Search NASA⌕ Search

SEARCH · Search NASA

Results for “EDEMA”

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.

At least 19 records
All sourcesNASA NTRSDOE OSTI
DOE OSTI2018

Progression of vasogenic edema induced by activated microglia under permanent middle cerebral artery occlusion

Highlights: • Vasogenic edema was visualized by superimposing TTC staining on T2WI. • Vasogenic edema moved from the ischemic core to the peripheral region. • Microglial activation was spread from the ischemic core to the peripheral region. • Microglial inhibition suppressed the progression of vasogenic edema. • Microglia are involved in vasogenic edema progression in ischemic stroke. Brain edema is a severe complication that accompanies ischemic stroke. Increasing evidence shows that inflammatory cytokines impair tight junctions of the blood-brain barrier, suggesting the involvement of microglia in brain edema. In this study, we examined the role of microglia in the progression of ischemic brain edema using mice with permanent middle cerebral artery occlusion. The intensity of T2-weighted imaging (T2WI) in the cerebral cortex and the striatum was elevated 3 h after occlusion and spread to peripheral regions of the ischemic hemisphere. Merged images of 2,3,5-triphenyl tetrazolium chloride staining and T2WI revealed the exact vasogenic edema region, which spread from the ischemic core to outside the ischemic region. Microglia were strongly activated in the ischemic region 3 h after occlusion and, notably, activated microglia were observed in the non-ischemic region 24 h after occlusion. Pretreatment with minocycline, an inhibitor of microglial activation clearly suppressed not only vasogenic edema but also infarct formation. We demonstrated in this study that vasogenic edema spreads from the ischemic core to the peripheral region, which can be elicited, at least in part, by microglial activation induced by ischemia.

60 APPLIED LIFE SCIENCES↗
NASA NTRSDate not supplied

B Complex 5-Methyltetrahydrofolate, Riboflavin, Pyridoxine, and Methylcobalamin Supplementation as a Non-Mechanical Countermeasure to Mitigate Optic Disc Edema Changes During Strict 6º Head-Down Tilt Bed Rest

A subset of astronauts on International Space Station missions have experienced optic disc edema, part of what is characterized as Spaceflight Associated Neuro-ocular Syndrome (SANS). While the precise cause of SANS is unknown, it is likely that there are multiple contributing factors, including genetic and environmental factors. Our recent work has shown that crewmembers with SANS have higher concentrations of metabolic biomarkers of impairments in the one-carbon metabolic pathway compared to unaffected astronauts - before, during, and after f light (1). B-vitamin status and the presence of one-carbon pathway single nucleotide polymorphism (SNP) variants predicted the incidence of SANS pathologies, including optic disc edema (2). Specifically, the G allele of methionine synthase reductase (MTRR) A66G and the C allele of serine hydroxymethyltransferase-1 (SHMT1) C1420T were associated with increased incidence of SANS pathologies (2). In a recent 30-d bed rest head-down tilt study with 0.5% CO2 exposure, 5 of 11 subjects developed optic disc edema (4) and the same SHMT1 C1420T and MTRR A66G genetic variants were associated with a larger increase in total retina thickness, a quantitative measure of optic disc edema (5). We published a multi-hit hypothesis of how genetics represents an indispensable element of SANS, which is a multifactorial problem (6). In brief: endothelial dysfunction secondary to genetic, biochemical/nutritional, and physiological (e.g., cardiovascular/fluid shift) f actors could lead to optic disc edema and the other ocular changes that occur in SANS. We expanded this hypothesis to include the possibility that genetic effects on B-vitamin status can alter nitric oxide synthesis and oxidative stress in the endothelium. This in turn could alter the turnover of structural components of the sclera, making it more susceptible to pathologic changes when faced with stressors related to the unrelenting headward fluid shift that occurs in weightlessness and strict head-down tilt bed rest (5). If the relationships that we have observed in flight and ground-based research hold true for the SANS Countermeasure Study, these genetic factors could predict who will be more susceptible to the development of SANS, and more importantly could also provide countermeasure options. As has been shown extensively in the literature, vitamin supplementation can serve to overcome genetic hindrances to one-carbon biochemistry and vascular physiology. Thus, based on our findings, publications, and hypotheses, supported by extensive supporting literature, we had hoped to test in the SANS Countermeasure Study the efficacy of a bioactive B-vitamin complex as a countermeasure to optimize function of the one-carbon pathway and prevent or mitigate optic disc edema during strict 6-degree head down tilt bed rest, and ultimately in space f light. While the supplement is no longer planned to be tested in the SANS Countermeasure Study because of laws regulating supplementation studies like this costing much more than initially planned, we will assess the contribution of one-carbon pathway genetics and B-vitamin status to SANS risk.

S R Zwart↗
NASA NTRSDate not supplied

Exploring Endothelial Function Risk Factors and Optic Disc Edema Changes During Strict 6º Head-Down Tilt Bed Rest

Approximately 20% of astronauts on International Space Station missions experience ophthalmic pathologies including optic disc edema, part of what is characterized as Spaceflight Associated Neuro-ocular Syndrome (SANS). While the cause of SANS is unknown, there are likely multiple contributing factors, including genetics, that may affect the response to spaceflight in affected individuals. B-vitamin status and the presence of specific one-carbon pathway single nucleotide polymorphism (SNP) alleles predicted the incidence of SANS pathologies in astronauts and in bed rest subjects. There are several hypotheses for how genetic variants could lead to SANS, specifically related to endothelial function. The biochemical pathway to which these genes are associated is intimately involved in maintaining endothelial function via nitric oxide synthase (eNOS) coupling and nitric oxide (NO) production. Furthermore, eNOS uncoupling can impair the functional status of the endothelial glycocalyx, which lines the entirety of the vascular lumen and affects endothelial function. Vascular distension, stasis and altered shear forces, which are associated with headward fluid shifts, may also contribute to glycocalyx dysfunction and shedding, resulting in endothelial dysfunction and increased vascular permeability and tissue edema, potentially contributing to optic nerve and optic disc edema in affected individuals. Given the findings relating genetics and the risk of optic disc edema in astronauts during flight and subjects during bed rest, further investigation is warranted. In this study, we will assess the same genetic variants in another bed rest study: AGBRESA. Some of the AGBRESA subjects developed optic disc edema, but their genetics have not been studied. Furthermore, we will test available urine samples from prior bed rest studies (VaPER and AGBRESA) for markers of glycocalyx degradation to expand our understanding of factors contributing to SANS.

S R Zwart↗
NASA NTRS2024

Development of optic disc edema during 30 days of hypercapnic head down tilt bed rest is associated with short sleep duration and blunted temperature amplitude

Consequences of sleep and circadian rhythm disturbances include many neurophysiological sequelae, especially when combined with spaceflight stressors, and are therefore hypothesized to contribute to the development of optic disc edema observed in astronauts. Additionally, chronically elevated carbon dioxide (CO 2 ) levels on the International Space Station may contribute to the observed sleep disturbances in astronauts. Here we determined if the spaceflight analogue head-down tilt bed rest (HDTBR) combined with elevated CO 2 levels influenced sleep and core temperature and was associated the development of optic disc edema. Healthy participants (5 female, 6 male) aged 25-50 years, underwent thirty days of strict 6° HDTBR in a mild hypercapnic environment (ambient PCO 2 = 4 mmHg) with measures of sleep, 24-hour core temperature, overnight arterialized CO2, and Frisén grade edema collected pre-HDTBR, on HDTBR days 4, 17, 28, and post-HDTBR days 4 and 10. During all HDTBR time points, sleep, core temperature, and overnight arterialized CO 2 were not statistically significantly different than the pre-HDTBR measurements. However, independent of the HDTBR intervention, the odds ratios (mean [95% CI]) for developing Frisén grade optic disc edema were statistically significant for each hour below the mean total sleep time (2.2 [1.1-4.4]) and stage 2 NREM sleep (4.8 [1.3-18.6]), and above the mean for wake after sleep onset (3.6 [1.2-10.6]) and for each 0.1°C decrease in core temperature amplitude below the mean (4.0 [1.4-11.7]).These data suggest that optic disc edema occurring during HDTBR was more likely to occur in those with short sleep duration and blunted temperature amplitude.

Kate H. Christian↗
DOE OSTI2019

Corpus luteum with ovarian stromal edema is associated with pelvic pain and confusion for ovarian torsion

Purpose: To distinguish the corpus luteum with adjacent ovarian stromal edema as an entity associated with pelvic pain, with confounding ultrasound features that may lead to false-positive diagnosis of ovarian torsion. Methods: This is a blinded, retrospective study of 243 corpora lutea on transvaginal ultrasound. Imaging parameters included ovarian and corpus luteum volumes, central cystic space within the corpus luteum, vascularity around the corpus luteum, peripherally displaced follicles, and complex free fluid. Residual volume (ovarian volume minus corpus luteum volume) was used as a surrogate for ovarian stromal edema. Clinical parameters included age, pregnancy, and location/acuity of pain if present. Concern for ovarian torsion in radiology reports was documented. Results: 51.0% (124/243) of patients presented with pain. Multivariate regression analysis of factors significantly associated with pain (including age, p = 0.001; larger corpus luteum volume, p = 0.002; larger residual volume, p < 0.001; complex free fluid, p = 0.002; and peripherally displaced follicles, p < 0.001) left only increased residual volume as significantly associated with pain [OR 1.02–1.16; p = 0.01]. False-positive concern for ovarian torsion on ultrasound was present in 12.9% (16/124) of patients with pain, associated with enlarged ovaries (p < 0.001) and peripherally displaced follicles (p < 0.001). High correlation between location of pain and side of the corpus luteum was demonstrated in patients with pain < 14 days duration (p < 0.001). Conclusion: Corpus luteum with ovarian stromal edema is associated with pelvic pain and can mimic ovarian torsion on ultrasound. Further research should explore diagnostically useful differences between cases of ovarian torsion and cases of ovarian edema related to corpora lutea.

62 RADIOLOGY AND NUCLEAR MEDICINE↗
DOE OSTI2018

Hypertonic saline regulates microglial M2 polarization via miR-200b/KLF4 in cerebral edema treatment

Highlights: • Hypertonic saline (HS) alleviates cerebral edema via regulating neuroinflammation. • miR-200b/KLF4 regulates microglial M2 polarization during HS treatment. • KLF4 directly binds to Arg1 promoter and induces its transcription. • Modulation of KLF4 in vivo affects HS treatment of cerebral edema. Hypertonic saline (HS) has been used clinically for treatment of cerebral edema for decades. Previously we have demonstrated that HS alleviates cerebral edema via regulating water/ion channel protein and attenuating neuroinflammation. However, whether HS treatment triggers microglia polarization and its regulatory mechanism during this process is unclear.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Central Corneal Edema with Scleral-Lens Wear

Purpose: To assess the safety of scleral-lens designs, we model and clinically assess central corneal edema induced by scleral-lens wear for healthy subjects. Materials and Methods: Typically, central corneal swelling during scleral-lens wear is measured using optical coherence tomography (OCT). Transport resistances are modeled for oxygen diffusion through the scleral lens and post-lens tear-film (PoLTF), and into the cornea. Oxygen deficiency in the cornea activates anaerobic metabolic reactions that induce corneal edema. Oxygen permeability, carbon-dioxide permeability, settled-lens PoLTF thickness, and scleral-lens thickness are varied in the calculations to mimic different lens fits. Results: Transport modeling predicts that for open eyes, increasing PoLTF thickness from 50 to 400 µm increases central corneal swelling by approximately 1–1.5% when oxygen transmissibility ( Dk/L ) is greater than 10 hBarrer/cm (i.e., hectoBarrer/cm). Although swelling is larger for oxygen Dk/L < 10 hBarrer/cm, PoLTF thickness has minimal impact in this range. For open eye, oxygen transmissibility of the lens plays a significant role in corneal edema, but is negligible when oxygen Dk/L is > 40 hBarrer/cm. For closed eye, central corneal swelling is greater than 5% for an oxygen Dk/L range of 0–100 hBarrer/cm with typical lens-fitting parameters. For carbon-dioxide transmissibilities increasing from 50 to 250 hBarrer/cm and with a fixed oxygen Dk/L of 25 hBarrer/cm, calculated swelling diminishes by an additional 0.5%. Comparison of model calculations to clinical-swelling data is within the error range of the clinical measurements. Conclusions: Oxygen/metabolite transport calculations for open-eye scleral-lens wear demonstrate that normal PoLTF thicknesses fitted by clinicians (i.e., PoLTF thicknesses < 400 µm) with modern scleral lenses (i.e., oxygen Dk/L > 25 hBarrer/cm) produce corneal swelling of less than 2% in agreement with experiment. Therefore, scleral lenses prescribed today evoke less than physiological hypoxic swelling (i.e., less than 4%) for healthy corneas during open-eye. Closed-eye wear, however, appears clinically unsafe.

60 APPLIED LIFE SCIENCES↗
NASA NTRS1992

VA/Q distribution during heavy exercise and recovery in humans: implications for pulmonary edema

Ventilation-perfusion (VA/Q) inequality has been shown to increase with exercise. Potential mechanisms for this increase include nonuniform pulmonary vasoconstriction, ventilatory time constant inequality, reduced large airway gas mixing, and development of interstitial pulmonary edema. We hypothesized that persistence of VA/Q mismatch after ventilation and cardiac output subside during recovery would be consistent with edema; however, rapid resolution would suggest mechanisms related to changes in ventilation and blood flow per se. Thirteen healthy males performed near-maximal cycle ergometry at an inspiratory PO2 of 91 Torr (because hypoxia accentuates VA/Q mismatch on exercise). Cardiorespiratory variables and inert gas elimination patterns were measured at rest, during exercise, and between 2 and 30 min of recovery. Two profiles of VA/Q distribution behavior emerged during heavy exercise: in group 1 an increase in VA/Q mismatch (log SDQ of 0.35 +/- 0.02 at rest and 0.44 +/- 0.02 at exercise; P less than 0.05, n = 7) and in group 2 no change in VA/Q mismatch (n = 6). There were no differences in anthropometric data, work rate, O2 uptake, or ventilation during heavy exercise between groups. Group 1 demonstrated significantly greater VA/Q inequality, lower vital capacity, and higher forced expiratory flow at 25-75% of forced vital capacity for the first 20 min during recovery than group 2. Cardiac index was higher in group 1 both during heavy exercise and 4 and 6 min postexercise. However, both ventilation and cardiac output returned toward baseline values more rapidly than did VA/Q relationships. Arterial pH was lower in group 1 during exercise and recovery. We conclude that greater VA/Q inequality in group 1 and its persistence during recovery are consistent with the hypothesis that edema occurs and contributes to the increase in VA/Q inequality during exercise. This is supported by observation of greater blood flows and acidosis and, presumably therefore, higher pulmonary vascular pressures in such subjects.

NASA Discipline Cardiopulmonary↗
NASA NTRS1991

Local fluid shifts and edema in humans during simulated microgravity

Local fluid shifts and edema in humans during simulated microgravity is studied. Recent results and significance and future plans on the following research topics are discussed: mechanisms of headward edema formation during head-down tilt; postural responses of head and foot microcirculations and their sensitivity to bed rest; and transcapillary fluid transport associated with lower body negative pressure (LBNP) with and without saline ingestion.

Hargens, Alan R.↗
NASA NTRS1996

Latest advances in edema

Basic concepts in the physiopathology of edema are reviewed. The mechanisms of fluid exchange across the capillary endothelium are explained. Interstitial flow and lymph formation are examined. Clinical disorders of tissue and lymphatic transport, microcirculatory derangements in venous disorders, protein disorders, and lymphatic system disorders are explored. Techniques for investigational imaging of the lymphatic system are explained.

Review, Tutorial↗
NASA NTRS1972

Pulmonary Edema and Plasma Volume Changes in Dysbarism

Two groups of anesthetized, fasted pigs were utilized. One group of 13 animals (8.5 to 16.6 kilograms) was exposed to a high-pressure environment, and the other group of eight animals (6.9 to 20.0 kilograms) constituted the control group. The experimental group was subjected to an atmosphere of 90 percent nitrogen and 10 percent oxygen at a pressure of 50 psig for 30 minutes and then decompressed at a rate 10 psi/min. Plasma volumes, using both iodine-125-tagged-albumin and chromium-51-tagged-cell dilution techniques, were measured before, immediately after, and at 30 and 60 minutes after decompression. Aortic and right-ventricular systolic pressures were also recorded. At 60 minutes after decompression, blood samples were taken, the animals were sacrificed, and the water content of the lungs, kidneys, livers, and spleens was estimated by measuring tissue wet weight and dry weight. Protein extravasation and tissue blood volumes were determined by measuring the iodine-125-tagged-albumin and chromium-51-tagged-cell spaces in homo-genates of the organs under investigation.

Joki, J. A.↗