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At least 109 records · Page 6

Fluid Redistribution and Heart Rate in Humans During Whole-Body Tilting, G(z) Centrifugation, and Lower Body Negative Pressure

Gravity creates blood pressure gradients which redistribute body fluids towards the feet. Positive G(z) centrifugation and lower body negative pressure (LBNP) have been proposed to simulate these and other effects of gravity during long-term existence in microgravity. We hypothesized that the magnitude of upper-to-lower body fluid redistribution would increase according to the following order: short-arm centrifugation (SAC), long-arm centrifugation (LAC), head-up tilt (HUT), and LBNP. To test this hypothesis, we employed strain gauge plethysmography of the neck, thigh and calf during HUT and supine SAC and LAC up to lG(z) at the feet, and during supine LBNP to 100 mm Hg. Supine 100 mm Hg LBNP generates footward force and produces transmural blood pressures in the foot approximately equal to 1 G(z) (90 deg) HUT. Heart rate was measured via cardiotachometry. Control measurements were made while supine. SAC and LAC elicited similar increases in thigh volume at 1 G(z) (2.3 +/- 0.4 and 2.1 +/- 0.1%, respectively; mean +/- se, n greater than or equal to 7). At 100 mm Hg LBNP, thigh volume increased (3.4 +/- 0.3%) significantly more than during l G(z) centrifugation (p less than 0.05). Surprisingly, due to a paradoxical 0.6% reduction of thigh volume between 0.8 and 1.0 G(z) HUT, thigh volume was increased only 0.6 +/- 0.3% at 1 G(z) HUT. The calf demonstrated similar, although less definitive, responses to the various gravitational stimuli. Neck volume tended to decrease less during HUT than during the other stimuli. Heart rate increased similarly during HUT (18 +/- 2 beats/min) and LAC (12 +/- 2 beats/min), and exhibited still greater elevation during LBNP (29 +/- 4 beats/min), yet did not increase during SAC. These results suggest upright posture activates mechanisms that counteract footward fluid redistribution which are not activated during supine applications of simulated gravity. LAC more closely approximated effects of normal gravity (HUT) than LBNP. Therefore, when considering LBNP to simulate gravity, these findings support efforts to reduce the cardiovascular stress imposed by LBNP, while preserving the gravity-like force generated by LBNP.

Watenpaugh, D. E.↗

Autonomic neural control of dynamic cerebral autoregulation in humans

BACKGROUND: The purpose of the present study was to determine the role of autonomic neural control of dynamic cerebral autoregulation in humans. METHODS AND RESULTS: We measured arterial pressure and cerebral blood flow (CBF) velocity in 12 healthy subjects (aged 29+/-6 years) before and after ganglion blockade with trimethaphan. CBF velocity was measured in the middle cerebral artery using transcranial Doppler. The magnitude of spontaneous changes in mean blood pressure and CBF velocity were quantified by spectral analysis. The transfer function gain, phase, and coherence between these variables were estimated to quantify dynamic cerebral autoregulation. After ganglion blockade, systolic and pulse pressure decreased significantly by 13% and 26%, respectively. CBF velocity decreased by 6% (P<0.05). In the very low frequency range (0.02 to 0.07 Hz), mean blood pressure variability decreased significantly (by 82%), while CBF velocity variability persisted. Thus, transfer function gain increased by 81%. In addition, the phase lead of CBF velocity to arterial pressure diminished. These changes in transfer function gain and phase persisted despite restoration of arterial pressure by infusion of phenylephrine and normalization of mean blood pressure variability by oscillatory lower body negative pressure. CONCLUSIONS: These data suggest that dynamic cerebral autoregulation is altered by ganglion blockade. We speculate that autonomic neural control of the cerebral circulation is tonically active and likely plays a significant role in the regulation of beat-to-beat CBF in humans.

Non-NASA Center↗

Neural Control of the Cardiovascular System in Space

During the acute transition from lying supine to standing upright, a large volume of blood suddenly moves from the chest into the legs. To prevent fainting, the blood pressure control system senses this change immediately, and rapidly adjusts flow (by increasing heart rate) and resistance to flow (by constricting the blood vessels) to restore blood pressure and maintain brain blood flow. If this system is inadequate, the brain has a backup plan. Blood vessels in the brain can adjust their diameter to keep blood flow constant. If blood pressure drops, the brain blood vessels dilate; if blood pressure increases, the brain blood vessels constrict. This process, which is called autoregulation, allows the brain to maintain a steady stream of oxygen, even when blood pressure changes. We examined what changes in the blood pressure control system or cerebral autoregulation contribute to the blood pressure control problems seen after spaceflight. We asked: (1) does the adaptation to spaceflight cause an adaptation in the blood pressure control system that impairs the ability of the system to constrict blood vessels on return to Earth?; (2) if such a defect exists, could we pinpoint the neural pathways involved?; and (3) does cerebral autoregulation become abnormal during spaceflight, impairing the body s ability to maintain constant brain blood flow when standing upright on Earth? We stressed the blood pressure control system using lower body negative pressure, upright tilt, handgrip exercise, and cold stimulation of the hand. Standard cardiovascular parameters were measured along with sympathetic nerve activity (the nerve activity causing blood vessels to constrict) and brain blood flow. We confirmed that the primary cardiovascular effect of spaceflight was a postflight reduction in upright stroke volume (the amount of blood the heart pumps per beat). Heart rate increased appropriately for the reduction in stroke volume, thereby showing that changes in heart rate regulation alone cannot be responsible for orthostatic hypotension after spaceflight. All of the astronauts in our study had an increase in sympathetic nerve activity during upright tilting on Earth postflight. This increase was well calibrated for the reduction in stroke volume induced by the upright posture. The results obtained from stimulating the sympathetic nervous system using handgrip exercise or cold stress were also entirely normal during and after spaceflight. No astronaut had reduced cerebral blood flow during upright tilt, and cerebral autoregulation was normal or even enhanced inflight. These experiments show that the cardiovascular adaptation to spaceflight does not lead to a defect in the regulation of blood vessel constriction via sympathetic nerve activity. In addition, cerebral autoregulation is well-maintained. It is possible that despite the increased sympathetic nerve activity, blood vessels did not respond with a greater degree of constriction than occurred preflight, possibly uncovering a limit of vasoconstrictor reserve.

Levine, Benjamin D.↗

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.↗

Role of physical countermaneuvers in the management of orthostatic hypotension: efficacy and biofeedback augmentation

OBJECTIVE: To evaluate the efficacy of various physical countermaneuvers in reducing orthostatic hypotension and its associated symptoms and to assess the efficacy of biofeedback training in enhancing the effectiveness of physical countermaneuvers. MATERIAL AND METHODS: In nine study subjects with neurogenic orthostatic hypotension, four training sessions on physical countermaneuvers were performed after tilt-up, three with visual feedback on the effect of physical countermaneuvers on blood pressure and other cardiovascular variables. Blood pressure change and orthostatic symptoms during tilt-up were determined, as were the changes in total peripheral resistance, stroke index, and heart rate. RESULTS: The five female and four male patients had a mean age of 53 years and a mean duration of symptoms of 4.2 years. On an orthostatic symptom scale of 0 to 10, these patients had a mean symptom score of 7.3. The increment in systolic blood pressure was better for some maneuvers (such as leg crossing and a combination) than others (such as neck flexion and abdominal contraction). Three patterns of responses to biofeedback were found. Simple maneuvers such as squatting did not improve with training; visual feedback was needed for maneuvers such as thigh contraction, and performance declined without biofeedback; the third pattern, seen in maneuvers such as leg crossing, showed continued improvement with training, even without biofeedback. A survey at 3 to 4 months after training revealed continued use of physical maneuvers (3.8 +/- 3.1 per day), increased standing time with each episode of presyncopal symptoms (8.3 +/- 5.8 minutes), and continued global symptomatic improvement. Total peripheral resistance, but not heart rate or stroke index, showed significant regression with blood pressure improvement. CONCLUSION: Physical countermaneuvers are efficacious in reducing orthostatic hypotension, can be augmented by use of biofeedback, and may significantly improve the functional outcome. The major mechanism of improvement is an increase in total peripheral resistance, presumably by reducing the vascular capacitance.

NASA Program Space Physiology and Countermeasures↗

Pressure ramp programmer; IMBLMS Phase B4 Additional Tasks: Task 3.0 pressure ramp programmer

A pressure ramp programmer model was designed, fabricated and tested. This model, in conjunction with an automatic blood pressure monitor, automatically controls the pressure in the blood pressure monitor arterial cuff. The cuff pressurization cycle is designed to maximize accuracy and repeatability of blood pressure measurements. The key feature of this automatic cycle is rapid blood pressure cuff bleed down from an initial setting until systolic (diastolic) pressure is encountered followed by a short repressurization and slow bleed, long enough to permit accurate systolic (diastolic) pressure determination. The system includes a pressure reservoir which bleeds the cuff through a precision needle valve; a solenoid valve which permits rapid pressurization from the reservoir; and a pressure sensor which provides information for bleed rate and set point controls. Korotkoff sound signals from a microphone in the blood pressure cuff (not part of the system) provide decision information to the digital control system. The system completed a series of engineering tests using simulated Korotkoff sound inputs. The system performed successfully in all cases and was stable over an extended period of time.

Fogal, G. L.↗

Vestibulosympathetic reflex during orthostatic challenge in aging humans

Aging attenuates the increase in muscle sympathetic nerve activity (MSNA) and elicits hypotension during otolith organ engagement in humans. The purpose of the present study was to determine the neural and cardiovascular responses to otolithic engagement during orthostatic stress in older adults. We hypothesized that age-related impairments in the vestibulosympathetic reflex would persist during orthostatic challenge in older subjects and might compromise arterial blood pressure regulation. MSNA, arterial blood pressure, and heart rate responses to head-down rotation (HDR) performed with and without lower body negative pressure (LBNP) in prone subjects were measured. Ten young (27 +/- 1 yr) and 11 older subjects (64 +/- 1 yr) were studied prospectively. HDR performed alone elicited an attenuated increase in MSNA in older subjects (Delta106 +/- 28 vs. Delta20 +/- 7% for young and older subjects). HDR performed during simultaneous orthostatic stress increased total MSNA further in young (Delta53 +/- 15%; P < 0.05) but not older subjects (Delta-5 +/- 4%). Older subjects demonstrated consistent significant hypotension during HDR performed both alone (Delta-6 +/- 2 mmHg) and during LBNP (Delta-7 +/- 2 mmHg). These data provide experimental support for the concept that age-related impairments in the vestibulosympathetic reflex persist during orthostatic challenge in older adults. Furthermore, these findings are consistent with the concept that age-related alterations in vestibular function might contribute to altered orthostatic blood pressure regulation with age in humans.

Clinical Trial↗

Exploring Heart and Lung Function in Space: ARMS Experiments

The Advanced Respiratory Monitoring System (ARMS) is a suite of monitoring instruments and supplies used to study the heart, lungs, and metabolism. Many experiments sponsored by the European Space Agency (ESA) will be conducted using ARMS during STS-107. The near-weightless environment of space causes the body to undergo many physiological adaptations, and the regulation of blood pressure is no exception. Astronauts also experience a decrease in blood volume as an adaptation to microgravity. Reduced blood volume may not provide enough blood pressure to the head during entry or landing. As a result, astronauts often experience light-headedness, and sometimes even fainting, when they stand shortly after returning to Earth. To help regulate blood pressure and heart rate, baroreceptors, sensors located in artery walls in the neck and near the heart, control blood pressure by sending information to the brain and ensuring blood flow to organs. These mechanisms work properly in Earth's gravity but must adapt in the microgravity environment of space. However, upon return to Earth during entry and landing, the cardiovascular system must readjust itself to gravity, which can cause fluctuation in the control of blood pressure and heart rate. Although the system recovers in hours or days, these occurrences are not easily predicted or understood - a puzzle investigators will study with the ARMS equipment. In space, researchers can focus on aspects of the cardiovascular system normally masked by gravity. The STS-107 experiments using ARMS will provide data on how the heart and lungs function in space, as well as how the nervous system controls them. Exercise will also be combined with breath holding and straining (the Valsalva maneuver) to test how heart rate and blood pressure react to different stresses. This understanding will improve astronauts' cardiopulmonary function after return to Earth, and may well help Earthbound patients who experience similar effects after long-term bed rest.

Andre Kuipers↗

Absence of arterial baroreflex modulation of skin sympathetic activity and sweat rate during whole-body heating in humans

1. Prior findings suggest that baroreflexes are capable of modulating skin blood flow, but the effects of baroreceptor loading/unloading on sweating are less clear. Therefore, this project tested the hypothesis that pharmacologically induced alterations in arterial blood pressure in heated humans would lead to baroreflex-mediated changes in both skin sympathetic nerve activity (SSNA) and sweat rate. 2. In seven subjects mean arterial blood pressure was lowered (approximately 8 mmHg) and then raised (approximately 13 mmHg) by bolus injections of sodium nitroprusside and phenylephrine, respectively. Moreover, in a separate protocol, arterial blood pressure was reduced via steady-state administration of sodium nitroprusside. In both normothermia and heat-stress conditions the following responses were monitored: sublingual and mean skin temperatures, heart rate, beat-by-beat blood pressure, skin blood flow (laser-Doppler flowmetry), local sweat rate and SSNA (microneurography from peroneal nerve). 3. Whole-body heating increased skin and sublingual temperatures, heart rate, cutaneous blood flow, sweat rate and SSNA, but did not change arterial blood pressure. Heart rate was significantly elevated (from 74 +/- 3 to 92 +/- 4 beats x min(-1); P < 0.001) during bolus sodium nitroprusside-induced reductions in blood pressure, and significantly reduced (from 92 +/- 4 to 68 +/- 4 beats x min(-1); P < 0.001) during bolus phenylephrine-induced elevations in blood pressure, thereby demonstrating normal baroreflex function in these subjects. 4. Neither SSNA nor sweat rate was altered by rapid (bolus infusion) or sustained (steady-state infusion) changes in blood pressure regardless of the thermal condition. 5. These data suggest that SSNA and sweat rate are not modulated by arterial baroreflexes in normothermic or moderately heated individuals.

Clinical Trial↗

Obstructive apnea during sleep is associated with peripheral vasoconstriction

Obstructive apnea during sleep is associated with a substantial transient blood pressure elevation. The mechanism of this pressor response is unclear. In this study we measured muscle sympathetic nerve activity (MSNA), mean arterial pressure (Psa), and mean limb blood velocity as an index of blood flow (MBV, Doppler) and calculated changes in limb vascular resistance during and after apneas during both wakefulness and sleep in patients with the obstructive sleep apnea syndrome. Immediately postapnea during sleep Psa increased significantly compared with the earlier stages of apnea and this was preceded by a rise of MSNA (n = 5). In contrast to blood pressure, MBV remained unchanged. Because resistance = blood pressure/blood flow, limb vascular resistance increased by 29 +/- 8% from late apnea to postapnea (n = 7, p < 0.002). Voluntary breathhold maneuvers during room air exposure evoked similar responses (n = 10). Supplemental oxygen administered via nonrebreather face mask attenuated the MSNA and vasoconstrictor responses to obstructive (n = 2) and voluntary apneas (n = 10). Our data suggest that obstructive apneas in patients with the obstructive apnea syndrome are accompanied by transient limb vasoconstriction. This vasoconstrictor response appears to be, at least in part, mediated by the sympathetic nervous system and may be linked to hypoxia.

NASA Discipline Cardiopulmonary↗

Sympathetic responses to Valsalva's manoeuvre following bed rest

The purpose of this study was to examine whether 14 days of head-down tilt bed rest (HDBR) alters autonomic regulation during Valsalva's manoeuvre (VM) and if this would predict blood pressure control during a 60 degrees head-up tilt (HUT) test. To examine autonomic control of blood pressure, we measured the changes in systolic (delta SBP) and diastolic (delta DBP) blood pressure between baseline and the early straining (Phase IIE) period of VM (20 sec straining to 40 mmHg; N = 7) in conjunction with changes in muscle sympathetic nerve activity (MSNA; microneurography) burst frequency (B/min) and total activity (% delta) from baseline over the 20-sec straining period. MSNA data were successfully recorded from 6 of the 7 individuals. The averaged responses from three repeated VMs performed in the supine position were compared between the pre- and post-HDBR tests. Compared with the pre-HDBR test, a greater reduction in SBP, DBP, and MAP was observed during Phase IIE following HDBR, p < 0.05. The increase in MSNA burst frequency during straining was augmented in the post- compared with the pre-HDBR test, p < 0.0001, as was the Phase IV blood pressure overshoot, p < 0.05. Although all subjects completed the 20-min pre-HDBR tilt test without evidence of hypotension or orthostatic intolerance, the post-HDBR test was stopped early in 5 of the 7 subjects due to systolic hypotension. The responses during the VM suggest that acute autonomic adjustments to rapid blood pressure changes are preserved after bed rest. Furthermore, MSNA and blood pressure responses during VM did not predict blood pressure control during orthostasis following HDBR.

NASA Discipline Musculoskeletal↗

Lower body negative pressure: Third manned Skylab mission

The objective of the Skylab Lower Body Negative Pressure experiment was to determine the extent and the time course of changes in orthostatic tolerance during the weightlessness of space flight and to determine whether in-flight data from the experiment would be useful in predicting the postflight status of orthostatic tolerance. Compared to preflight results, lower body negative pressure produced exaggerated blood pressure and heart rate responses during the first in-flight test of the Skylab 2 crewmen and showed no clear-cut trend toward preflight levels during the 28-day flight. During the second manned mission, Skylab 3, similar exaggeration of blood pressure and heart rate responses occurred during the first in-flight test. Again no definite trend toward preflight values could be seen during the first 28 days but cardiovascular responses to lower body negative pressure appeared to become more stable by the sixth to eighth week of flight. In general, the test results in-flight served to predict quite well the orthostatic tolerance of the individual crewmen in the immediate postflight period.

Johnson, R. L.↗

Comparison of cardiovascular function during the early hours of bed rest and space flight

This paper reviews the cardiovascular responses of six healthy male subjects to 6 hours in a 5 degrees head-down bed rest model of weightlessness, and compares these responses to those obtained when subjects were positioned in head-up tilts of 10 degrees, 20 degrees, and 42 degrees, simulating 1/6, 1/3, and 2/3 G, respectively. Thoracic fluid index, cardiac output, stroke volume, and peak flow were measured using impedance cardiography. Cardiac dimensions and volumes were determined from two-dimensional guided M-mode echocardiograms in the left lateral decubitus position at 0, 2, 4, and 6 hours. Cardiovascular response to a stand test were compared before and after bed rest. The impedance values were related to tilt angle for the first 2 hours of tilt; however, after 3 hours, at all four angles, values began to converge, indicating that cardiovascular homeostatic mechanisms seek a common adapted state, regardless of effective gravity level (tilt angle) up to 2/3 G. Echocardiography revealed that left ventricular end-diastolic and end-systolic volume, stroke volume, ejection fraction, heart rate, and cardiac output had returned to control values by hour 6 for all tilt angles. The lack of a significant immediate change in left ventricular end-diastolic volume, despite decrements in stroke volume (P < .05) and heart rate (not significant), indicates that multiple factors may play a role in the adaptation to simulated hypogravity. The echocardiography data indicated that no angle of tilt, whether head-down or head-up for 4 to 6 hours, mimicked exactly the changes in cardiovascular function recorded after 4 to 6 hours of space flight. Changes in left ventricular end-diastolic volume during space flight and tilt may be similar, but follow a different time course. Nevertheless, head-down tilt at 5 degrees for 6 hours mimics some (stroke volume, systolic and diastolic blood pressure, mean arterial blood pressure, and total resistance), but not all, of the changes occurring in an equivalent time of space flight. The magnitude of the change in the mean heart rate response to standing was greater after six hours of tilt at -5 degrees or 10 degrees. Thus, results from the stand test after 6 hours of bed rest at -5 degrees and 10 degrees, but not at 20 degrees or 42 degrees, are similar to those obtained after space flight.

Space Flight↗

Effect of perturbations and a meal on superior mesenteric artery flow in patients with orthostatic hypotension

Our aims were to evaluate to role of superior mesenteric blood flow in the pathophysiology of orthostatic hypotension in patients with generalized autonomic failure. METHODS: Twelve patients with symptomatic neurogenic orthostatic hypotension and 12 healthy controls underwent superior mesenteric artery flow measurements using Doppler ultrasonography during head-up tilt and tilt plus meal ingestion. Autonomic failure was assessed using standard tests of the function of the sympathetic adrenergic, cardiovagal and postganglionic sympathetic sudomotor function. RESULTS: Superior mesenteric flow volume and time-averaged velocity were similar in patients and controls at supine rest; however, responses to cold pressor test and upright tilt were attenuated (p < 0.05) in patients compared to controls. Head-up tilt after the meal evoked a profound fall of blood pressure and mesenteric blood flow in the patients; the reduction of mesenteric blood flow correlated (r = 0.89) with the fall of blood pressure in these patients, providing another manifestation of failed baroreflexes. We make the novel finding that the severity of postprandial orthostatic hypotension regressed negatively with the postprandial increase in mesenteric flow in patients with orthostatic hypotension. CONCLUSION: Mesenteric flow is under baroreflex control, which when defective, results in, or worsens orthostatic hypotension. Its large size and baroreflexivity renders it quantitatively important in the maintenance of postural normotension. The effects of orthostatic stress can be significantly attenuated by reducing the splanchnic-mesenteric volume increase in response to food. Evaluation of mesenteric flow in response to eating and head-up tilt provide important information on intra-abdominal sympathetic adrenergic function, and the ability of the patient to cope with orthostatic stress.

Non-NASA Center↗