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Search indexed NASA NTRS and DOE OSTI research on propulsion, heat transfer, battery materials and energy systems. Follow report and document links to the original sources.

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At least 109 records · Page 6
All sourcesNASA NTRSDOE OSTI
NASA NTRS1995

'Non-hypotensive' hypovolaemia reduces ascending aortic dimensions in humans

1. The notion that small, 'non-hypotensive' reductions of effective blood volume alter neither arterial pressure nor arterial baroreceptor activity is pervasive in the experimental literature. We tested two hypotheses: (a) that minute arterial pressure and cardiac autonomic outflow changes during hypovolaemia induced by lower body suction in humans are masked by alterations in breathing, and (b) that evidence for arterial baroreflex engagement might be obtained from measurements of thoracic aorta dimensions. 2. In two studies, responses to graded lower body suction at 0 (control), 5, 10, 15, 20 and 40 mmHg were examined in twelve and ten healthy young men, respectively. In the first, arterial pressure (photoplethysmograph), R-R interval, and respiratory sinus arrhythmia amplitude (complex demodulation) were measured during uncontrolled and controlled breathing (constant breathing frequency and tidal volume). In the second, cross-sectional areas of the ascending thoracic aorta were calculated from nuclear magnetic resonance images. 3. Lower body suction with controlled breathing resulted in an increased arterial pulse pressure at mild levels (5-20 mmHg; ANOVA, P < 0.05) and a decreased arterial pulse pressure at moderate levels (40 mmHg; ANOVA, P < 0.05). Both R-R intervals and respiratory sinus arrhythmia were negatively related to lower body suction level, whether group averages (general linear regression, r > 0.92) or individual subjects (orthogonal polynomials, 12 of 12 subjects) were assessed. 4. Aortic pulse area decreased progressively and significantly during mild lower body suction, with 47% of the total decline occurring by 5 mmHg. 5. These results suggest that small reductions of effective blood volume reduce aortic baroreceptive areas and trigger haemodynamic adjustments which are so efficient that alterations in arterial pressure escape detection by conventional means.

NASA Discipline Cardiopulmonary↗
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 NTRS1985

Predictions of cardiovascular responses during STS reentry using mathematical models

The physiological adaptation to weightless exposure includes cardiovascular deconditioning arising in part from a loss of total circulating blood volume and resulting in a reduction of orthostatic tolerance. The crew of the Shuttle orbiter are less tolerant to acceleration forces in the head-to-foot direction during the reentry phase of the flight at a time they must function at a high level of performance. The factors that contribute to orthostatic intolerance during and following reentry and to predict the likelihood of impaired crew performance are evaluated. A computer simulation approach employing a mathematical model of the cardiovascular system is employed. It is shown that depending on the severity of blood volume loss, the reentry acceleration stress may be detrimental to physiologic function and may place the physiologic status of the crew near the borderline of some type of impairment. They are in agreement with conclusions from early ground-based experiments and from observations of early Shuttle flights.

Leonard, J. I.↗
NASA NTRS1995

Catecholaminergic effects of prolonged head-down bed rest

Prolonged head-down bed rest (HDBR) provides a model for examining responses to chronic weightlessness in humans. Eight healthy volunteers underwent HDBR for 2 wk. Antecubital venous blood was sampled for plasma levels of catechols [norepinephrine (NE), epinephrine, dopamine, dihydroxyphenylalanine, dihydroxyphenylglycol, and dihydroxyphenylacetic acid] after supine rest on a control (C) day and after 4 h and 7 and 14 days of HDBR. Urine was collected after 2 h of supine rest during day C, 2 h before HDBR, and during the intervals 1-4, 4-24, 144-168 (day 7), and 312-336 h (day 14) of HDBR. All subjects had decreased plasma and blood volumes (mean 16%), atriopeptin levels (31%), and peripheral venous pressure (26%) after HDBR. NE excretion on day 14 of HDBR was decreased by 35% from that on day C, without further trends as HDBR continued, whereas plasma levels were only variably and nonsignificantly decreased. Excretion rates of dihydroxyphenylglycol and dihydroxyphenylalanine decreased slightly during HDBR; excretion rates of epinephrine, dopamine, and dihydroxyphenylacetic acid and plasma levels of catechols were unchanged. The results suggest that HDBR produces sustained inhibition of sympathoneural release, turnover, and synthesis of NE without affecting adrenomedullary secretion or renal dopamine production. Concurrent hypovolemia probably interferes with detection of sympathoinhibition by plasma levels of NE and other catechols in this setting. Sympathoinhibition, despite decreased blood volume, may help to explain orthostatic intolerance in astronauts returning from spaceflights.

Non-NASA Center↗
NASA NTRS2010

NIRS-Derived Tissue Oxygen Saturation and Hydrogen Ion Concentration Following Bed Rest

Long-term bed rest (BR), a model of spaceflight, results in a decrease in aerobic capacity and altered submaximal exercise responses. The strongest BR-induced effects on exercise appear to be centrally-mediated, but longer BR durations may result in peripheral adaptations (e.g., decreased mitochondrial and capillary density) which are likely to influence exercise responses. PURPOSE: To measure tissue oxygen saturation (SO2) and hydrogen ion concentration ([H+]) in the vastus lateralis (VL) using near infrared spectroscopy (NIRS) during cycle ergometry before and after . 30 d of BR. METHODS: Eight subjects performed a graded exercise test on a cycle ergometer to volitional fatigue 7 d before (pre-BR) and at the end or 1 day after BR (post-BR). NIRS spectra were collected from a sensor adhered to the skin overlying the VL. Oxygen consumption (VO2) was measured by open circuit spirometry. Blood volume (BV) was measured before and after BR using the carbon monoxide rebreathing technique. Changes in pre- and post-BR SO2 and [H+] data were compared using mixed model analyses. BV and peak exercise data were compared using paired t-tests. RESULTS: BV (pre-BR: 4.3+/-0.3, post-BR: 3.7+/-0.2 L, mean+/-SE, p=.01) and peak VO2 (pre-BR: 1.98+/-0.24, post-BR: 1.48 +/-0.21 L/min, p<.01) were reduced after BR. As expected, SO2 decreased with exercise before and after BR. However, SO2 was lower post compared with pre-BR throughout exercise, including at peak exercise (pre-BR: 50+/-3, post-BR: 43+/-4%, p=.01). After BR, [H+] was higher at the start of exercise and did not increase at the same rate as pre-BR. Peak [H+] was not different from pre to post-BR (pre-BR: 36+/-2; post-BR: 38+/-2 nmol/L). CONCLUSIONS: Lower SO2 during exercise suggests that oxygen extraction in the VL is higher after BR, perhaps due to lower circulating blood volume. The higher [H+] after BR suggests a greater reliance upon glycolysis during submaximal exercise, although [H+] at peak exercise was unchanged. Taken together, these data suggest that longer duration BR induces a number of changes that result in peripheral adaptations which contribute to cardiovascular and muscular deconditioning as measured by NIRS-derived SO2 and [H+] in the VL and may contribute to lower post-BR exercise tolerance. Supported by the National Space Biomedical Research Institute through NASA NCC 9-58

Lee, S. M. C.↗
NASA NTRS1976

Pre- and postflight systolic time intervals during LBNP - The second manned Skylab mission

Before and after the 59 day Skylab 3 flight, the astronauts were stressed with lower body negative pressure (LBNP), and their vectorcardiograms, pneumograms, phonocardiograms, and carotid pulse tracings were monitored together with the intervals of systole. In the immediate postflight period elevations in heart rate and blood pressure were observed in response to -50 mm Hg of LBNP. Postflight abnormalities in the systolic time intervals (STI) at rest and during stress were due to an increase in afterload and a decrease in preload. As blood volume was restored and blood pressure reduced, STI abnormalities persisted as long as one month, suggesting a possible reduction in ventricular contractility and/or a functional impairment to venous return.

Bergman, S. A., Jr.↗
NASA NTRS1979

Fluid volumes changes induced by spaceflight

The blood volume (BV), plasma volume (PV), and extracellular fluid volume changes produced in crewmembers during spaceflights of 11-84 days were compared to changes after 14 or 28 days of bedrest. Spaceflight and bedrest produce approximately equal BV changes but the recorded PV change after spaceflight was less. However, the diurnal change in PV may explain the smaller decreases recorded after spaceflight. The cardiovascular deconditioning caused by spaceflight and bedrest was compared using the mean heart rate response to lower body negative pressure (LBNP) testing at -50 mmHg pressure. These tests show approximately equal LBNP produced heart rate changes after bedrest and spaceflight. A countermeasure which includes 4 hr of LBNP treatment at -30 mmHg and the ingestion of one l. of saline was studied and found capable of returning the heart rate response and the PV of bedrested subjects to control (prebedrest) levels suggesting that it would be useful to the crewmembers after a spaceflight.

Johnson, P. C.↗
NASA NTRS1988

Cardiovascular effects of weightlessness and ground-based simulation

A large number of animal and human flight and ground-based studies were conducted to uncover the cardiovascular effects of weightlessness. Findings indicate changes in cardiovascular function during simulations and with spaceflight that lead to compromised function on reambulation and/or return to earth. This altered state termed cardiovascular deconditioning is most clearly manifest when in an erect body state. Hemodynamic parameters inidicate the presence of excessive tachnycardia, hypotension (leading to presyncope in one-third of the subjects), decreased heart volume, decreased plasma and circulating blood volumes and loss of skeletal muscle mass, particularly in the lower limbs. No clinically harmful effects were observed to date, but in-depth follow-ups were limited, as was available physiologic information. Available data concerning the causes for the observed changes indicate significant roles for mechanisms involved with body fluid-volume regulation, altered cardiac function, and the neurohumoral control of the control of the peripheral circulation. Satisfactory measures are not found. Return to preflight state was variable and only slightly dependent on flight duration. Future progress awaits availability of flight durations longer than several weeks.

Sandler, Harold↗
NASA NTRS1997

Interaction of central venous pressure, intramuscular pressure, and carotid baroreflex function

Seven healthy volunteer men participated in an experiment involving lower body positive pressure (LBPP) of 30 Torr and acute volume expansions of 5-6% (VE-I) and 9-10% (VE-II) of their total blood volume (TBV) to differentiate the effect of increased intramuscular pressure and central venous pressure (CVP) on the maximal gain (Gmax) of the carotid baroreflex. During each experimental condition, the heart rate (HR), mean arterial pressure (MAP; intraradial artery or Finapres), and CVP (at the 3rd-4th intercostal space) were monitored continuously. Gmax was derived from the logistic modeling of the HR and MAP responses to ramped changes in carotid sinus transmural pressure using a protocol of pulsatile changes in neck chamber pressure from +40 to -65 Torr. The increase in CVP during +30-Torr LBPP was 1.5 mmHg (P < 0.05) and was similar to that observed during VE-I (1.7 mmHg, P > 0.05). The Gmax of the carotid baroreflex of HR and MAP was significantly decreased during LBPP by -0.145 +/- 0.039 beats x min(-1) x mmHg(-1) (38%) and -0.071 +/- 0.013 mmHg/mmHg (25%), respectively; however, VE-I did not affect Gmax. During VE-II, CVP was significantly greater than that elicited by LBPP, and the Gmax of the carotid baroreflex of the HR and MAP responses was significantly reduced. We conclude that carotid baroreflex responsiveness was selectively inhibited by increasing intramuscular pressure, possibly resulting in an activation of the intramuscular mechanoreceptors during LBPP. Furthermore, it would appear that the inhibition of the carotid baroreflex, via cardiopulmonary baroreceptor loading (increased CVP), occurred when a threshold pressure (CVP) was achieved.

NASA Discipline Cardiopulmonary↗
NASA NTRS1987

Measurement of Human Blood and Plasma Volumes

Report reviews techniques for measuring blood-plasma volume in humans. Common technique of using radioactive iodine isotope to label plasma albumin involves unwarranted risks from low-level radiation. Report emphasizes techniques using Evans-blue-dye (T-1824) labeling of albumin, hematocrit or hemoglobin/hematocrit measurements, or blood densitometry. In Evans-blue-dye technique, plasma volume determined from decrease in dye concentration occurring after small amount of dye solution injected into circulatory system. Subjection of Evans blue dye to test for carcinogenicity gave negative results.

Greenleaf, J. E.↗
NASA NTRS1993

Hormonal and electrolyte responses to acute isohemic volume expansion in unanesthetized rats

This study was undertaken to explore the time course of the metabolic response to isohemic blood volume expansion (30%) in normotensive, unanesthetized Sprague-Dawley rats. Whole blood, drawn from a femoral artery catheter of conscious donor rats, was infused into the jugular vein of recipient rats. Blood samples were drawn from a carotid artery of recipient rats at time points beginning immediately post-volume expansion (IPVE) up through 5 days post-volume expansion (PVE). To characterize the attendant compensatory mechanisms, the plasma concentrations of electrolytes and fluid regulatory hormones were determined. Hematocrit began to raise IPVE and was significantly elevated above control IPVE 20, 30, 40, 60, and 90 min, and 2, 4, 6, 8, 12, and 24 hr PVE. Consistent with our current understanding of the hormonal response to excess volume, atrial natriuretic factor was significantly increased above the prevolume expansion (control) values 0-30 min PVE. Surprisingly, plasma aldosterone levels were significantly increased above control at 20 and 30 min and 6 hr PVE, whereas plasma renin activity was significantly decreased 30-40 min PVE. Plasma sodium was not changed from control values except for a significant increase at 6 hr post-volume expansion. Plasma potassium, osmolality, and arginine vasopressin levels were not altered by the volume expansion. These studies delineate the physiologic time scheme operative in the regulation of fluid volume during acute ischemic volume expansion.

NASA Discipline Cardiopulmonary↗
NASA NTRS2000

Time Course and Variability of Polycythemic Response in Men at High Altitude

Ten young men were exposed to 4,300 m (PB 460 Torr) for three weeks. Plasma volume (PV, Evans Blue dye). and blood volume (BV, carbon monoxide) measured simultaneously, and red cell volume (RCV) calculated from hematocrit, were determined twice at sea level and after 9-11 and 19-20 days at high altitude. After 19-20 days. half the subjects increased RCV +19.4 +/- 1.8% (p<0.001); the other 5 subjects had no significant change in RCV. All 10 subjects had a sustained decrease in PV (-16.2 +/- 1.9%, p<0.05) at altitude. Consequently, compared with sea level values, BV was unchanged (-3.1 +/- 1.8%) in the group with increased RCV, but BV decreased significantly (-12.2 +/- 1.4%, p<0.05) in the other group. Variability in RCV response was not explained by differences, in hypoxemic stimulus or the erythropoictin and reticulocyte responses. Since RCV reflects the balance between red cell. production and destruction, accelerated red cell destruction may have occurred in those individuals with no net change in RCV.

Grover, R. F.↗
NASA NTRS2001

Ischemia causes muscle fatigue

The purpose of this investigation was to determine whether ischemia, which reduces oxygenation in the extensor carpi radialis (ECR) muscle, causes a reduction in muscle force production. In eight subjects, muscle oxygenation (TO2) of the right ECR was measured noninvasively and continuously using near infrared spectroscopy (NIRS) while muscle twitch force was elicited by transcutaneous electrical stimulation (1 Hz, 0.1 ms). Baseline measurements of blood volume, muscle oxygenation and twitch force were recorded continuously, then a tourniquet on the upper arm was inflated to one of five different pressure levels: 20, 40, 60 mm Hg (randomized order) and diastolic (69 +/- 9.8 mm Hg) and systolic (106 +/- 12.8 mm Hg) blood pressures. Each pressure level was maintained for 3-5 min, and was followed by a recovery period sufficient to allow measurements to return to baseline. For each respective tourniquet pressure level, mean TO2 decreased from resting baseline (100% TO2) to 99 +/- 1.2% (SEM), 96 +/- 1.9%, 93 +/- 2.8%, 90 +/- 2.5%, and 86 +/- 2.7%, and mean twitch force decreased from resting baseline (100% force) to 99 +/- 0.7% (SEM), 96 +/- 2.7%, 93 +/- 3.1%, 88 +/- 3.2%, and 86 +/- 2.6%. Muscle oxygenation and twitch force at 60 mm Hg tourniquet compression and above were significantly lower (P < 0.05) than baseline value. Reduced twitch force was correlated in a dose-dependent manner with reduced muscle oxygenation (r = 0.78, P < 0.001). Although the correlation does not prove causation, the results indicate that ischemia leading to a 7% or greater reduction in muscle oxygenation causes decreased muscle force production in the forearm extensor muscle. Thus, ischemia associated with a modest decline in TO2 causes muscle fatigue.

Non-NASA Center↗
NASA NTRS1975

Response of local vascular volumes to lower body negative pressure stress

The present study involved an intravenous injection of radioactive iodinated serum albumin, equilibration of this isotope within the vascular space, and the continuous measurement of isotope activity over selected anatomical areas before, during and following multiple human LBNP tests. Both rate and magnitude of vascular pooling were distinctly different within each of five selected lower body anatomical areas. In the upper body, all areas except the abdomen showed depletions from their resting vascular volumes during LBNP. The presence of uniquely different pooling patterns in the lower body, the apparent stability of abdominal vascular volumes, and a possible decrease in cerebral blood volume during LBNP represent the major findings of this study.

Wolthuis, R. A.↗
NASA NTRS1991

Cardiovascular adaptation to O-G (Experiment 294) - Instrumentation for invasive and noninvasive studies

Many astronauts returning from space have difficulties regulating blood pressure, some to the point of fainting during quiet standing. Experiment 294 was designed to study this and other cardiovascular effects of adaptation to microgravity and to understand the mechanisms behind it. To accomplish this several cardiovascular variables had to be measured accurately. Heart rate, blood pressure, cardiac output (blood pumped by the heart each minute), stroke volume (blood pumped by the heart with each beat), limb flow, limb compliance, heart size and central venous pressure all had to been recorded during various stresses to understand fully the adaptation to space and the readaptation to earth's gravity. Numerous pieces of equipment were used. Some were purpose-built for the Spacelab mission and others were derived from commercial hardware. Developing spaceflight hardware is challenging and costly, but can lead to significant new information in the unique environment of space.

Buckey, Jay C.↗
NASA NTRS1993

Adaptation of Baroreflexes and Orthostatic Hypotension

The footward shift of blood volume and compensatory autonomic reflex responses initiated during the assumption of the upright posture in terrestrial gravity is a common feature in humans. When regular exposure to upright posture is removed, the headward redistribution of blood induces numerous physiological adaptations which compromise this normal response and the development of low blood pressure upon standing (orthostatic hypotension) can ensue. Such microgravity conditions can be produced by prolonged exposure to spaceflight or prolonged bed rest. Since the reduction of blood and plasma volume during exposure to microgravity has been associated with orthostatic instability following spaceflight and bed rest, it has been a reasonable assumption that hypovolemia may be a primary contributing factor to the development of orthostatic hypotension. This view was supported by the observation that the attempt to restore vascular volume in astronauts by drinking saline solutions just prior to re-entry had proven effective in reducing orthostatic instability after spaceflights of short duration. However, as the duration of spaceflight lengthens, orthostatic instability persists despite fluid loading procedures, suggesting that mechanisms other than hypovolemia may contribute to orthostatic hypotension following prolonged exposure to microgravity conditions. Recent evidence has been generated from spaceflight and groundbase experiments that supports the notion that changes in autonomic baroreflexes that control cardiac and vascular responses during orthostatic challenges may be affected by longer periods of microgravity exposure and can contribute to postflight orthostatic instability.

Convertino, Victor A.↗
NASA NTRS1993

Characterization of fluid physics effects on cardiovascular response to microgravity (G-572)

The recognition and understanding of cardiovascular adaptation to spaceflight has experienced substantial advancement in the last several years. In-flight echocardiographic measurements of astronaut cardiac function on the Space Shuttle have documented a 15 percent reduction in both left ventricular volume index and stroke volume with a compensatory increase in heart rate to maintain cardiac output. To date, the reduced cardiac size and stroke volume have been presumed to be the consequence of the reduction in circulating fluid volume following diuresis and other physiological processes to reduce blood volume within a few days after orbital insertion. However, no specific mechanism for the reduced stroke volume has been elucidated. The following investigation proposes the use of a hydraulic model of the cardiovascular system to examine the possibility that the observed reduction in stroke volume may, in part, be related to fluid physics effects on heart function. The automated model is being prepared to fly as a GAS payload. The experimental apparatus consists of a pneumatically actuated, elliptical artificial ventricle connected to a closed-loop, hydraulic circuit with compliance and resistance elements to create physiologic pressure and flow conditions. The ventricle is instrumented with high-fidelity, acceleration-insensitive, catheter-tip pressure transducers (Millar Instruments) in the apex and base to determine the instantaneous ventricular pressures and (delta)P(sub LV) across the left ventricle (LVP(sub apex)-LVP(sub base). The ventricle is also instrumented with a flow probe and pressure transducers immediately upstream of the inflow valve and downstream of the outflow valve. The experiment will be microprocessor controlled with analog signals stored on the FM data tape recorder. By varying the circulating fluid volume, ventricular function can be determined for varying preload pressures with fixed afterload pressure. Pilot experiments on board the NASA KC-135 aircraft have demonstrated proof-of-concept and provided early support for the proposed hypothesis. A review of the pilot experiments and developmental progress on the GAS version of this experiment will be presented.

Pantalos, George M.↗