for the decreases in maximal oxygen uptaken during exercise after bedrest. Tabulated test data are included.

Hyatt, K. H.↗
NASA NTRS2000

Bed Rest and Orthostatic-Hypotensive Intolerance

Orthostatic tolerance may be defined as the ability of humans to maintain cerebral perfusion and consciousness upon movement from a supine or sitting position to the upright posture; for example, subjects can stand suddenly or be tilted to the head-up body position. Similar but not identical physiological responses can be induced by positive G(sub Z) (head to foot) acceleration or exposure to lower body negative pressure (LBNP). The objective is to suddenly shift blood to the lower body to determine how effectively cardiovascular and neural-hormonal compensatory responses react to maintain blood pressure. In the most precise method for measuring tolerance, individuals would be stressed until they faint (syncope). However, the potential consequences and discomforts of such a test usually prohibit such a procedure so that few investigators actually induce syncope. In a more common approach, subjects are exposed to a given level of stress, for example, head-up tilt for 15 min, and any increases in heart rate or decreases in blood pressure are interpreted as indicators of progress toward syncope. Presumably, the greater the perturbation of heart rate and blood pressure, the closer to "tolerance," i.e., point of unconsciousness. Another more appropriate approach is to induce a progressively increasing hypotensive stress until pre-determined physiological responses or pre-syncopal symptoms appear. The physiological criteria may include a sudden drop in systolic blood pressure (greater than 25 mm/min), a sudden drop in heart rate (greater than 15 beats/min), or a systolic blood pressure less than 70 mmHg. The most common pre-syncopal symptoms include lightheadedness, stomach awareness or distress, feelings of warmth, tingly skin, and light to profuse sweating. Usually a combination of physiological responses and symptoms occurs such that, on different days, the tolerance time to the same orthostatic protocol is reproducible for a given individual. The assumption is that by taking subjects to near fainting, one can determine their tolerance. This latter pre-syncopal approach is better for estimating orthostatic or hypotensive tolerance than the former measurement of heart rate and blood pressure responses to a given stress. There is considerable variability in individual responses to orthostasis. For example, some subjects are "heart-rate responders" and have a pronounced cardiovascular response similar to that when performing moderately hard aerobic exercise, whereas others may experience pre-syncopal symptoms with very little increase in heart rate. Some individuals have a slow, gradual fall in blood pressure to orthostasis, and others have little change in blood pressure until a sudden precipitous fall in pressure occurs just prior to fainting. With both tilt and LBNP tests there is a low correlation between heart-rate or blood-pressure responses to a sub-tolerance stress as a measure of pre-syncopal limited orthostatic-hypotensive tolerance.

Schneider, Suzanne M.↗
NASA NTRS1994

Cerebral versus systemic hemodynamics during graded orthostatic stress in humans

BACKGROUND: Orthostatic syncope is usually attributed to cerebral hypoperfusion secondary to systemic hemodynamic collapse. Recent research in patients with neurocardiogenic syncope has suggested that cerebral vasoconstriction may occur during orthostatic hypotension, compromising cerebral autoregulation and possibly contributing to the loss of consciousness. However, the regulation of cerebral blood flow (CBF) in such patients may be quite different from that of healthy individuals, particularly when assessed during the rapidly changing hemodynamic conditions associated with neurocardiogenic syncope. To be able to interpret the pathophysiological significance of these observations, a clear understanding of the normal responses of the cerebral circulation to orthostatic stress must be obtained, particularly in the context of the known changes in systemic and regional distributions of blood flow and vascular resistance during orthostasis. Therefore, the specific aim of this study was to examine the changes that occur in the cerebral circulation during graded reductions in central blood volume in the absence of systemic hypotension in healthy humans. We hypothesized that cerebral vasoconstriction would occur and CBF would decrease due to activation of the sympathetic nervous system. We further hypothesized, however, that the magnitude of this change would be small compared with changes in systemic or skeletal muscle vascular resistance in healthy subjects with intact autoregulation and would be unlikely to cause syncope without concomitant hypotension. METHODS AND RESULTS: To test this hypothesis, we studied 13 healthy men (age, 27 +/- 7 years) during progressive lower body negative pressure (LBNP). We measured systemic flow (Qc is cardiac output; C2H2 rebreathing), regional forearm flow (FBF; venous occlusion plethysmography), and blood pressure (BP; Finapres) and calculated systemic (SVR) and forearm (FVR) vascular resistances. Changes in brain blood flow were estimated from changes in the blood flow velocity in the middle cerebral artery (VMCA) using transcranial Doppler. Pulsatility (systolic minus diastolic/mean velocity) normalized for systemic arterial pressure pulsatility was used as an index of distal cerebral vascular resistance. End-tidal PACO2 was closely monitored during LBNP. From rest to maximal LBNP before the onset of symptoms or systemic hypotension, Qc and FBF decreased by 29.9% and 34.4%, respectively. VMCA decreased less, by 15.5% consistent with a smaller decrease in CBF. Similarly, SVR and FVR increased by 62.8% and 69.8%, respectively, whereas pulsatility increased by 17.2%, suggestive of a mild degree of small-vessel cerebral vasoconstriction. Seven of 13 subjects had presyncope during LBNP, all associated with a sudden drop in BP (29 +/- 9%). By comparison, hyperventilation alone caused greater changes in VMCA (42 +/- 2%) and pulsatility but never caused presyncope. In a separate group of 3 subjects, superimposition of hyperventilation during highlevel LBNP caused a further decrease in VMCA (31 +/- 7%) but no change in BP or level of consciousness. CONCLUSIONS: We conclude that cerebral vasoconstriction occurs in healthy humans during graded reductions in central blood volume caused by LBNP. However, the magnitude of this response is small compared with changes in SVR or FVR during LBNP or other stimuli known to induce cerebral vasoconstriction (hypocapnia). We speculate that this degree of cerebral vasoconstriction is not by itself sufficient to cause syncope during orthostatic stress. However, it may exacerbate the decrease in CBF associated with hypotension if hemodynamic instability develops.

NASA Discipline Cardiopulmonary↗
NASA NTRS1995

Simultaneous cerebrovascular and cardiovascular responses during presyncope

BACKGROUND AND PURPOSE: Presyncope, characterized by symptoms and signs indicative of imminent syncope, can be aborted in many situations before loss of consciousness occurs. The plasticity of cerebral autoregulation in healthy humans and its behavior during this syncopal prodrome are unclear, although systemic hemodynamic instability has been suggested as a key factor in the precipitation of syncope. Using lower body negative pressure (LBNP) to simulate central hypovolemia, we previously observed falling mean flow velocities (MFVs) with maintained mean arterial blood pressure (MABP). These findings, and recent reports suggesting increased vascular tone within the cerebral vasculature at presyncope, cannot be explained by the classic static cerebral autoregulation curve; neither can they be totally explained by a recent suggestion of a rightward shift in this curve. METHODS: Four male and five female healthy volunteers were exposed to presyncopal LBNP to evaluate their cerebrovascular and cardiovascular responses by use of continuous acquisition of MFV from the right middle cerebral artery with transcranial Doppler sonography, MABP (Finapres), and heart rate (ECG). RESULTS: At presyncope, MFV dropped on average by 27.3 +/- 14% of its baseline value (P < .05), while MABP remained at 2.0 +/- 27% above its baseline level. Estimated cerebrovascular resistance increased during LBNP. The percentage change from baseline to presyncope in MFV and MABP revealed consistent decreases in MFV before MABP. CONCLUSIONS: Increased estimated cerebrovascular resistance, falling MFV, and constant MABP are evidence of an increase in cerebral vascular tone with falling flow, suggesting a downward shift in the cerebral autoregulation curve. Cerebral vessels may have a differential sensitivity to sympathetic drive or more than one type of sympathetic innervation. Future work to induce dynamic changes in MABP during LBNP may help in assessing the plasticity of the cerebral autoregulation mechanism.

Non-NASA Center↗
NASA NTRS2007

Medical Monitoring during Short Radius Centrifugation in Bed-rested Subjects

The artificial gravity pilot project was designed to investigate the efficacy of daily exposure to a Gz acceleration gradient for counteracting the physiologic decrements induced by prolonged bed rest. A short radius centrifuge was used to produce a Gz gradient such that 1 g was applied at the level of the subject s heart and 2.5 g at the feet. For inclusion in the study, subjects were required to complete a 75-minute screening spin on the centrifuge. During the study, each active treatment subject was scheduled for a 60-minute spin each day for 20 consecutive days. During centrifugation, subjects were continuously monitored by a physician for signs and symptoms of pre-syncope, motion sickness, arrhythmias, joint/muscle pain and any other unanticipated problems. The physician was also present to provide emergency care in the case of a medical emergency. Cameras mounted on the centrifuge were used to provide a means of observing the subject s face and torso. Audio communication was continuously maintained. Other monitoring tools included two-lead EKG tracings, pulse oximetry, intermittent sphygmomanometer readings, lights in the peripheral visual field, and continuous blood pressure readout from a tonometry device. Thirty screening runs were attempted using twenty-seven subjects. Seven of these runs were terminated early for symptoms of pre-syncope, motion sickness, or GI distress. A total of eight subjects completed the active treatment arm of the study. Of the 160 centrifuge runs that were scheduled for these eight treatment subjects, 152 were completed, seven were terminated early, and one was not attempted. Of the seven early terminations, four were related to symptoms of pre-syncope, one to leg pain, one to GI discomfort, and one to equipment failure. Three terminations for adverse symptoms occurred on the first treatment day. Three terminations occurred on day nineteen of treatment and within 24 hours after scheduled soleus and quadriceps muscle biopsies. We have summarized the relative usefulness of the information obtained by the various monitoring modalities in making a decision to terminate a centrifuge run. The video and audio communication information was essential to the decision-making process. Heart rate and EKG tracings are considered valuable, even though no spins were terminated due to significant arrhythmias. The tonometer device was generally not reliable in this application. Our observations suggest that subjects may be less tolerant of centrifugation just after starting bed rest and after invasive procedures.

Reinertson, Randal↗
NASA NTRSDate not supplied

Dynamical Decoupling for Measuring and Suppressing Crosstalk

Dynamical decoupling (DD) is a noise-mitigating strategy in which sequences of pulses are applied to single qubits to average out their interaction with the environment. DD has been extensively studied and demonstrated for suppressing single-qubit decoherence and can be tailored for different noise spectrum. We report another important adaptation of DD where crosstalk between qubits are suppressed. We demonstrate the efficiency of this procedure on quantum circuits on superconducting transmon-based quantum devices. We designed a family of syncopated DD sequences that effectively suppress ZZ coupling between qubit pairs, which is the dominating crosstalk form on the device. We insert DD to a quantum circuit whenever single qubits are idle (often during two-qubits gates on other qubits). While standard periodic DD suppress crosstalk between these qubits and their neighbors, the syncopated DD further decouples crosstalk between these qubits. We further designed short sequences that maximize the application of DD without adding time to the quantum circuit execution. Such DD sequences yield significant improvement of the performance of the algorithm on the hardware. The performance is further boosted by combining DD with another mitigation strategy, randomized compilation. Our work demonstrated that syncopated DD is effective and practical way to suppress crosstalk in quantum circuits and serves as a great probe to characterize the crosstalk and inform hardware design.

Quantum Computing↗
DOE OSTI2021

Classification of orthostatic intolerance through data analytics

Imbalance in the autonomic nervous system can lead to orthostatic intolerance manifested by dizziness, lightheadedness, and a sudden loss of consciousness (syncope); these are common conditions, but they are challenging to diagnose correctly. Uncertainties about the triggering mechanisms and the underlying pathophysiology have led to variations in their classification. This study uses machine learning to categorize patients with orthostatic intolerance. Here we use random forest classification trees to identify a small number of markers in blood pressure, and heart rate time-series data measured during head-up tilt to (a) distinguish patients with a single pathology and (b) examine data from patients with a mixed pathophysiology. Next, we use Kmeans to cluster the markers representing the time-series data. We apply the proposed method analyzing clinical data from 186 subjects identified as control or suffering from one of four conditions: postural orthostatic tachycardia (POTS), cardioinhibition, vasodepression, and mixed cardioinhibition and vasodepression. Classification results confirm the use of supervised machine learning. We were able to categorize more than 95% of patients with a single condition and were able to subgroup all patients with mixed cardioinhibitory and vasodepressor syncope. Clustering results confirm the disease groups and identify two distinct subgroups within the control and mixed groups. The proposed study demonstrates how to use machine learning to discover structure in blood pressure and heart rate time-series data. The methodology is used in classification of patients with orthostatic intolerance. Diagnosing orthostatic intolerance is challenging, and full characterization of the pathophysiological mechanisms remains a topic of ongoing research. This study provides a step toward leveraging machine learning to assist clinicians and researchers in addressing these challenges.

60 APPLIED LIFE SCIENCES↗
NASA NTRS2002

Cerebral blood flow velocity declines before arterial pressure in patients with orthostatic vasovagal presyncope

OBJECTIVES: We studied hemodynamic changes leading to orthostatic vasovagal presyncope to determine whether changes of cerebral artery blood flow velocity precede or follow reductions of arterial pressure. BACKGROUND: Some evidence suggests that disordered cerebral autoregulation contributes to the occurrence of orthostatic vasovagal syncope. We studied cerebral hemodynamics with transcranial Doppler recordings, and we closely examined the temporal sequence of changes of cerebral artery blood flow velocity and systemic arterial pressure in 15 patients who did or did not faint during passive 70 degrees head-up tilt. METHODS: We recorded photoplethysmographic arterial pressure, RR intervals (electrocardiogram) and middle cerebral artery blood flow velocities (mean, total, mean/RR interval; Gosling's pulsatility index; and cerebrovascular resistance [mean cerebral velocity/mean arterial pressure, MAP]). RESULTS: Eight men developed presyncope, and six men and one woman did not. Presyncopal patients reported light-headedness, diaphoresis, or a sensation of fatigue 155 s (range: 25 to 414 s) before any cerebral or systemic hemodynamic change. Average cerebral blood flow velocity (CBFV) changes (defined by an iterative linear regression algorithm) began 67 s (range: 9 to 198 s) before reductions of MAP. Cerebral and systemic hemodynamic measurements remained constant in nonsyncopal patients. CONCLUSIONS: Presyncopal symptoms and CBFV changes precede arterial pressure reductions in patients with orthostatic vasovagal syncope. Therefore, changes of cerebrovascular regulation may contribute to the occurrence of vasovagal reactions.

Non-NASA Center↗
NASA NTRS1994

Orthostatic responses to dietary sodium restriction during heat acclimation

Several studies have shown that individuals consuming low-salt diets and working in the heat have an increased risk or incidence of heat injury, suggestive of inadequate cardiovascular adjustment. Furthermore, others have shown that prolonged work in hot climates can precipitate orthostatic hypotension and syncope. This study was designed to evaluate the effects of moderate-salt (MS) and low-salt (LS) diets on the circulatory responses and incidence of presyncopal symptoms to an orthostatic test (OT) during successive days of heat acclimation (HA). Seventeen unacclimatized male soldiers (mean +/- SE: age 20+/-1 yrs) participated in this two-phase study. The first phase consisted of a seven day dietary stabilization period during which all subjects consumed similar diets of about 4000 kcal/day containing 8g NaCl and lived in a dormitory setting (21 C, 30% RH). The second phase commenced on day eight and consisted of dietary NaCl restriction and 10 days HA (days 8-17). Volunteers were randomly assigned to either the MS diet (n=9) providing 8g NaCl/day or the LS diet (n=8) furnishing just 4g NaCl/day. The acquisition of HA was manifested in both groups by reductions in exercising rectal temperature and heart rate (HR); these characteristics were similar in the MS and LS diets. The OT was performed at 21 C on day seven of the stabilization phase and on days 9, 11, 13, 15, and 17 of the HA phase, before and after 8.5 hr of intermittent treadmill walking in a hot environment. Blood pressure (BP) and HR responses at 1,2, and 4 min and any presyncopal symptoms were recorded after assuming an upright position from recumbency. All subjects completed the OT before and after prolonged exercise in the heat without incidence of either hypotension or presyncopal symptoms irrespective of dietary-salt intake and day of HA. The results indicate that the prolonged work in the heat can be performed without orthostatic hypotension or syncope while consuming 4g NaCl/day with adequate fluid replacement. Furthermore, the circulatory responses to OT showed no improvement with successive days of HA irrespective of dietary-salt intake.

Szlyk, Patricia C.↗
NASA NTRS1992

Comparison of saline and fludrocortisone as fluid-loading countermeasures following exposure to simulated microgravity

Saline loading (SL) within hours of reentry is currently used as a countermeasure against postflight orthostatic hypotension in astronauts. However, its effects on blood volume expansion is not quantified and its effectiveness has proved marginal at best. The purposes of the present study were: (1) to quantify the effects of SL on plasma volume and orthostatic tolerance following exposure to simulated microgravity and (2) to compare these effects with the use of a pharacological fluid expander, fludrcortisone (F). Method: Eleven men (30-45 yr.) underwent a 15-minute stand test before and immediately after 7 days of head-down bedrest (BR). Five subjects ingested SL (8 g salt tablets with 1 liter of water) 2 hours before standing at the end of BR while the other 6 subjects received 0.2 mg oral doses of F at 0800 and 2200 hours the day before and 0800 hours the day the subjects got out of bed (i.e., 2 hours before standing). Plasma volume (PV) was measured before BR on day 7 of BR and after the final SL and F treatments just before the post-BR stand test. Blood pressure and heart rate were measured continuously during the stand tests. Results: BR decreased PV from 40.7 plus or minus 1.9 mml/kg to 35.9 plus or minus 1.1 ml/kg (minus 11.8 percent P less than 0.05). Following SL, PV remained at 36.4 plus or minus 1.5 ml/kg while F returned PV to 39.1 plus or minus 1.8 ml/kg. The post BR stand test was completed without syncopal symptoms by 5 of 6 F subjects but only 2 of 5 SL subjects. Conclusions: SL may be ineffective in restoring PV to preflight levels and may provide inadequate protection against postflight orthostatic hypotension. In contrast, F may provide a promising countermeasure since it restored PV and reduced the incidence of syncope following exposure to simulated microgravity in the present study.

Vernikos, J.↗
NASA NTRS1996

Effect of +Gz Acceleration on the Oxygen Uptake-Excercise Load Relationship during Lower Extremity Ergometer Excercise

Long term spaceflight and habitation of a space station and/or the moon require that astronauts be provided with sufficient environmental and physiological support so that they can not only function in microgravity but be returned to earth safely. As the duration of habitation in microgravity increase the effects of the concomitant deconditioning of body systems becomes a concern for added exercise in space and for reentry to Earth gravity. Many countermeasures have been proposed to maintain proper functioning of the body, but none have proved sufficient, especially when the cost of crew time spent in these activities is considered. The issue of appropriate countermeasures remains unresolved. Spaceflight deconditioning decreases tolerance to +Gz acceleration, head to foot, the direction which is experienced during reentry; the result is that the crew member is more prone to becoming pre-syncopal or syncopal, thus exacerbating the orthostatic intolerance. All ground-based research using microgravity analogues has produced this same lowered G tolerance. When intermittent exposure to +1 to +4 Gz acceleration training was used, some alleviation of orthosatic intolerance and negative physiological effects of deconditioning occurred. Exercise alone was not as effective; but the added G force was. The physiological responses to acceleration added to exercise training have not been clearly shown. We will test the hypothesis that there will be no difference in the exercise oxygen uptake-exercise load relationship with added +Gz acceleration. We wi also compare oxygen uptake during graded exercise-acceleration loads in the human-powered short arm centrifuge with those from normal supine exercise loads. The human-powered short arm centrifuge was built by NASA engineers at Ames Research Center.

Jackson, Catherine G. R.↗
NASA NTRS1999

Low LBNP Tolerance in Men is Associated With Attenuated Activation of Renin-Angiotensin System

Vasoactive hormone concentrations (epinephrine (pE), norepinephrine (pNE), angiotensin II (pATII), vasopressin (pVP), endothelin 1 (pET1)] and plasma renin activity (pRA) were measured during lower body negative pressure (LBNP) to test the hypothesis that responsiveness of the reninangiotensin system is related to LBNP tolerance. Healthy men (2,822 cal per day, 2 mmol per kilogram per day Na (+)) were exposed to 30 min of progressive LBNP to -50mmHg. LBNP was uneventful for 7 men (2512 yr, HiTol group), but 8 men (26 plus or minus 3 yr) reached pre-syncope after 11 plus or minus 1 min (P less than 0.001, LoTol group). Mean arterial pressure was unchanged. Central venous pressure and left atrial diameter decreased in both groups (5-6 mmHg by 30%, P less than 0.05). Control [hormone] were similar but, pRA differed between groups (LoTol 0.6 plus or minus 0.1, HiTol 1.2 plus or minus 0.1 ng Ang1 per milliliter per hour, per hour, P less than 0.05). LBNP increased (P less than 0.05) pRA and pATII more in HiTol (9.9 plus or minus 2.2 ng Ang1 per milliliter per hour and 58 plus or minus 12 pg per milliliter) than LoTol (4.3 plus or minus 0.9 ng Angl per milliliter per hour and 28 plus or minus 6 pg per milliliter). In contrast, pVP was higher (P less than 0.05) in LoTol than in HiTol. The response of the renin-angiotensin system seems linked to the occurrence of pre-syncope, and measurement of resting pRA may be predictive.

Greenleaf, John E.↗