Understanding Oxygenated Blood Pulse Transit Times during Hypoxia Induction for Characterization of Cognitive Impairment
Explore the source record for details and available documents.
SEARCH · Engineering Papers
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.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Lymphocytes are naturally exposed to genotoxic stresses. DNA damage occurs during the entire lymphocyte’s life span and is induced mainly by reactive oxygen species (ROS), replication fork collapse, or telomere shortening during the immune response or intense cell proliferation phases. Strong evidence for the influence of immune function on DNA repair comes from studies of SCID disease. SCID mice not only have a deficient V(D)J recombination but are also unable to repair double strand breaks, leading to increased radiation sensitivity. The leukocytes’ transcriptome of 8 ISS crew members revels a dysregulated immune function and activation of cellular survival pathways in response to space environment. We have performed PCR analysis in peripheral mononuclear cells from the same crew members. A list of 62 genes were carefully selected addressing immunological and cell survival pathways. Differentially expressed genes indicated changes in chemokine receptor activity, chemokine binding, toll-like receptors, adhesion molecules and cellular response to DNA damage.
Lymphocytes are naturally exposed to genotoxic stresses. DNA damage occurs during the entire lymphocyte’s life span and is induced mainly by reactive oxygen species (ROS), replication fork collapse, or telomere shortening during the immune response or intense cell proliferation phases. Strong evidence for the influence of immune function on DNA repair comes from studies of SCID disease. SCID mice not only have a deficient V(D)J recombination but are also unable to repair double strand breaks, leading to increased radiation sensitivity. The leukocytes’ transcriptome of 8 ISS crew members revels a dysregulated immune function and activation of cellular survival pathways in response to space environment. We have performed PCR analysis in peripheral mononuclear cells from the same crew members. A list of 62 genes were carefully selected addressing immunological and cell survival pathways. Differentially expressed genes indicated changes in chemokine receptor activity, chemokine binding, toll-like receptors, adhesion molecules and cellular response to DNA damage.
Explore the source record for details and available documents.
IEEE SIgnal Processing Society (SPS) and Women in Signal Processing (WiSP) Webinar (https://signalprocessingsociety.org/blog/webinar-wisp-blood-platelets-classification-earth-system-digital-twins-career-computer-vision): Join us for an interactive session with Dr. Jacqueline Le Moigne, Manager of the NASA Science Mission Directorate Earth Science Technology Office’s Advanced Information Systems Technology Program. In this webinar, Dr. Le Moigne will share her journey through academia, the private sector, and her pivotal roles at NASA, emphasizing her work in signal processing, computer vision, and related technologies. The webinar will conclude with an interactive Q&A session, providing attendees the opportunity to engage directly with Dr. Le Moigne about her experiences and insights. Dr. Jacqueline Le Moigne manages NASA's Advanced Information Systems Technology Program, focusing on novel technologies that support Earth Science missions. She previously held roles at NASA Goddard, including Assistant Chief for Technology, and has worked on NASA's Space Technology Research Grants Program and Technology Roadmaps. Before NASA, she was a Research Scientist at the University of Maryland's Computer Vision Laboratory and also gained experience in the private sector. Jacqueline earned her Ph.D. in Computer Science from the University Pierre and Marie Curie in Paris. Her research interests include Image Registration, Computer Vision, Artificial Intelligence, Autonomous Systems, Distributed Spacecraft Missions (DSM), and Earth System Digital Twins (ESDT), as well as high-performance and onboard computing. She has authored over 180 publications, including books and patents, and has received multiple awards, including the NASA Exceptional Service Medal and the Goddard Information Science and Technology Award in 2012.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
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.
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.
Prolonged exposure to microgravity or its analogues impairs thermoregulation in humans evidenced by higher internal temperatures following the exposure during a thermal challenge. Although the mechanism leading to this response has not been clearly delineated, we identified that prolonged head-down tilt (HDT) markedly impairs thermoregulatory reflex control of skin blood flow, as demonstrated by an increased internal temperature threshold for cutaneous vasodilation, and by a reduced slope of the relationship between the elevation in skin blood flow relative to the elevation in internal temperature. Recently, Fortney et al. identified similar responses in two individuals following 115 days of microgravity exposure. One possible mechanism leading to altered cutaneous vasodilation during a thermal challenge following actual or simulated microgravity exposure may be associated with baroreflex-mediated attenuation in the elevation of skin blood flow. During a heat stress the elevation in skin blood flow is accomplished through a combination of increased cutaneous vascular conductance and cardiac output, both of which result in central venous pressure (CVP) decreasing 2-6 mmHg. Reductions in CVP of this magnitude in normothermia decrease muscle blood flow and skin blood flow presumably through unloading the cardiopulmonary baroreceptors. It is unclear whether the reduction in CVP, and accompanying cardiopulmonary baroreceptor unloading, during passive heating buffers the elevation in skin blood flow. That is, would the elevation in skin blood flow be greater if CVP did not decrease, or decreased to a lesser extent during the heat stress? Conversely, if CVP decreased to a greater extend during a thermal challenge following a perturbation such as prolonged HDT, would the elevation in skin blood flow be attenuated during that thermal challenge? Given that prolonged HDT decreases plasma volume and central venous pressure, such a finding would provide a plausible hypothesis to explain why skin blood flow does not increase to the same extent during a heat stress following simulated or actual microgravity exposure. Thus, the purpose of this project was to identify whether cardiopulmonary baroreceptor unloading coincident with heat stress buffers the elevation in skin blood flow.
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.
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.