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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 NTRS1996

Relationship of the time course of venous gas bubbles to altitude decompression illness

The correlation is low between the occurrence of gas bubbles in the pulmonary artery, called venous gas emboli (VGE), and subsequent decompression illness (DCI). The correlation improves when a "grade" of VGE is considered; a zero to four categorical classification based on the intensity and duration of the VGE signal from a Doppler bubble detector. Additional insight about DCI might come from an analysis of the time course of the occurrence of VGE. Using the NASA Hypobaric Decompression Sickness Databank, we compared the time course of the VGE outcome between 322 subjects who exercised and 133 Doppler technicians who did not exercise to evaluate the role of physical activity on the VGE outcome and incidence of DCI. We also compared 61 subjects with VGE and DCI with 110 subjects with VGE but without DCI to identify unique characteristics about the time course of the VGE outcome to try to discriminate between DCI and no-DCI cases. The VGE outcome as a function of time showed a characteristic short lag, rapid response, and gradual recovery phase that was related to physical activity at altitude and the presence or absence of DCI. The average time for DCI symptoms in a limb occurred just before the time of the highest fraction of VGE in the pulmonary artery. It is likely, but not certain, that an individual will report a DCI symptom if VGE are detected early in the altitude exposure, the intensity or grade of VGE rapidly increases from a limb region, and the intensity or grade of VGE remains high.

NASA Discipline Environmental Health↗
NASA NTRS1999

New approaches to the Doppler echocardiographic assessment of diastolic function: from research laboratory to clinical practice

Over the past decade, Doppler echocardiography has become a well-established tool for the diagnosis of left ventricular diastolic dysfunction. Unfortunately, in many clinical situations traditional Doppler indices of transmittal and pulmonary venous flow are inconclusive, primarily due to their dependence on left atrial pressure. Recently, new Doppler indices that are much less dependent on preload have been developed, based on intraventricular flow propagation and intrinsic myocardial velocity. These methodologies provide direct assessment of ventricular relaxation and the small intraventricular pressure gradients essential to efficient filling of the ventricle. We review in this article the theoretical and experiment background of these new echo techniques as well as how they can be implemented in routine clinical practice.

NASA Discipline Cardiopulmonary↗
NASA NTRS1991

Pathophysiology of spontaneous venous gas embolism

The use of controllable degrees and durations of continuous isobaric counterdiffusion venous gas embolism to investigate effects of venous gas embolism upon blood, cardiovascular, and respiratory gas exchange function, as well as pathological effects upon the lung and its microcirculation is discussed. Use of N2O/He counterdiffusion permitted performance of the pathophysiologic and pulmonary microstructural effects at one ATA without hyperbaric or hypobaric exposures.

Lambertsen, C. J.↗
NASA NTRS2003

Protein turnover in atrophying muscle: from nutritional intervention to microarray expression analysis

PURPOSE OF REVIEW: In response to decreased usage, skeletal muscle undergoes adaptive reductive remodeling due to the decrease in tension on the weight bearing components of the musculo-skeletal system. This response occurs with uncomplicated disuse (e.g. bed rest, space flight), as a secondary consequence of several widely prevalent chronic diseases for which activity is reduced (e.g. chronic obstructive pulmonary disease and chronic heart failure) and is part of the aging process. The problem is therefore one of considerable clinical importance. RECENT FINDINGS: The impaired function and exercise intolerance is related more to the associated muscle wasting rather than to the specific organ system primarily impacted by the disease. Progress has continued in describing the use of anabolic drugs and dietary manipulation. The major advance in the field has been: (i) the discovery of the atrogin-1 gene and (ii) the application of microarray expression analysis and proteomics with the objectives of obtaining comprehensive understanding of the pathways changed with disuse atrophy. SUMMARY: Disuse atrophy is a common clinical problem. There is a need for therapeutic interventions that do not involve exercise. A better understanding of the changes, particularly at the molecular level, could indicate hitherto unsuspected sites for nutritional and pharmacological intervention.

Non-NASA Center↗
NASA NTRS1997

Hypergravity Alters the Susceptibility of Cells to Anoxia-Reoxygenation Injury

Gravity is a physical force, much like shear stress or mechanical stretch, and should affect organ and cellular function. Researchers have shown that gravity plays a role in ventilation and blood flow distribution, gas exchange, alveolar size and mechanical stresses within the lung. Short exposure to microgravity produced marked alterations in lung blood flow and ventilation distribution while hypergravity exaggerated the regional differences in lung structure and function resulting in reduced ventilation at the base and no ventilation of the upper half of the lung. Microgravity also decreased metabolic activity in cardiac cells, WI-38 embryonic lung cells, and human lymphocytes. Rats, in the tail-suspended head-down tilt model, experienced transient loss of lung water, contrary to an expected increase due to pooling of blood in the pulmonary vasculature. Hypergravity has also been found to increase the proliferation of several different cell lines (e.g., chick embryo fibroblasts) while decreasing cell motility and slowing liver regeneration following partial hepatectomy. These studies show that changes in the gravity environment will affect several aspects of organ and cellular function and produce major change in blood flow and tissue/organ perfusion. However, these past studies have not addressed whether ischemia-reperfusion injury will be exacerbated or ameliorated by changes in the gravity environment, e.g., space flight. Currently, nothing is known about how gravity will affect the susceptibility of different lung and vascular cells to this type of injury. We conducted studies that addressed the following question: Does the susceptibility of lung fibroblasts, vascular smooth muscle, and endothelial cells to anoxia/reoxygenation injury change following exposure to hypergravity conditions?

McCloud, Henry↗
NASA NTRS1999

Role of microtubules in the contractile dysfunction of hypertrophied myocardium

OBJECTIVES: We sought to determine whether the ameliorative effects of microtubule depolymerization on cellular contractile dysfunction in pressure overload cardiac hypertrophy apply at the tissue level. BACKGROUND: A selective and persistent increase in microtubule density causes decreased contractile function of cardiocytes from cats with hypertrophy produced by chronic right ventricular (RV) pressure overloading. Microtubule depolymerization by colchicine normalizes contractility in these isolated cardiocytes. However, whether these changes in cellular function might contribute to changes in function at the more highly integrated and complex cardiac tissue level was unknown. METHODS: Accordingly, RV papillary muscles were isolated from 25 cats with RV pressure overload hypertrophy induced by pulmonary artery banding (PAB) for 4 weeks and 25 control cats. Contractile state was measured using physiologically sequenced contractions before and 90 min after treatment with 10(-5) mol/liter colchicine. RESULTS: The PAB significantly increased RV systolic pressure and the RV weight/body weight ratio in PAB; it significantly decreased developed tension from 59+/-3 mN/mm2 in control to 25+/-4 mN/mm2 in PAB, shortening extent from 0.21+/-0.01 muscle lengths (ML) in control to 0.12+/-0.01 ML in PAB, and shortening rate from 1.12+/-0.07 ML/s in control to 0.55+/-0.03 ML/s in PAB. Indirect immunofluorescence confocal microscopy showed that PAB muscles had a selective increase in microtubule density and that colchicine caused complete microtubule depolymerization in both control and PAB papillary muscles. Microtubule depolymerization normalized myocardial contractility in papillary muscles of PAB cats but did not alter contractility in control muscles. CONCLUSIONS: Excess microtubule density, therefore, is equally important to both cellular and to myocardial contractile dysfunction caused by chronic, severe pressure-overload cardiac hypertrophy.

NASA Discipline Cardiopulmonary↗
NASA NTRS2002

Numerical simulation of the influence of gravity and posture on cardiac performance

A numerical model of the cardiovascular system was used to quantify the influences on cardiac function of intrathoracic pressure and intravascular and intraventricular hydrostatic pressure, which are fundamental biomechanical stimuli for orthostatic response. The model included a detailed arterial circulation with lumped parameter models of the atria, ventricles, pulmonary circulation, and venous circulation. The venous circulation was divided into cranial, central, and caudal regions with nonlinear compliance. Changes in intrathoracic pressure and the effects of hydrostatic pressure were simulated in supine, launch, sitting, and standing postures for 0, 1, and 1.8 G. Increasing intrathoracic pressure experienced with increasing gravity caused 12% and 14% decreases in cardiac output for 1 and 1.8 G supine, respectively, compared to 0 G. Similar results were obtained for launch posture, in which the effects of changing intrathoracic pressure dominated those of hydrostatic pressure. Compared to 0 G, cardiac output decreased 0.9% for 1 G launch and 15% for 1.8 G launch. In sitting and standing, the position of the heart above the hydrostatic indifference level caused the effects of changing hydrostatic pressure to dominate those of intrathoracic pressure. Compared to 0 G, cardiac output decreased 13% for 1 G sitting and 23% for 1.8 G sitting, and decreased 17% for 1 G standing and 31% for 1.8 G standing. For a posture change from supine to standing in 1 G, cardiac output decreased, consistent with the trend necessary to explain orthostatic intolerance in some astronauts during postflight stand tests. Simulated lower body negative pressure (LBNP) in 0 G reduced cardiac output and mean aortic pressure similar to I G standing, suggesting that LBNP provides at least some cardiovascular stimuli that may be useful in preventing postflight orthostatic intolerance. A unifying concept, consistent with the Frank-Starling mechanism of the heart, was that cardiac output was proportional to cardiac diastolic transmural pressure for all postures and gravitational accelerations.

Non-NASA Center↗
NASA NTRS1977

Mathematical modelling of a human external respiratory system

A closed system of algebraic and common differential equations solved by computer is investigated. It includes equations which describe the activity pattern of the respiratory center, the phrenic nerve, the thrust produced by the diaphragm as a function of the lung volume and discharge frequency of the phrenic nerve, as well as certain relations of the lung stretch receptors and chemoreceptors on various lung and blood characteristics, equations for lung biomechanics, pulmonary blood flow, alveolar gas exchange and capillary blood composition equations to determine various air and blood flow and gas exchange parameters, and various gas mixing and arterial and venous blood composition equations, to determine other blood, air and gas mixing characteristics. Data are presented by means of graphs and tables, and some advantages of this model over others are demonstrated by test results.

Source record↗
NASA NTRS1997

Pulmonary tissue volume, cardiac output, and diffusing capacity in sustained microgravity

In microgravity (microG) humans have marked changes in body fluids, with a combination of an overall fluid loss and a redistribution of fluids in the cranial direction. We investigated whether interstitial pulmonary edema develops as a result of a headward fluid shift or whether pulmonary tissue fluid volume is reduced as a result of the overall loss of body fluid. We measured pulmonary tissue volume (Vti), capillary blood flow, and diffusing capacity in four subjects before, during, and after 10 days of exposure to microG during spaceflight. Measurements were made by rebreathing a gas mixture containing small amounts of acetylene, carbon monoxide, and argon. Measurements made early in flight in two subjects showed no change in Vti despite large increases in stroke volume (40%) and diffusing capacity (13%) consistent with increased pulmonary capillary blood volume. Late in-flight measurements in four subjects showed a 25% reduction in Vti compared with preflight controls (P < 0.001). There was a concomittant reduction in stroke volume, to the extent that it was no longer significantly different from preflight control. Diffusing capacity remained elevated (11%; P < 0.05) late in flight. These findings suggest that, despite increased pulmonary perfusion and pulmonary capillary blood volume, interstitial pulmonary edema does not result from exposure to microG.

Clinical Trial↗
NASA NTRS2012

Developing Physiologic Models for Emergency Medical Procedures Under Microgravity

Several technological enhancements have been made to METI's commercial Emergency Care Simulator (ECS) with regard to how microgravity affects human physiology. The ECS uses both a software-only lung simulation, and an integrated mannequin lung that uses a physical lung bag for creating chest excursions, and a digital simulation of lung mechanics and gas exchange. METI's patient simulators incorporate models of human physiology that simulate lung and chest wall mechanics, as well as pulmonary gas exchange. Microgravity affects how O2 and CO2 are exchanged in the lungs. Procedures were also developed to take into affect the Glasgow Coma Scale for determining levels of consciousness by varying the ECS eye-blinking function to partially indicate the level of consciousness of the patient. In addition, the ECS was modified to provide various levels of pulses from weak and thready to hyper-dynamic to assist in assessing patient conditions from the femoral, carotid, brachial, and pedal pulse locations.

Parker, Nigel↗
NASA NTRS2012

Developing Physiologic Models for Emergency Medical Procedures Under Microgravity

Several technological enhancements have been made to METI's commercial Emergency Care Simulator (ECS) with regard to how microgravity affects human physiology. The ECS uses both a software-only lung simulation, and an integrated mannequin lung that uses a physical lung bag for creating chest excursions, and a digital simulation of lung mechanics and gas exchange. METI s patient simulators incorporate models of human physiology that simulate lung and chest wall mechanics, as well as pulmonary gas exchange. Microgravity affects how O2 and CO2 are exchanged in the lungs. Procedures were also developed to take into affect the Glasgow Coma Scale for determining levels of consciousness by varying the ECS eye-blinking function to partially indicate the level of consciousness of the patient. In addition, the ECS was modified to provide various levels of pulses from weak and thready to hyper-dynamic to assist in assessing patient conditions from the femoral, carotid, brachial, and pedal pulse locations.

Parker, Nigel↗
NASA NTRS2002

Pulmonary venous flows reflect changes in left atrial hemodynamics during mitral balloon valvotomy

Patients with mitral stenosis have usually blunted pulmonary venous (PV) flow, because of decreased mitral valve area and diastolic dysfunction. The authors compared changes in Doppler PV velocities by using transesophageal echocardiography (TEE) against hemodynamics parameters before and after mitral balloon valvotomy to observe relevance of PV velocities and endsystolic left atrial (LA) pressure-volume relationship. In 25 patients (aged 35 +/- 17 years) with mitral stenosis in sinus rhythm, changes in LA pressure and volumes were compared with PV velocities before and after valvotomy. Mitral valve area, mitral gradients, and deceleration time were obtained. Mitral valve area and mitral gradients changed from 1 +/- 0.2 cm2 and 14.6 +/- 5.4 mmHg to 1.9 +/- 0.3 cm2 and 6.3 +/- 1.7 mmHg, respectively (p<0.001). AR peak reverse flow velocity and AR duration decreased from 29 +/- 13 cm/s and 110 =/- 30 msec to 19 +/- 6 cm/s and 80 +/- 29 msec respectively (p<0.001). Transmitral Doppler E wave deceleration time decreased from 327 +/- 85 to 209 +/- 61 s and cardiac output increased from 4.2 +/- 1.0 to 5.2 +/- 1.1 L/minute (p<0.001). The changes in LA pressure were correlated with changes in S/D (r=0.57, p<0.05). The changes in endsystolic LA pressure-volume relationship were also correlated with changes in S/D (r=0.52, p<0.05). Endsystolic LA pressure-volume relationship decreased after mitral balloon valvotomy, as a result of a large decrease in pressure. PV systolic/diastolic (S/D) waves ratio reflects endsystolic LA pressure-volume relationship and may be used as another indicator of successful valvotomy.

Non-NASA Center↗
NASA NTRS2000

Endogenous circulating sympatholytic factor in orthostatic intolerance

Sympathotonic orthostatic hypotension (SOH) is an idiopathic syndrome characterized by tachycardia, hypotension, elevated plasma norepinephrine, and symptoms of orthostatic intolerance provoked by assumption of an upright posture. We studied a woman with severe progressive SOH with blood pressure unresponsive to the pressor effects of alpha(1)-adrenergic receptor (AR) agonists. We tested the hypothesis that a circulating factor in this patient interferes with vascular adrenergic neurotransmission. Preincubation of porcine pulmonary artery vessel rings with patient plasma produced a dose-dependent inhibition of vasoconstriction to phenylephrine in vitro, abolished vasoconstriction to direct electrical stimulation, and had no effect on nonadrenergic vasoconstrictive stimuli (endothelin-1), PGF-2alpha (or KCl). Preincubation of vessels with control plasma was devoid of these effects. SOH plasma inhibited the binding of an alpha(1)-selective antagonist radioligand ([(125)I]HEAT) to membrane fractions derived from porcine pulmonary artery vessel rings, rat liver, and cell lines selectively overexpressing human ARs of the alpha(1B) subtype but not other AR subtypes (alpha(1A) and alpha(1D)). We conclude that a factor in SOH plasma can selectively and irreversibly inhibit adrenergic ligand binding to alpha(1B) ARs. We propose that this factor contributes to a novel pathogenesis for SOH in this patient. This patient's syndrome represents a new disease entity, and her plasma may provide a unique tool for probing the selective functions of alpha(1)-ARs.

Case Reports↗
NASA NTRS1988

Vascular pressures and passage of gas emboli through the pulmonary circulation

Doppler technique was used to measure the pulmonary vascular pressure gradients in dogs that received venous air emboli (VAE) at the rate of 0.35 ml/kg per min, at which the spillover of bubbles into the systemic arteries occur. It was found that, in 60 percent of dogs, venous bubbles spilled over into the arterial circulation at the pulmonary vascular pressure gradient of about 34.7 mm Hg. When the pulmonary vascular pressure gradient was raised to about 52 mm Hg, the spillover of venous bubbles occurred 100 percent of time. It is concluded that venous bubbles can cross the lungs of anesthetized dogs when the driving pressures are sufficient to overcome the normal filtering function.

Butler, B. D.↗
DOE OSTI2026

Lethality is Local, but Survival is Systemic: Temporal and Multi-Organ Responses to Chlorine Gas Exposure in a Murine Model

Chlorine gas (Cl2) is a highly toxic chemical associated with both localized lung injury and systemic health effects. While pulmonary damage has been well characterized, the systemic inflammatory and metabolic responses remain poorly understood. We aimed to define the temporal and multi-organ responses to Cl2 exposure in a murine model, with a focus on identifying spatiotemporal inflammation and its impact on survival and lethality. SKH1 mice were exposed for 10 min to varying concentrations of Cl2 (94.4–810 ppm, representative of non-lethal, LD10, and LD50 doses) and monitored for respiratory function, perfusion, and acidosis using organ-specific imaging. At multiple time points (40 min, 6 h, 24 h, and 7 d), we measured phosphoproteins, cytokines, chemokines, growth factors, and metabolic hormones in the lungs, heart, cortex, and plasma. Statistical modeling and logistic regression were used to identify biomarkers associated with lethality and survival. We found that lung injury was the primary cause of potential lethality, particularly via early phosphoprotein signaling disruptions. However, survival correlated with early systemic coordination of inflammatory and metabolic signals across organs. Perfusion and acidosis imaging were strongly associated with chemokine and hormone responses. Key survival-associated plasma biomarkers included decreased insulin, increased ghrelin, and decreased eotaxin. While potential lethality from Cl2 exposure is locally driven by pulmonary injury, survival depends on systemic, multi-organ responses that occur rapidly post-exposure. Within this model, our findings identify a potential therapeutic window to enhance survival and suggest candidate biomarkers that may be explored translationally for both triage and treatment of chlorine-related incidents.

chlorine gas↗
NASA NTRS2000

Effects of JP-8 Jet Fuel on Homeostasis of Clone 9 Rat Liver Cells

Chronic exposure to JP-8 and other kerosene-based petroleum distillates has been associated with hepatic, renal, neurologic, pulmonary, and immune toxicity. However, the effects of kerosene-type jet fuels on cellular homeostasis hitherto have not been reported. Fluorescence imaging using a Meridian Ultima laser scanning fluorescence microscope was used to evaluate the effect of JP-8 jet fuel on a communication competent rat liver cell line. Several endpoints of cellular function were measured including gap junctional intercellular communication (GJIC), mitochondrial and plasma membrane potential (MMP and PMP, respectively), intracellular glutathione (GSH) concentration, glutathione-S-transferase (GST) activity, and reactive oxygen species (ROS) generation. Cells were treated with JP-8 (0.01 to 2% in ethanol (EtOH)) for the following time points: 1 h, 24 h, 48 h, and analysis immediately after addition of jet fuel. GJIC analyzed directly after addition of 1% JP-8 was reduced 4.9-fold relative to EtOH-dosed control groups and further reduction (12.6-fold) was observed in cells treated for 1 h. Moreover, GJIC was not recoverable in cells treated with 1% JP-8 for 1 h and subsequently washed and incubated in fresh medium for 1 h. Significant changes in GSH content and GST activity were observed in cells analyzed directly after addition of 1% JP-8. GSH content increased in cells treated for 1 h with less than 2% JP-8 whereas treatment with 2% JP-8 for 1 h resulted in a 50% reduction in intracellular GSH relative to EtOH-dosed controls. Cells treated with 1% JP-8 for 48 h exhibited changes in GSH levels. However, higher JP-8 concentrations exhibited more pronounced changes in GSH and GST, which led to suppression of GSH synthesis. ROS increased in a dose-responsive fashion at JP-8 concentrations up to 1%, but decreased to 80% of control values at 2% and 3% JP-8. A 25% reduction in PMP was observed in cells treated for 1 h with 1% JP-8. In contrast, cells treated for 48 h with 2% JP-8 exhibited a 25% increase when compared to control. No significant changes were noted in the 0.01 and 1% treatment groups. Moreover, no significant changes were observed in MMP or intracellular calcium concentrations in cells treated with 0.01 to 2% JP-8 for up to 48 h. In summary, the most significant effects observed in the present study which may contribute to the toxicity of JP-8 jet fuel in cultured rat liver cells include effects on GJIC, ROS production, and GSH depletion at high (i.e., greater than 2%) JP-8 concentrations.

Wilson, C. L.↗
NASA NTRS2000

Reduced xenon diffusion for quantitative lung study--the role of SF(6)

The large diffusion coefficients of gases result in significant spin motion during the application of gradient pulses that typically last a few milliseconds in most NMR experiments. In restricted environments, such as the lung, this rapid gas diffusion can lead to violations of the narrow pulse approximation, a basic assumption of the standard Stejskal-Tanner NMR method of diffusion measurement. We therefore investigated the effect of a common, biologically inert buffer gas, sulfur hexafluoride (SF(6)), on (129)Xe NMR and diffusion. We found that the contribution of SF(6) to (129)Xe T(1) relaxation in a 1:1 xenon/oxygen mixture is negligible up to 2 bar of SF(6) at standard temperature. We also measured the contribution of SF(6) gas to (129)Xe T(2) relaxation, and found it to scale inversely with pressure, with this contribution approximately equal to 1 s for 1 bar SF(6) pressure and standard temperature. Finally, we found the coefficient of (129)Xe diffusion through SF(6) to be approximately 4.6 x 10(-6) m(2)s(-1) for 1 bar pressure of SF(6) and standard temperature, which is only 1.2 times smaller than the (129)Xe self diffusion coefficient for 1 bar (129)Xe pressure and standard temperature. From these measurements we conclude that SF(6) will not sufficiently reduce (129)Xe diffusion to allow accurate surface-area/volume ratio measurements in human alveoli using time-dependent gas diffusion NMR.

Non-NASA Center↗
NASA NTRS1973

Mechanisms of inert gas narcosis

Experiments describing the mechanism of inert gas narcosis are reported. A strain of mice, genetically altered to increase susceptibility to botulin poisoning (synaptic response) appears to increase metabolic rates while breathing argon; this infers a genetically altered synaptic response to both botulin toxin and narcotic gases. Studies of metabolic depression in human subjects breathing either air or a 30% mixture of nitrous oxide indicate that nitrous oxide narcosis does not produce pronounced metabolic depression. Tests on mice for relative susceptibilities to narcosis and oxygen poisoning as a function of fatty membrane composition show that alteration of the fatty acid composition of phospholipids increases resistance to metabolically depressant effects of argon but bas no effect on nitrous oxide narcosis. Another study suggests that acclimatization to low tension prior to high pressure oxygen treatment enhances susceptibility of mice to convulsions and death; developing biochemical lesions cause CNS metabolite reductions and pulmonary damage.

Source record↗