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At least 145 records · Page 8
All sourcesNASA NTRSDOE OSTI
NASA NTRS2002

Quantitative analysis of aortic regurgitation: real-time 3-dimensional and 2-dimensional color Doppler echocardiographic method--a clinical and a chronic animal study

BACKGROUND: For evaluating patients with aortic regurgitation (AR), regurgitant volumes, left ventricular (LV) stroke volumes (SV), and absolute LV volumes are valuable indices. AIM: The aim of this study was to validate the combination of real-time 3-dimensional echocardiography (3DE) and semiautomated digital color Doppler cardiac flow measurement (ACM) for quantifying absolute LV volumes, LVSV, and AR volumes using an animal model of chronic AR and to investigate its clinical applicability. METHODS: In 8 sheep, a total of 26 hemodynamic states were obtained pharmacologically 20 weeks after the aortic valve noncoronary (n = 4) or right coronary (n = 4) leaflet was incised to produce AR. Reference standard LVSV and AR volume were determined using the electromagnetic flow method (EM). Simultaneous epicardial real-time 3DE studies were performed to obtain LV end-diastolic volumes (LVEDV), end-systolic volumes (LVESV), and LVSV by subtracting LVESV from LVEDV. Simultaneous ACM was performed to obtain LVSV and transmitral flows; AR volume was calculated by subtracting transmitral flow volume from LVSV. In a total of 19 patients with AR, real-time 3DE and ACM were used to obtain LVSVs and these were compared with each other. RESULTS: A strong relationship was found between LVSV derived from EM and those from the real-time 3DE (r = 0.93, P <.001, mean difference (3D - EM) = -1.0 +/- 9.8 mL). A good relationship between LVSV and AR volumes derived from EM and those by ACM was found (r = 0.88, P <.001). A good relationship between LVSV derived from real-time 3DE and that from ACM was observed (r = 0.73, P <.01, mean difference = 2.5 +/- 7.9 mL). In patients, a good relationship between LVSV obtained by real-time 3DE and ACM was found (r = 0.90, P <.001, mean difference = 0.6 +/- 9.8 mL). CONCLUSION: The combination of ACM and real-time 3DE for quantifying LV volumes, LVSV, and AR volumes was validated by the chronic animal study and was shown to be clinically applicable.

Validation Studies↗
NASA NTRS1992

Effect of hemorrhage on cardiac output, vasopressin, aldosterone, and diuresis during immersion in men

The purpose of this research was to test the hypotesis that a reduction in blood volume would attenuate or eliminate immersion-induced increases in cardiac output (Q(sub co)) and urine excretion, and to investigate accompanying vasoactive and fluid-electrolyte hormonal responses. Eight men (19-23 yr) were supine during a 2-hr control period in air, and then sat for 5-hr test periods in air at 20 C (dry control, DC); water at 34.5 C (wet control, WC); and water (34.5 C) after hemorrhage (WH) of 14.8 plus or minus 0.3 percent of their blood volume. Blood volume was -11.6 plus or minus 0.6 percent at immersion (time 0). Mean (bar-X hrs 1-5) Q(sub co) was unchanged in WC (5.3 plus or minus 0.01 l/min) and in WH (4.5 plus or minus 0.1 l/min), but decreased (P less than 0.05) in DC to 3.6 plus or minus 0.1 l/min. Mean urine excretion rates were 1.0 plus or minus 0.2 ml/min for DC and 1.1 plus or minus 0.2 ml/min for WH; both were lower (P less than 0.05) than that for WC of 2.0 plus or minus 0.4 ml/min. Plasma (Na+) and (Osm) were unchanged in all experiments. Mean plasma vasopressin (PVP) (bar-X hrs 1-5) was 1.1 plus or minus 0.1 pg/ml in WC, and higher (P less than 0.05) in DC (2.1 plus or minus 0.2 pg/ml)and WH (2.1 plus or minus 0.1 pg/ml); it was unchanged during air and water test periods. Thus, hemorrhage attenuated the immersion-induced increase in Q(sub co), eliminated the WC diuresis, maintained plasma renin activity and PVP at DC levels and did not change immersion-induced aldosterone suppression; the osmotic diuresis during control immersion is apparently not due to either aldosterone suppression or vasopressin suppression.

Greenleaf, J. E.↗
NASA NTRS2000

Deconditioning and Reconditioning: Humans in Stressful Environments

Deconditioning is an integrated physiological response of the body to a reduction in metabolic rate; that is, to a reduction in energy use or in exercise level. While it may involve assumption of a horizontal body position, it certainly perturbs bodily homeostasis - at least temporarily. The reduction in physical activity that causes deconditioning is often associated with an increase in the time spent, for whatever reason, in a sitting or horizontal position. As a result, orthostatic factors may also contribute to the deconditioning mechanism. The word decondition may be defined as "1: to cause extinction of (a conditioned response) 2: to cause to lose physical fitness". This definition implies that psychological/emotional factors may accompany physical deconditioning, and it is this interpretation of the word that is used throughout this volume. It is apparent that deconditioning plays a major role in the mechanism of the general adaptive (homeostatic) response that is initiated by exposure to prolonged bed rest (BR). And the total homeostatic response to BR involves more than deconditioning per se. For example, it has been shown that the restoration of plasma volume and maximal work capacity after 4 weeks of BR deconditioning left other bodily functions (submaximal exercise oxygen uptake and cardiac output, leg proprioception and posterior leg muscle thickness and volume, head-up tilt tolerance, and sleep quality) functioning at decreased levels. The precise effect of deconditioning on BR homeostasis is difficult to determine, because the fundamental interactive neuro-endocrine-immune control networks that facilitate conditioning and deconditioning also act to maintain basic wholebody homeostasis. For example, is the mechanism of BR-induced deconditioning independent of the mechanism that provokes concomitant orthostatic intolerance; that is, fainting? Assumption of the recumbent body position for prolonged periods of time, results in a new adaptive-homeostatic state. This state occurs in response to the mutually interactive effects of the change in bodily position (hydrostatic pressure), to the virtual elimination of longitudinal pressure on the bones, to the increased confinement with possible reduction in total daily energy (exercise) expenditure, to the reorientation of stimuli within the vestibular organs, and (often) to altered socio-psychological conditions. The exercise-training (reconditioning) syndrome affects total body homeostasis by facilitating increases in work capacity and endurance, whereas deconditioning decreases physical performance. There are many interrelated factors that influence the control parameters that seek to maintain the adaptive conditioning-deconditioning syndrome. These control parameters can be better elucidated by subjecting otherwise healthy ambulatory people to various stresses, such as exercise training and prolonged spaceflight, bed rest, water immersion, hyperbaria, and isolation and confinement. Changes in control parameters will be manifested in muscle function, orthostatic tolerance, cardiorespiratory responses, musculo-skeletal systems, free-radical processes, and body thermoregulation with overarching effects on the subjects' psycho-sociological states. A discussion of these factors and the control parameters constitutes the substance of this volume. Special emphasis is placed on delineating practical applications of the findings that will be of special interest to physicians, nurses, and other health-care workers.

Greenleaf, John E.↗
NASA NTRS1996

Submaximal exercise VO2 and Qc during 30-day 6 degrees head-down bed rest with isotonic and isokinetic exercise training

BACKGROUND: Maintaining intermediary metabolism is necessary for the health and well-being of astronauts on long-duration spaceflights. While peak oxygen uptake (VO2) is consistently decreased during prolonged bed rest, submaximal VO2 is either unchanged or decreased. METHODS: Submaximal exercise metabolism (61 +/- 3% peak VO2) was measured during ambulation (AMB day-2) and on bed rest days 4, 11, and 25 in 19 healthy men (32-42 yr) allocated into no exercise (NOE, N = 5) control, and isotonic exercise (ITE, N = 7) and isokinetic exercise (IKE, N = 7) training groups. Exercise training was conducted supine for two 30-min periods per day for 6 d per week: ITE training was intermittent at 60-90% peak VO2; IKE training was 10 sets of 5 repetitions of peak knee flexion-extension force at a velocity of 100 degrees s-1. Cardiac output was measured with the indirect Fick CO2 method, and plasma volume with Evans blue dye dilution. RESULTS: Supine submaximal exercise VO2 decreased significantly (*p < 0.05) by 10.3%* with ITE and by 7.3%* with IKE; similar to the submaximal cardiac output decrease of 14.5%* (ITE) and 20.3%* (IKE), but different from change in peak VO2 (+1.4% with ITE and -10.2%* with IKE) and decrease in plasma volume of -3.7% (ITE) and -18.0%* (IKE). Reduction of submaximal VO2 during bed rest correlated 0.79 (p < 0.01) with submaximal Qc, but was not related to change in peak VO2 or plasma volume. CONCLUSION: Reduction in submaximal oxygen uptake during prolonged bed rest is related to decrease in exercise but not resting cardiac output; perturbations in active skeletal muscle metabolism may be involved.

NASA Discipline Regulatory Physiology↗
NASA NTRS1980

Instantaneous stroke volume by PDE during and after constant LBNP (-50 torr)

Six male subjects were exposed to -50 torr lower body negative pressure (LBNP) for 10 min while stroke volume was recorded beat by beat at regular intervals before, during and after release of LBNP. Stroke volume was calculated from the systolic velocity integral in the ascending aorta by pulsed Doppler echocardiography (PDE) and the cross sectional area of the vessel by M mode echocardiography. Changes in leg volume were recorded continuously and blood pressure was taken every minute. Stroke volume dropped by 51% of the control in the first 33 sec of LBNP and continued to decline slowly to -62% toward the end. Heart rate increased by 15% in the first 10 sec and was 22% above control at the end of exposure. The resulting cardiac output closely followed the course of stroke volume (-47% at 33 sec, -53% at 8 min) showing that the modest increase in heart rate did little to offset the drop in stroke volume. Leg volume increased markedly within the first 10 sec with a more gradual rise reaching +3.5% at the end. Upon sudden release of LBNP, leg volume dropped significantly during the first 3 sec simultaneously with an increase in stroke volume followed by a substantial decline in heart rate below the baseline.

Source record↗
NASA NTRS1971

Circulatory responses to hypoxia in experimental myocardial infarction.

Three levels of decreased arterial oxygen saturation elicited a graded circulatory response in dogs, manifested by stepwise increases in cardiac output, left ventricular dp/dt, and stroke volume, and decreases in systemic vascular resistance. Responses to similar hypoxia challenges after experimental myocardial infarction were qualitatively similar but quantitatively less. Although the circulatory compensation for hypoxia was less effective after myocardial infarction, no further deterioration of the haemodynamics was noted.

Schroll, M.↗
NASA NTRS1979

Cardiopulmonary readjustments in passive tilt

The readjustment of cardiopulmonary variables in human volunteers at various tilt angles on a tilt board is studied. Five healthy subjects (18-31 yr) with thorough knowledge of the experimental protocol are tested, passively tilted from the supine to the upright position in 15-deg increments in random sequence. The parameters measured are cardiac output (Q), heart rate (HR), stroke volume (SV), minute and alveolar ventilation /V(E) and V(A)/, functional residual capacity (FRC), and arterial-end-tidal P(CO2) pressure difference. It is found that changes in Q and FRC are linearly related to the sine of the tilt angle, indicating that either reflexes are absent or their net effect is proportional to the effects of gravity. This is clearly not the case for other variables /HR, SV, V(E), V(A)/, where it is possible to demonstrate threshold values for the appearance of secondary changes.

Matalon, S. V.↗
NASA NTRS2008

Graded Compression Stockings Prevent Post-spaceflight Orthostatic Hypotension

Post-spaceflight orthostatic intolerance is characterized by hypotension and presyncope in 20-30% of returning astronauts. Previous data from our laboratory suggests that this is largely a result of decreased venous return. Currently, NASA astronauts wear an anti-gravity suit (AGS) which consists of inflatable air bladders over the calves, thighs and abdomen, which are typically pressurized from 0.5 to 1.5 PSI (~27 to 78 mmHg). ISS crew members sometimes wear Russian Kentavr suits which consist of laced compression shorts and gaiters, providing ~30 mmHg nominally. While these garments are effective during reentry, there are a number of drawbacks that make them impractical for postflight use. We studied the ability of commercially available, custom fit, graded compression stockings (Jobst, 55 mmHg at ankle to 6 mmHg at top of thigh, 25 mmHg mean compression) to prevent postflight orthostatic intolerance, hypothesizing that these garments would prevent orthostatic intolerance following short duration space flight. Crew members from a single Space Shuttle flight were tilted to 80 degrees for 10 min while wearing the stockings (n=5 males) upon arrival at the clinic (~2 hrs after landing). Hemodynamic data were compared to data from all crewmembers tilted (without countermeasures) since return to flight (n=9). Two-way, repeated measures ANOVA, using the entire tilt time curve (0-10 min) show that systolic blood pressure (SBP, group effect p=0.008), stroke volume (SV, group effect p=0.003), and cardiac output (CO, group effect p=0.004) were higher in crewmembers who wore the Jobst stockings. A one-way ANOVA comparing the last minute standing also showed that SV (p=0.001) and CO (p less than 0.001) were higher and SBP tended to be higher (p=0.06) in Jobst subjects compared to controls. Control subjects had a higher rate of presyncope than Jobst subjects (3/9 vs 0/5) during the tilt on landing day. Orthostatic hypotension continues to present following spaceflight, despite fluid loading and other countermeasures. This preliminary study shows that commercially available compression stockings may ameliorate this problem. These stockings are readily available, inexpensive, and can be worn for days following landing. We have observed similar protection against orthostatic intolerance in ground-based studies of hypovolemic test subjects. Further refinements to the design and compression of the stockings are in progress.

Platts, S. H.↗
NASA NTRS2016

Influence of Population Variation of Physiological Parameters in Computational Models of Space Physiology

The earliest manifestations of Visual Impairment and Intracranial Pressure (VIIP) syndrome become evident after months of spaceflight and include a variety of ophthalmic changes, including posterior globe flattening and distension of the optic nerve sheath. Prevailing evidence links the occurrence of VIIP to the cephalic fluid shift induced by microgravity and the subsequent pressure changes around the optic nerve and eye. Deducing the etiology of VIIP is challenging due to the wide range of physiological parameters that may be influenced by spaceflight and are required to address a realistic spectrum of physiological responses. Here, we report on the application of an efficient approach to interrogating physiological parameter space through computational modeling. Specifically, we assess the influence of uncertainty in input parameters for two models of VIIP syndrome: a lumped-parameter model (LPM) of the cardiovascular and central nervous systems, and a finite-element model (FEM) of the posterior eye, optic nerve head (ONH) and optic nerve sheath. Methods: To investigate the parameter space in each model, we employed Latin hypercube sampling partial rank correlation coefficient (LHSPRCC) strategies. LHS techniques outperform Monte Carlo approaches by enforcing efficient sampling across the entire range of all parameters. The PRCC method estimates the sensitivity of model outputs to these parameters while adjusting for the linear effects of all other inputs. The LPM analysis addressed uncertainties in 42 physiological parameters, such as initial compartmental volume and nominal compartment percentage of total cardiac output in the supine state, while the FEM evaluated the effects on biomechanical strain from uncertainties in 23 material and pressure parameters for the ocular anatomy. Results and Conclusion: The LPM analysis identified several key factors including high sensitivity to the initial fluid distribution. The FEM study found that intraocular pressure and intracranial pressure had dominant impact on the peak strains in the ONH and retro-laminar optic nerve, respectively; optic nerve and lamina cribrosa stiffness were also important. This investigation illustrates the ability of LHSPRCC to identify the most influential physiological parameters, which must therefore be well-characterized to produce the most accurate numerical results.

biomechanics↗
NASA NTRS1992

Role of atrial natriuretic peptide in systemic responses to acute isotonic volume expansion

A hypothesis is proposed that a temporal relationship exists between increases in cardiac filling pressure and plasma artrial natriuretic peptide (ANP) concentration and also between ANP elevation and vasodilation, fluid movement from plasma to interstitium, and increased urine volume (UV). To test the hypothesis, 30 ml/kg isotonic saline were infused in supine male subjects over 24 min and responses were monitored for 3 h postinfusion. Results show that at end infusion, mean arterial pressure (RAP), heart rate and plasma volume exhibited peak increases of 146, 23, and 27 percent, respectively. Mean plasma ANP and UV peaked (45 and 390 percent, respectively) at 30 min postinfusion. Most cardiovascular variables had returned toward control levels by 1 h postinfusion, and net reabsorption of extravascular fluid ensued. It is concluded that since ANP was not significantly increased until 30 min postinfusion, factors other than ANP initiate responses to intravascular fluid loading. These factors include increased vascular pressures, baroreceptor-mediated vasolidation, and hemodilution of plasma proteins. ANP is suggested to mediate, in part, the renal response to saline infusion.

Watenpaugh, Donald E.↗
NASA NTRS1997

Resistance exercise training and the orthostatic response

Resistance exercise has been suggested to increase blood volume, increase the sensitivity of the carotid baroreceptor cardiac reflex response (BARO), and decrease leg compliance, all factors that are expected to improve orthostatic tolerance. To further test these hypotheses, cardiovascular responses to standing and to pre-syncopal limited lower body negative pressure (LBNP) were measured in two groups of sedentary men before and after a 12-week period of either exercise (n = 10) or no exercise (control, n = 9). Resistance exercise training consisted of nine isotonic exercises, four sets of each, 3 days per week, stressing all major muscle groups. After exercise training, leg muscle volumes increased (P < 0.05) by 4-14%, lean body mass increased (P = 0.00) by 2.0 (0.5) kg, leg compliance and BARO were not significantly altered, and the maximal LBNP tolerated without pre-syncope was not significantly different. Supine resting heart rate was reduced (P = 0.03) without attenuating the heart rate or blood pressure responses during the stand test or LBNP. Also, blood volume (125I and 51Cr) and red cell mass were increased (P < 0.02) by 2.8% and 3.9%, respectively. These findings indicate that intense resistance exercise increases blood volume but does not consistently improve orthostatic tolerance.

NASA Discipline Musculoskeletal↗
NASA NTRS1998

Low level CO2 effects on pulmonary function in humans

The purpose of the study was to determine whether chamber exposure to low levels of CO2 results in functional alterations in gas mixing and closing volume in humans. Four healthy volunteer subjects were exposed to 0.7% CO2 and to 1.2% CO2. Spirometry, lung volumes, single breath nitrogen washout, diffusing capacity for carbon monoxide (DLCO) by two methods, and cardiac output were measured in triplicate. Values were obtained over two non-consecutive days during the training period (control) and on days 2 or 3, 4, 6, 10, 13, and 23 of exposure to each CO2 level. Measurements were made during the same time of day. There was one day of testing after exposure, while still in the chamber but off carbon dioxide. The order of testing, up until measurements of DLCO and cardiac output, were randomized to avoid presentation effects. The consistent findings were a reduction in diffusing capacity for carbon monoxide and a fall in cardiac output, occurring to a similar degree with both exposures. For the group as a whole, there was no indication of major effects on spirometry, lung volumes, gas mixing or dead space. We conclude that small changes may occur in the function of distal gas exchanging units; however, these effects were not associated with any adverse health effects. The likelihood of pathophysiologic changes in lung function or structure with 0.7 or 1.2% CO2 exposure for this period of time, is therefore, low.

NASA Discipline Cardiopulmonary↗
NASA NTRS2001

Regulation of sympathetic nervous system function after cardiovascular deconditioning

Humans subjected to prolonged periods of bed rest or microgravity undergo deconditioning of the cardiovascular system, characterized by resting tachycardia, reduced exercise capability, and a predisposition for orthostatic intolerance. These changes in cardiovascular function are likely due to a combination of factors, including changes in control of body fluid balance or cardiac alterations resulting in inadequate maintenance of stroke volume, altered arterial or venous vascular function, reduced activation of cardiovascular hormones, and diminished autonomic reflex function. There is evidence indicating a role for each of these mechanisms. Diminished reflex activation of the sympathetic nervous system and subsequent vasoconstriction appear to play an important role. Studies utilizing the hindlimb-unloaded (HU) rat, an animal model of deconditioning, evaluated the potential role of altered arterial baroreflex control of the sympathetic nervous system. These studies indicate that HU results in blunted baroreflex-mediated activation of both renal and lumbar sympathetic nerve activity in response to a hypotensive stimulus. HU rats are less able to maintain arterial pressure during hemorrhage, suggesting that diminished ability to increase sympathetic activity has functional consequences for the animal. Reflex control of vasopressin secretion appears to be enhanced following HU. Blunted baroreflex-mediated sympathoexcitation appears to involve altered central nervous system function. Baroreceptor afferent activity in response to changes in arterial pressure is unaltered in HU rats. However, increases in efferent sympathetic nerve activity for a given decrease in afferent input are blunted after HU. This altered central nervous system processing of baroreceptor inputs appears to involve an effect at the rostral ventrolateral medulla (RVLM). Specifically, it appears that tonic GABAA-mediated inhibition of the RVLM is enhanced after HU. Augmented inhibition apparently arises from sources other than the caudal ventrolateral medulla. If similar alterations in control of the sympathetic nervous system occur in humans in response to cardiovascular deconditioning, it is likely that they play an important role in the observed tendency for orthostatic intolerance. Combined with potential changes in vascular function, cardiac function, and hypovolemia, the predisposition for orthostatic intolerance following cardiovascular deconditioning would be markedly enhanced by blunted ability to reflexly activate the sympathetic nervous system.

Review, Tutorial↗
NASA NTRS1975

Fluctuations in O2 stores and gas exchange with passive changes in posture

The purpose of the present study is to determine the effects of changes in posture on oxygen transfer at the mouth and pulmonary capillary membrane and to observe concomitant subtle changes in ventilation under specified assumptions. Breath-by-breath calculations are carried out with a box-balloon spirometer and mass spectrometer. Measurements are made before, during, and after passive tilt to 60 deg and on return to recumbency after 10 min erect. It is found that from supine to upright oxygen stores in the lung increases rapidly and oxygen stores in the blood drops slowly, creating a net deficit in oxygen transfer at the mouth of 130 ml in 10 min. Changes in oxygen stores in the blood result from shifts in blood volume and flow more than from changes in cardiac output. Refilling of oxygen stores in the blood is found to cause transient hypoxia with substantial hyperpnea.

Loeppky, J. A.↗
NASA NTRS1984

Analysis of head-down tilt as an analog of weightlessness using a methematical simulation model

Antiorthostasis or head down tilt of a moderate degree was used as a ground based analog of weightless space flight to study headward fluid shifts, decreased plasma volume, orthostatic intolerance and muscular skeletal degradation. A mathematical model was used to help interpret these observations. The model proved most valuable for these studies was originally developed as a description of the major circulatory, fluid and electrolyte control systems. Two different experimental studies are employed to validate the model. The first is a 24 hour head down tilt study and the second is a 7 day head down bed rest study. The major issues addressed include the reduction in plasma volume, the dynamic changes of venous pressure and cardiac output, the extent of central hypervolemia during long term zero g exposure, the existence of an early diuresis, the mechanisms which alter the renal regulating hormones during the short term and long term periods, the significance of potassium loss on other zero g responses, and the role of transcapillary filtration in adjusting fluid shifts. The use of mathematical models as an interpretive and analysis technique for experimental research for space life science is illustrated.

Leonard, J. I.↗
NASA NTRS2011

Human Cardiovascular Adaptation to Weightlessness

Entering weightlessness (0 G) induces immediately a shift of blood and fluid from the lower to the upper parts of the body inducing expansion of the cardiac chambers (Bungo et al. 1986; Charles & Lathers 1991; Videbaek & Norsk 1997). For many years the effects of sudden 0 G on central venous pressure (CVP) was discussed, and it puzzled researchers that CVP compared to the 1-G supine position decreased during the initial hours of spaceflight, when at the same time left atrial diameter increased (Buckey et al. 1996). By measuring esophageal pressure as an estimate of inter-pleural pressure, it was later shown that this pressure decreases more than CVP does during 0 G induced by parabolic flights (Videbaek & Norsk 1997). Thus, transmural CVP is increased, which distends the cardiac chambers. This unique lung-heart interaction whereby 1) inter-pleural pressure decreases and 2) central blood volume is expanded is unique for 0 G. Because transmural CVP is increased, stroke volume increases according to the law of Frank-Starling leading to an increase in cardiac output, which is maintained increased during months of 0 G in space to levels of some 25% above that of the 1-G seated position (Norsk unpublished). Simultaneously, sympathetic nervous activity is at the level of the upright 1-G posture, which is difficult to explain based on the high stroke volume and decreased blood pressure and systemic vascular resistance. This paradox should be explored and the mechanisms revealed, because it might have implications for estimating the cardiovascular risk of travelling in space.

Norsk, Peter↗