Academic literature on the topic 'Extracellular fluid volume'

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Journal articles on the topic "Extracellular fluid volume"

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Sánchez, M., M. Jiménez-Lendínez, M. Cidoncha, M. J. Asensio, E. Herrero, A. Collado, and M. Santacruz. "Comparison of Fluid Compartments and Fluid Responsiveness in Septic and Non-Septic Patients." Anaesthesia and Intensive Care 39, no. 6 (November 2011): 1022–29. http://dx.doi.org/10.1177/0310057x1103900607.

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Our objective was to study the response to a fluid load in patients with and without septic shock, the relationship between the response and baseline fluid distributions and the ratios of the various compartments. A total of 18 patients with septic shock and 14 control patients without pathologies that increase capillary permeability were evaluated prospectively. We used transpulmonary thermodilution to measure the extravascular lung water index, intrathoracic blood volume index and pulmonary blood volume. For the measurement of the initial distribution volume of glucose, plasma volume and extracellular water, we used dilutions of glucose, indocyanine green and sinistrin respectively. Transpulmonary thermodilution and dilutions of glucose were repeated 75 minutes after the beginning of the fluid load.The patients in the septic group had higher volumes of extracellular water (median 295 vs 234 ml/kg, P <0.001), lower intrathoracic blood volume index (median 894 vs 1157 ml/m2, P <0.003), higher pulmonary permeability ratios (extravascular lung water/pulmonary blood volume) (P <0.003) and higher systemic permeability ratios (interstitial/plasma volume) (P <0.04). The intrathoracic blood volume index increase after fluid loading was lower in the septic group (10 vs 145 ml/m2). The pulmonary permeability ratios did not correlate with the systemic permeability ratios, and in the septic group, the percentage volume retained in the intrathoracic blood volumes after fluid loading did not correlate with the systemic permeability ratios. Septic shock can cause a redistribution of fluids. Fluid administration in these patients produced a minimal increase in intrathoracic blood volume, and the percentage of volume retained in this space was not correlated with the interstitial/plasma volume ratio.
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Blaustein, M. P. "Sodium chloride, extracellular fluid volume, and hypertension." Hypertension 7, no. 5 (September 1985): 834–35. http://dx.doi.org/10.1161/01.hyp.7.5.834.

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Snelling, Hayley L. R., Myron B. Ciapryna, Philippe F. Bowles, Daphne M. Glass, Maria T. Burniston, and A. Michael Peters. "Extracellular fluid volume in patients with cancer." Nuclear Medicine Communications 31, no. 5 (May 2010): 359–65. http://dx.doi.org/10.1097/mnm.0b013e3283359073.

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Peters, A. Michael, Daphne M. Glass, and Nicholas J. Bird. "Extracellular fluid volume and glomerular filtration rate." Nuclear Medicine Communications 32, no. 7 (July 2011): 649–53. http://dx.doi.org/10.1097/mnm.0b013e3283457466.

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Simpson, John, and Terence Stephenson. "Regulation of extracellular fluid volume in neonates." Early Human Development 34, no. 3 (October 1993): 179–90. http://dx.doi.org/10.1016/0378-3782(93)90175-t.

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Peters, A. Michael. "Estimation of extracellular fluid volume in children." Pediatric Nephrology 27, no. 7 (March 16, 2012): 1149–55. http://dx.doi.org/10.1007/s00467-012-2117-9.

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Wong, William W. "Influence of ovariectomy on extracellular fluid volume in rats: Assessment of extracellular fluid volume by means of bromide." Journal of Laboratory and Clinical Medicine 135, no. 4 (April 2000): 298–99. http://dx.doi.org/10.1067/mlc.2000.105291.

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Bolscher, Marieke Dijkgraaf-ten, Rob Barto, Daphne A. Voorn, Dirk Compas, J. Coen Netelenbos, and Wim J. F. van der Vijgh. "Influence of ovariectomy on extracellular fluid volume in rats: Assessment of extracellular fluid volume by means of bromide." Journal of Laboratory and Clinical Medicine 135, no. 4 (April 2000): 303–8. http://dx.doi.org/10.1067/mlc.2000.105292.

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Hamlyn, J. M., and M. P. Blaustein. "Sodium chloride, extracellular fluid volume, and blood pressure regulation." American Journal of Physiology-Renal Physiology 251, no. 4 (October 1, 1986): F563—F575. http://dx.doi.org/10.1152/ajprenal.1986.251.4.f563.

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Data from humans and experimental animals indicate that hypertensive diseases triggered by extracellular fluid volume expansion are characterized, in their chronic phases, by relatively normal blood volume (BV) and heightened pressure-volume relationship may be viewed as corresponding to a condition of "virtual hypervolemia," where BV is inappropriately "high" relative to blood pressure. The limited data available on the phasic relationship between these variables indicate that the BV expansion appears to be a prerequisite to alterations in vascular ion metabolism, that both of these changes precede the rise in blood pressure, and that structures within the central nervous system may be a critical link between the body fluid volumes and vascular functional changes. In contrast, hypertensive diseases triggered by secretion of pressor agents or their precursors appear to be characterized in their chronic phases by low BV. These relationships and the associated alterations in plasma aldosterone and renin levels are summarized for a variety of clinical syndromes, including essential hypertension and pregnancy-induced hypertension. Direct or indirect evidence of a primary or secondary defect in renal function is apparent as an underlying event in many of these diseases.
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Manning, R. Davis. "Dynamics of extracellular fluid volume changes during hyperproteinemia." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 275, no. 6 (December 1, 1998): R1878—R1884. http://dx.doi.org/10.1152/ajpregu.1998.275.6.r1878.

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The dynamics of fluid volume distribution between the blood and interstitium during hyperproteinemia were studied in 12 anephric, conscious dogs during several states of hydration. After recovery from splenectomy and unilateral nephrectomy, plasma protein concentration was elevated to 8.4–8.7 g/dl by daily intravenous infusion of 330 ml of previously collected autologous plasma for 11 days. The remaining kidney was then removed, and the next day lactated Ringer solution equivalent to 10 or 20% of body weight was infused intravenously. By the end of the 25-h postinfusion period, Ringer infusion had increased circulating protein mass 20.9 ± 9.1% (mean ± SE) in the 10% group ( P< 0.05) and decreased it 10.5 ± 3.3% in the 20% group ( P < 0.05). The average increase in blood volume and arterial pressure during the postinfusion period was 27.4 ± 2.5 and 20.7 ± 3.7%, respectively, in the 10% group but only 17.8 ± 2.4 and 12 ± 1.6% in the 20% group (all changes significant compared with respective control). The relationship between blood volume and sodium space was similar to that found during normoproteinemia, such that elevations in sodium space of 40–50% increased blood volume but greater elevations in sodium space caused no further increases in blood volume. Overhydration during chronic hyperproteinemia causes hypervolemia and hypertension, but, in contrast to those in short-term studies, the increases in blood volume and arterial pressure are not greater than those achieved during normoproteinemia.
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Dissertations / Theses on the topic "Extracellular fluid volume"

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Reyhani, Vahid. "Extracellular Matrix and Actin Cytoskeleton - the Control Unit of Interstitial Fluid Volume." Doctoral thesis, Uppsala universitet, Institutionen för medicinsk biokemi och mikrobiologi, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-217027.

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The regulation of fluid (water) volume in the body is crucial for tissue homeostasis. The interstitial fluid, which comprises almost 20% of the body fluid, is stored in the loose connective tissue and its volume is actively regulated by components of this tissue. The loose connective tissue provides a path for fluid flow from capillaries to the tissue and lymphatics. This fluid is partially stored in the interstitium and the remainder is directed to the lymphatics. The fibroblasts in the loose connective tissue actively compact the fibrous extracellular matrix (ECM) through mechanotransduction via integrins. This in turn, maintains the interstitial fluid pressure and keeps the ground substance underhydrated. The interstitial fluid pressure is part of the forces that regulate the efflux of fluid from capillaries and keep the ground substance underhydrated. The underhydrated ground substance has a potential to take up fluid 3-fold the plasma volume. Therefore, the active contraction of the ECM via fibroblasts is crucial to prevent the risk of evacuation of fluid from capillaries. During pathologies, such as inflammation and carcinogenesis, the interstitial fluid pressure and hence the interstitial fluid volume is altered. The results presented in this thesis show that the signaling events downstream of αVβ3 integrin, collagen-binding β1 integrins, and platelet-derived growth factor receptor β, that induce cell-mediated matrix contraction, included paired function of PI3K and PLCγ, cofilin activation, actin turnover, and generation of actomyosin forces. Furthermore, the results highlight new potential roles for fibrin and αVβ3 integrins, for instance during clearance of edema. Notably, fibrin extravasation at inflammatory sites induced αVβ3 integrin-dependent matrix contraction, leading to normalization of the altered interstitial fluid volume. It also reprograms the expression of ECM-related genes and hence induces ECM turnover. Taken together, these results provide further insight into the regulatory mechanism through which the loose connective tissue actively regulates the interstitial fluid volume.
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Serwaah, Bonsu Amma. "Comparative retrospective analysis assessment of extracellular volume excess in hypertensive hemodialysis patients." Doctoral diss., University of Central Florida, 2011. http://digital.library.ucf.edu/cdm/ref/collection/ETD/id/5040.

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Cardiovascular disease, including hypertension, accounts for almost 50% of the deaths in patients with end stage renal disease (ESRD) on hemodialysis (HD) yet hypertension remains very poorly controlled in this population. The purpose of this study was to retrospectively compare control of hypertension in hemodialysis (HD) patients when extracellular volume (ECV) was assessed and managed by clinical parameters and physical assessment data alone with control of hypertension when data from blood volume monitoring (BVM) technology was also used to assess and manage ECV in a freestanding outpatient hemodialysis unit. The main cause of hypertension in the ESRD population has been identified as increased ECV most likely secondary to increased interdialytic weight gain and failure to attain and maintain patient's dry weight. HD nurses often employ clinical parameters along with physical examination to determine a patient's pre, intra, and post dialytic fluid status and this approach can have a high index of error. BVM technology is being used in many hemodialysis units to assist with assessment of ECV. A comparative retrospective chart review was used to collect data for this project. A descriptive, cross-sectional design was employed to answer the question: "Are hypertensive hemodialysis patients who dialyze in a freestanding dialysis unit, where BVM technology is utilized, more likely to be normotensive as defined by a pre dialysis blood pressure of less than 140/90 and post dialysis blood pressure less than 130/80"? A pilot study was conducted to determine if the patient population and data were available in existing patient records for extrapolation. Approval for the study was obtained from the University IRB. A convenience sample was obtained from the records of patients meeting the inclusion criteria.; Variables were measured and analyzed using descriptive statistics such as sampled paired T-test to compare pre and post BVM systolic, diastolic blood pressures, intradialytic weight gain, serum Albumin and sodium levels, and hemoglobin. A p-value of 0.05 was assigned for statistical significance. Data analysis showed there were statisticaly significant differences in the pre dialysis systolic blood pressure, post BVM, and the serum sodium pre and post BVM when the two groups were compared These statistically significant findings support a correlation between reduction in the HD patient's ECV and improved blood pressure control. The reduction of pre-dialysis SBP was significant because many patients on hemodialysis have systolic hypertension that may or may not coexist with diastolic hypertension. The findings of this study may be used to formulate a protocol to be used in the HD units where the BVM is available. The protocol would rely on accurate nursing assessment of clinical parameters, patient verbalizations of symptoms, and the routine use of the BVM in order to continuously assess the patient's fluid status. Future research recommendations include conducting the study in a population closer to the national sample, a study where glucose readings and /or hemoglobin A1C levels are measured to assess the impact of glucose on ECV, and which antihypertensive class of medication works best with BVM technology to effectively manage hypertension in this population.
ID: 029808737; System requirements: World Wide Web browser and PDF reader.; Mode of access: World Wide Web.; Thesis (D.N.P.)--University of Central Florida, 2011.; Includes bibliographical references (p. 74-81).
D.N.P.
Doctorate
Nursing
Nursing Practice
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Faucon, Anne-Laure. "Volume extracellulaire : évolution et valeur pronostique au cours de la maladie rénale chronique." Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASR002.

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Le volume extracellulaire (VEC) est étroitement régulé par les reins, via l’homéostasie sodée. Au cours de la maladie rénale chronique (MRC), il existe une altération de l’excrétion tubulaire de sodium, à l’origine d’une augmentation du VEC. L’évolution du VEC et sa valeur pronostique au cours de la MRC restent mal connues. En effet, si chez les patients dialysés chroniques, il est clairement établi que la surcharge hydro-sodée constitue un facteur indépendant de mortalité, les résultats des études pionnières menées chez des patients suivis pour une MRC restent controversés. L’analyse de l’impact de l’augmentation du VEC au cours de la MRC est un point important puisque celui-ci peut être modulé grâce à l’adaptation du traitement diurétique et de la consommation alimentaire de sodium. Par ailleurs, plusieurs applications cliniques – comme quantification du degré d’hypo ou d’hypervolémie, ou la mesure du débit de filtration glomérulaire – nécessitent une estimation précise du VEC théorique individuel. La valeur du VEC étant variable selon les caractéristiques anthropométriques et la composition corporelle, il donc est indispensable de développer un outil permettant d’estimer facilement le VEC théorique individuel. Les deux premiers axes d’études ont été menés chez les patients de la cohorte prospective hospitalière tricentrique NephroTest – cohorte qui inclut 2084 patients atteints de MRC de stade 1 à 5, de toutes étiologies – dont le VEC et le débit de filtration glomérulaire ont été mesurés par méthode de référence (i.e. volume de distribution et clairance d’un traceur exogène, respectivement). Dans la première partie, nous avons montré, grâce à l’utilisation de modèles de Cox cause-spécifiques, que le VEC constituait un facteur indépendant de mortalité, de progression de la MRC et d’insuffisance rénale chronique terminale. Dans la seconde partie, les résultats des modèles conjoints à effets aléatoires partagés avec prise en compte des risques compétitifs ont montré que le VEC augmentait avec la progression de la MRC, et que ces variations au cours du temps étaient associées aux risques de mortalité et d’insuffisance rénale chronique terminale. Dans la troisième partie, l’évaluation des différentes formules d’estimation du VEC théorique a montré que la précision et l’exactitude de ces dernières étaient faibles, questionnant leur utilisation en pratique clinique courante. Nous avons donc développé et validé une nouvelle équation d’estimation du VEC théorique, facilement utilisable en clinique ou en recherche, mais qui nécessite d’être validée à plus large échelle. L’ensemble de ces résultats corrobore le fait que le VEC est une cible thérapeutique très importante à considérer dans la prise en charge des patients suivis pour une MRC. Un outil d’estimation du VEC théorique facilement utilisable permettant de quantifier avec précision le degré d’hypervolémie reste nécessaire chez les patients ayant une MRC
Extracellular fluid volume (ECF) is tightly regulated by the kidneys, through sodium homeostasis. Chronic kidney disease (CKD) is characterized by an impairment of tubular sodium excretion, leading to ECF expansion. Change in ECF over time and its prognostic value remain poorly studied in CKD. Indeed, if several large-scaled studies have shown that fluid overload was a strong and independent risk factor for mortality in hemodialysis patients, results from pioneer studies conducted in non-dialysis CKD patients yielded conflicting results. Analysis of the impact of ECF during CKD is thus important in the clinical management of patients with CKD, as it may be corrected with diuretics and decreased sodium intake. Moreover, a precise and accurate estimation of the individual theoretical ECF is useful for several clinical settings, such as appreciation of how ECF may deviate from the normal condition, and glomerular filtration rate measurement (GFR) based on single-sample plasma clearance method. As ECF value varies according to anthropometric parameters, the development of a tool which allows estimation of individual theoretical ECF would be useful in clinical practice.The two first research topics have been conducted in patients from the prospective tricentric hospital-based NephroTest cohort – which included 2084 patients with CKD stage 1 to 5 of all etiologies – who underwent ECF and GFR measurements by gold standard methods (i.e. distribution volume and renal clearance of an exogenous tracer, respectively). In the first part, using cause-specific Cox models, we showed that ECF was an independent factor for mortality and end-stage kidney disease, and was associated with a faster GFR decline. In the second part, results from joint model for competing time-to-events with shared random effects showed that ECF increased over time in patients with CKD, and that this change in ECF was associated with the risks of mortality and end-stage kidney disease. In the third part, we showed that all ECF estimating equations displayed poor precision and accuracy, questioning their suitability in routine clinical practice. We thus developed and validated a new equation to estimate ECF. External validation in several cohorts including patients of extreme age and body mass index remains needed.All these results highlight the fact that ECF is an important therapeutic target in the clinical management of CKD patients. A readily applicable tool to accurately assess ECF excess in patients with CKD is needed
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Mathavakkannan, Suresh. "Techniques to assess volume status and haemodynamic stability in patients on haemodialysis." Thesis, University of Hertfordshire, 2010. http://hdl.handle.net/2299/4811.

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Volume overload is a common feature in patients on haemodialysis (HD). This contributes significantly to the cardiovascular disease burden seen in these patients. Clinical assessments of the volume state are often inaccurate. Techniques such as interdialytic blood pressure, relative blood volume monitoring, bioimpedance are available to improve clinical effectives. However all these techniques exhibit significant shortcomings in their accuracy, reliability and applicability at the bed side. We evaluated the usefulness of a dual compartment monitoring technique using Continuous Segmental Bioimpedance Spectroscopy (CSBIS) and Relative Blood Volume (RBV) as a tool to assess hydration status and determine dry weight. We also sought to evaluate the role of Atrial Natriuretic Peptide (ANP) and B-type Natriuretic Peptide (BNP) as a volume marker in dialysis patients. The Retrospective analysis of a historical cohort (n = 376, 55 Diabetic) showed a significant reduction in post-dialysis weights in the first three months of dialysis (72.5 to 70kg, p<0.027) with a non-significant increase in weight between months 6-12. The use of anti-hypertensive agents reduced insignificantly in the first 3 months, increased marginally between months 3-6 and significantly increased over the subsequent 6 months. The residual urea clearance (KRU) fell and dialysis times increased. The cohort was very different to that dialysing at Tassin and showed a dissociation between weight reduction and BP control. This may relate to occult volume overload. CSBIS-RBV monitoring in 9 patients with pulse ultrafiltration (pulse UF) showed distinct reproducible patterns relating to extra cellular fluid (ECF) and RBV rebound. An empirical Refill Ratio was then used to define the patterns of change and this was related to the state of their hydration. A value closer to unity was consistent with the attainment of best achievable target weight. The refill ratio fell significantly between the first (earlier) and third (last) rebound phase (1.97 ± 0.92 vs 1.32 ± 0.2). CSBIS monitoring was then carried out in 31 subjects, whilst varying dialysate composition, temperature and patient posture to analyse the effects of these changes on the ECF trace and to ascertain whether any of these interventions can trigger a change in the slope of the ECF trace distinct to that caused by UF. Only, isovolemic HD caused a change in both RBV and ECF in some patients that was explained by volume re-distribution due to gravitational shifts, poor vascular reactivity, sodium gradient between plasma and dialysate and the use of vasodilating antihypertensive agents. This has not been described previously. These will need to be explored further. The study did demonstrate a significant lack of comparability of absolute values of RECF between dialysis sessions even in the same patient. This too has not been described previously. This is likely to be due to subtle changes in fluid distribution between compartments. Therefore a relative changes must be studied. This sensitivity to subtle changes may increase the usefulness of the technique for ECF tracking through dialysis. The potential of dual compartment monitoring to track volume changes in real time was further explored in 29 patients of whom 21 achieved weight reductions and were able to be restudied. The Refill Ratio decreased significantly in the 21 patients who had their dry weights reduced by 0.95 ± 1.13 kg (1.41 ± 0.25 vs 1.25 ± 0.31). Blood pressure changes did not reach statistical significance. The technique was then used to examine differences in vascular refill between a 36oC and isothermic dialysis session in 20 stable prevalent patients. Pulse UF was carried out in both these sessions. There were no significant differences in Refill Ratios, energy removed and blood pressure response between the two sessions. The core temperature (CT) of these patients was close to 36oC and administering isothermic HD did not confer any additional benefit. Mean BNP levels in 12 patients during isovolemic HD and HD with UF did not relate to volume changes. ANP concentrations fell during a dialysis session in 11 patients from a mean 249 ± 143 pg/ml (mean ± SD) at the start of dialysis to 77 ± 65 pg/ml at the end of the session (p<0.001). During isolated UF levels did not change but fell in the ensuing sham phase indicating a time lag between volume loss and decreased generation. (136±99 pg/ml to 101±77.2 pg/ml; p<0.02) In a subsequent study ANP concentrations were measured throughout dialysis and in the post-HD period for 2 hours. A rebound in ANP concentration was observed occurring at around 90 min post-HD. The degree of this rebound may reflect the prevailing fluid state and merit further study. We have shown the utility of dual compartment monitoring with CSBIS-RBV technique and its potential in assessing volume changes in real time in haemodialysis patients. We have also shown the potential of ANP as an independent marker of volume status in the same setting. Both these techniques merit further study.
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Gregoriades, Jeannine Marie Crum. "Functions of the apical Na+/ K+/ 2Cl- Cotransporter 1 in choroid plexus epithelial cells." Wright State University / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=wright150367502359194.

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Friedman, Oded. "Role of Extracellular Fluid Volume in Inducing or Aggravating Obstructive Sleep Apnea-hypopnea in Patients with Resistant Hypertension." Thesis, 2009. http://hdl.handle.net/1807/18300.

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Accumulating evidence suggests that volume overload in drug-resistant hypertension (RH) may contribute to the high prevalence of obstructive sleep apnea-hypopnea (OSAH). Upon recumbency, leg fluid volume moves rostrally causing an increase in nuchal and peripharyngeal fluid content, subsequently obstructing airflow. Rostral fluid displacement following lower body positive pressure (LBPP) application and occurring spontaneously overnight were evaluated in subjects with RH (n = 25) and controlled hypertension (n = 15). In both groups, the reduction in mean upper airway cross-sectional area with LBPP strongly related to the amount of fluid displaced from the legs (R2 = 0.41; p<0.0001), although its magnitude was greater in the RH group (p=0.001; adjusted for propensity score). In both groups, the apnea-hypopnea index strongly related to the amount of fluid spontaneously displaced from the legs during sleep (R2 = 0.56; p<0.0001), although its magnitude was greater in the RH group (p=0.01; adjusted for propensity score).
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Antolić, AnaMaria. "The effect of extracellular osmolality on cell volume and resting skeletal muscle metabolism." 2006. http://www.oregonpdf.org.

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Vanderboom, Russell John. "The binding of follicular fluid glycosaminoglycans and extracellular matrix proteins." 1989. http://catalog.hathitrust.org/api/volumes/oclc/20077951.html.

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Thesis (M.S.)--University of Wisconsin--Madison, 1989.
Typescript. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 63-80).
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Books on the topic "Extracellular fluid volume"

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Hahn, Robert G. Fluid and electrolyte physiology in anaesthetic practice. Edited by Jonathan G. Hardman. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0003.

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The maintenance of body fluid homeostasis is an essential task in perioperative care. Body fluid volumes are tightly controlled by the nervous system, by hormones, and by the kidneys. All these systems are affected by anaesthesia and surgery in ways that must be appreciated by the anaesthetist. Administration of infusion fluids is the key tool to prevent major derangements of the body fluid volumes during before, during, and after surgery. By varying its composition, an infusion fluid can be made to selectively expand or shrink a body fluid compartment. The total osmolality determines whether the infused volume distributes over the total body water or over the extracellular fluid volume, or even attracts fluid from intracellular space. Infusion fluid is the first-line tool in the management of the vasodilation that is induced by both general and regional anaesthesia. Fluids are also an essential component in the treatment of haemorrhage, in which a reduction in arterial pressure implies that 20% of the blood volume has been lost. Capillary refill restores the blood volume, but too slowly to prevent haemorrhagic shock. In this situation, prompt intravenous fluid therapy is life-saving. Electrolyte derangements may be induced by disease and/or medication. The most essential ones to consider during anaesthesia are sodium, potassium, calcium, and bicarbonate.
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Delaney, Anthony. Physiology of body fluids. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0068.

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An understanding of the physiology of body fluids is essential when considering appropriate fluid resuscitation and fluid replacement therapy in critically-ill patients. In healthy humans, the body is composed of approximately 60% water, distributed between intracellular and an extracellular compartments. The extracellular compartment is divided into intravascular, interstitial and transcellular compartments. The movement of fluids between the intravascular and interstitial compartments, is classically described as being governed by Starling forces, leading to a small net efflux of fluid from the intravascular to the interstitial compartment. More recent evidence suggests that a model incorporating the effect of the endothelial glycoclayx layer, a web of glycoproteins and proteoglycans that are bound on the luminal side of the vascular endothelium, better explains the observed distribution of fluids. The movement of fluid to and from the intracellular compartment and the interstitial fluid compartment, is governed by the relative osmolarities of the two compartments. Body fluid status is governed by the difference between fluid inputs and outputs; fluid input is regulated by the thirst mechanism, with fluid outputs consisting of gastrointestinal, renal, and insensible losses. The regulation of intracellular fluid status is largely governed by the regulation of the interstitial fluid osmolarity, which is regulated by the secretion of antidiuretic hormone from the posterior pituitary gland. The regulation of extracellular volume status is regulated by a complex neuro-endocrine mechanism, designed to regulate sodium in the extracellular fluid.
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Turner, Neil, and Premil Rajakrishna. Pathophysiology of oedema in nephrotic syndrome. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0053.

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The mechanism by which loss of serum proteins into the urine causes expansion of extracellular fluid volume and oedema has become clearer. A key initiating abnormality is avid sodium retention by the kidney, leading to increased whole-body sodium and increased extracellular fluid volume. This appears to be driven primarily by overactivation of the amiloride-sensitive epithelial sodium channel (ENaC) in the collecting duct, activated proteolytically through abnormal filtration of plasminogen, and its activation to plasmin in the nephron. Conventional explanations for nephrotic oedema focused on low colloid osmotic pressure as a consequence of loss of serum proteins, leading to egress of extracellular fluid from the intravascular compartment. It was hypothesized that this led to underfilling of the circulation and a drive to sodium retention. While low osmotic pressure may play a part in the clinical picture of nephrotic syndrome, a variety of observations suggest that underfilling is not a common feature except in the most severe nephrotic syndrome. Furthermore the gradient in colloid osmotic pressure between serum and interstitium tends to be preserved in nephrotic syndrome. The distribution of excess extracellular fluid is markedly different in patients with nephrotic syndrome from that seen in patients who have reduced glomerular filtration rate as the cause of sodium retention. This is not fully understood but hypotheses centre on capillary permeability and colloid osmotic pressure effects.
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Bohn, Desmond. Fluids and Electrolytes. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199918027.003.0011.

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This chapter provides essential information on the distribution of body water and key electrolytes (sodium and potassium) in children, including the extracellular and intracellular components of total body water. Guidelines are provided for the composition and volume of fluids needed to maintain homeostasis, including maintenance intravenous fluids and fluids needed for specific circumstances, such as postoperatively. Water and electrolyte compositions of commonly used intravenous fluids and electrolytes in body fluids are provided in table format. Approaches are also given for disorders of fluid and electrolyte balance, including etiology and treatment of those related to antidiuretic hormone secretion, hyponatremia, hypernatremia, hypokalemia, and hyperkalemia.
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Houillier, Pascal. Magnesium homeostasis. Edited by Robert Unwin. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0027.

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Magnesium is critically important in the process of energy release. Although most magnesium is stored outside the extracellular fluid compartment, the regulated concentration appears in blood. Urinary magnesium excretion can decrease rapidly to low values when magnesium entry rate into the extracellular fluid volume is low, which has several important implications: cell and bone magnesium do not play a major role in the defence of blood magnesium concentration; while a major role is played by the kidney and especially the renal tubule, which adapts to match the urinary magnesium excretion and net entry of magnesium into extracellular fluid. In the kidney, magnesium is reabsorbed in the proximal tubule, the thick ascending limb of the loop of Henle (TALH), and the distal convoluted tubule (DCT). Magnesium absorption is mainly paracellular in the proximal tubule and TALH, whereas it is transcellular in the DCT. The hormone(s) regulating renal magnesium transport and blood magnesium concentration are not fully understood. Renal tubular magnesium transport is altered by a number of hormones, mainly in the TALH and DCT. Parathyroid hormone, calcitonin, arginine vasopressin, ß-adrenergic agonists, and epidermal growth factor, all increase renal tubular magnesium reabsorption; in contrast, prostaglandin E2 decreases magnesium reabsorption. Non-hormonal factors also influence magnesium reabsorption: it is decreased by high blood concentrations of calcium and magnesium, probably via the action of divalent cations on the calcium-sensing receptor; metabolic acidosis decreases, and metabolic alkalosis increases, renal magnesium reabsorption.
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Egan, Brian N. Hyponatremia/Hypernatremia. Edited by Matthew D. McEvoy and Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0037.

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lSodium is the most abundant cation in the extracellular fluid and is important for regulation of plasma water concentrations and cell volume. Sodium cannot readily cross the blood-brain barrier, and changes in plasma sodium levels by altering free water movement can expand or shrink brain cells. Changes in brain cell volume can cause brain cell dysfunction and apoptosis. Correction of both high and low sodium levels must be done gradually, as rapid correction of dysnatremias can also damage brain cells. In this chapter we review the physiology of sodium regulation, and discuss the clinical implications of these disorders as well as present a treatment plan for safe correction.
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Marples, David, and Søren Nielsen. Water homeostasis. Edited by Robert Unwin. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0022_update_001.

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Under normal circumstances, the maintenance of water balance is a question of balancing urine output against oral water intake, after allowance for the largely unregulated loss of water through other routes (respiratory, transcutaneous, and via the gastrointestinal tract). Normally, this is managed by the feedback mechanisms controlling thirst and diuresis, but in a medical context it is important to allow for other forms of administration that may not be under the control of the patient, and other routes of fluid loss, such as haemorrhage and drains. Electrolyte and water homeostasis are closely interrelated: the major trigger for both antidiuretic hormone (vasopressin) release (and hence renal water retention) and thirst is plasma osmolality. Sodium and chloride are the major solutes in extracellular fluid so are major determinants of body water content and circulating volume.
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O’Callaghan, Chris A. Renal function. Edited by Rutger Ploeg. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0126.

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The kidneys play a central role in homeostasis by maintaining extracellular fluid composition and volume. They do this by continuous filtration of plasma in the renal glomeruli and then subsequent modification of the filtered fluid as it passes along the nephron. The filtration process excludes large molecules, but most small molecules and ions are freely filtered. The filtrate that is produced in the glomeruli has a similar composition to plasma with respect to small molecules and ions. Most of the water and solutes are reabsorbed along the tubules and this process requires high levels of metabolic activity. In addition, a range of compounds and ions are secreted into the tubules along the nephron. Renal function is central to homeostasis and an appreciation of normal renal physiology is essential to understand the role of the kidney in a wide variety of disease processes.
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Schild, Laurent. Sodium transport and balance. Edited by Robert Unwin. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0021.

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The kidney maintains the extracellular fluid volume and blood pressure by regulating urinary sodium (Na+) excretion to precisely balance daily Na+ intake. Genetic and experimental evidence support a central role for the distal nephron in the fine tuning of urinary Na+ excretion. The cellular and molecular aspects of the transporters involved in Na+ reabsorption in the distal nephron, and their regulation linked to complex signaling pathways are discussed. Na+ absorption can be viewed as a continuum in the activities of specific transport processes along the distal nephron. The crosstalk between these different and complex reabsorptive processes is important for the adaptation of Na+ excretion in various physiological, pathophysiological, and pharmacological conditions.
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Hoorn, Ewout J., and Robert Zietse. Approach to the patient with hyponatraemia. Edited by Robert Unwin. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0028.

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Hyponatraemia is the most common electrolyte disorder in hospitalized patients and is primarily a water balance disorder. Therefore, hyponatraemia is due to a relative excess of water in comparison with sodium in the extracellular fluid volume. Hyponatraemia is usually due to the release of vasopressin despite hypo-osmolality; this secretion is either ‘appropriate’ (i.e. due to a low intravascular volume) or ‘inappropriate’. The diagnostic approach to hyponatraemia relies on the assessment of the time of development, symptoms, and volume status, along with laboratory parameters such as urine sodium and urine osmolality. Complications are mainly neurological and usually depend on the rate of development and correction. If hyponatraemia develops acutely, treatment should be directed towards counteracting the water shift to or brain cells. Conversely, in more chronic cases of hyponatraemia, treatment should be directed at the underlying cause, while avoiding over-correction.
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Book chapters on the topic "Extracellular fluid volume"

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Reddi, Alluru S. "Disorders of Extracellular Fluid Volume: Basic Concepts." In Fluid, Electrolyte and Acid-Base Disorders, 53–57. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-9083-8_6.

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Reddi, Alluru S. "Disorders of Extracellular Fluid Volume: Basic Concepts." In Fluid, Electrolyte and Acid-Base Disorders, 57–61. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-60167-0_6.

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Palmer, Biff F. "Extracellular Fluid Volume in the Hypoalbuminemic Diabetic Patient." In The Kidney in Heart Failure, 51–65. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-3694-2_5.

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Henriksen, Jens H. "Regulation of the Extracellular Fluid Volume and Renal Function." In Chronic Liver Failure, 239–67. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-866-9_12.

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London, G. M., and M. E. Safar. "Venous system, extracellular fluid volume and the kidney in essential hypertension." In Developments in Cardiovascular Medicine, 95–102. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-009-3303-3_7.

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Chester-Jones, I., P. M. Ingleton, and J. G. Phillips. "Integration of Hormonal Actions to Regulate Extracellular Fluid Volume and Composition." In Fundamentals of Comparative Vertebrate Endocrinology, 481–95. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4899-3617-2_12.

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Syková, E., A. Chvátal, L. Vargová, and I. Vorišek. "Extracellular space ionic composition, volume and geometry during neuronal activity and pathological states." In Intracranial and Intralabyrinthine Fluids, 9–22. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-80163-1_2.

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Mulroney, Susan E., and Adam K. Myers. "Regulation of Extracellular Fluid Volume and Osmolarity." In Netter's Essential Physiology, 225–29. Elsevier, 2009. http://dx.doi.org/10.1016/b978-1-4160-4196-2.50031-9.

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Koeppen, Bruce M., and Bruce A. Stanton. "Regulation of Extracellular Fluid Volume and Nacl Balance." In Renal Physiology, 93–114. Elsevier, 2013. http://dx.doi.org/10.1016/b978-0-323-08691-2.00006-5.

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"REGULATION OF EXTRACELLULAR FLUID VOLUME AND NaCl BALANCE." In Renal Physiology, 91–111. Elsevier, 2007. http://dx.doi.org/10.1016/b978-0-323-03447-0.50012-4.

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Conference papers on the topic "Extracellular fluid volume"

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Fansan Zhu, Franz Kappel, Edward F. Leonard, Peter Kotanko, and Nathan W. Levin. "Modeling of change in blood volume and extracellular fluid volume during hemodialysis." In 2013 35th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2013. http://dx.doi.org/10.1109/embc.2013.6609798.

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Choi, JungHun. "Characteristics of Intracellular and Extracellular Fluid Ratio for the Varying Body Impedances in Fixed Total Body Fluid." In 2017 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2017. http://dx.doi.org/10.1115/dmd2017-3309.

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A bioelectrical impedance analysis is a proven method to measure body composition in clinical situations. It uses the relation between the body fluid and the impedances in a variety of frequencies. A body model can be simplified as a parallel combination of a capacitor and two resistors which represent a cell membrane, Intracellular Fluid (ICF), and Extracellular Fluid (ECF). Low frequency current passes through ECF and high frequency current also passes through ICF in a body. A Cole-Cole plot is a graphical interpretation of the path of impedances and each axis represents resistance and reactance with variable frequencies. A high value of resistance in a horizontal axis is a resistance value of ECF and a low value of resistance at a high frequency presents ICF. Interpolation technique is needed to find out the exact cross-point between impedance values and the horizontal axis. The two estimated impedance values are used to derive Total Body Water (TBW), ICF, ECF, Fat Free Mass (FFM), and Fat Mass (FM) from various published equations [1]. Minimizing the possible error of fluid volume assessment and accurate prediction of fluid status in a human body is essential for appropriate therapy. Different techniques of fluid status assessment in a human body can be applicable, such as physical examination, orthostatic vital signs, blood volume measurement, acoustic cardiograph, chest radiography, and thoracic ultrasonography [2]. In this study, a bioelectrical impedance spectroscopy device and simple body models were used to collect data such as TBW, ICF, ECF, FM, and FFM. The ratio between ICF and ECF was investigated for the same values of TBW, FM, and FFM by varying impedance values.
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Boss, Andreas, Petros Martirosian, Ferruh Artunc, Teut Risler, Claus D. Claussen, Heinz-Peter Schlemmer, and Fritz Schick. "Quantification of glomerular filtration rate by measurement of gadobutrol clearance from the extracellular fluid volume: comparison of a TurboFLASH and a TrueFISP approach." In Medical Imaging, edited by Armando Manduca and Xiaoping P. Hu. SPIE, 2007. http://dx.doi.org/10.1117/12.709101.

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Hulme, Paul, Simon Chi, Dominic Young, John Matyas, and Neil A. Duncan. "Enzymatic Digestion Technique Influences Regulatory Volume Decrease of Isolated Bovine Chondrocytes." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-32671.

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Cell volume regulation has been observed in almost all cell types examined to date. When cells are exposed to hypotonic solutions a quick increase in volume is followed by a more gradual return, termed regulatory volume decrease (RVD). The mechanism associated with RVD depends upon cell type and species, but in bovine chondrocytes the non-selective osmolyte channels are mainly responsible [1]. In a chondrocyte, volume control is critical for the maintenance of metabolism, and biosynthesis. Volume fluctuations can be due to changes in hydrostatic pressure, fluid flows, deformation, and extracellular matrix (ECM) hydration. Alterations in hydration can occur during static loading of articular cartilage or during the early stages of osteoarthritis [1], which have been correlated with changes in cellular metabolism. The swelling behaviour of chondrocytes, and the mechanism by which they sense and respond to changes in their physico-chemical environment, are not well understood [1]. To investigate the effects of osmotic environment on chondrocyte behaviour it is often beneficial to isolate cells from the ECM, which can be achieved by a variety of techniques. To investigate the effect of isolation technique on the swelling behaviour of bovine chondrocytes, two enzymatic digestion techniques were chosen for this study.
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Banerjee, Rupak K., Peter M. Bungay, Malisa Sarntinoranont, and Srinivas Chippada. "Generalizing the Theory of Microdialysis." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-32970.

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The efficiency of sampling or delivering solutes (analytes) by in vivo microdialysis is influenced by the diffusive permeabilities of the probe and the tissue in which the probe is implanted. In tissue, processes removing the analyte from the extracellular space are as important as diffusion in determining permeability. In addition to diffusion, analyte permeation through these media may be augmented or diminished by bulk fluid movement (transmembrane and interstitial convection). Within the perfusate, the dominant process is axial convection. Both diffusive and convective determinants of probe efficiency may be influenced by probe geometry (Figure 1; longitudinal cross-sectional view). The main geometric parameters are the probe membrane length and radii, but inner cannula geometry can also be an appreciable factor. The objective of this study is to generalize the mathematical description of microdialysis. The treatment extends in several ways previous mathematical models (Bungay et al. [1]; Morrison et al. [2]; Morrison et al. [3]; Wallgren et al. [4]). In addition to removing some simplifications and approximations and adding convective transport, the revised theory is applicable to low-molecular-weight lipophilic, as well as hydrophilic solutes. This is achieved by incorporating transcellular solute movement as a pathway paralleling interstitial diffusion. This change accompanies employing the combined intracellular and extracellular volumes, rather than the interstitial volume, as the basis for solute mass balances.
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Chen, Hsiu-hung, and Dayong Gao. "A Microfluidic Perfusion Chamber Utilized in the Study of Biophysical Properties of Cell Membrane and Its Fluidic Evaluation." In ASME 2009 Second International Conference on Micro/Nanoscale Heat and Mass Transfer. ASMEDC, 2009. http://dx.doi.org/10.1115/mnhmt2009-18393.

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A microfluidic system is demonstrated here to measure the kinetic changes of cell volume under various extracellular conditions, in order to determine cell membrane transport properties. The system is comprised of microchannels, a cell immobilization chamber, an inlet and an outlet, and is made of poly(dimethylsiloxane) (PDMS) using softlithographic method. During experiments, mouse dendritic cells (mDCs), mixed with media of known concentrations, are quickly injected to the inlet of such microfluidic device, flow through a microchannel, and are then immobilized by a sieving structure, where kinetic images of cell volume response are captured by a CCD camera lively. The fluid keeps flowing due to the continuous suction from the outlet by a programmable syringe pump. Two sets of experiments have been performed: the cells are mixed with (1) solutions prepared in different concentrations of non-permeating solutes, and (2) solutions containing a permeating cryoprotective agent (CPA) plus non-permeating solute, respectively. Based on the captured images, both cell inactive volumes (Vb), permeability coefficients of water (Lp) and of CPA (Ps) through cell membranes of mDCs at different temperatures (10°C, 22°C, and 34°C) can be determined by least-squared curve fittings, respectively. A quantitative evaluation conducted using ImageJ will be performed in order to validate the microfluidic perfusion system, as well as help us understand the dynamic concentration changes around those immobilized cells. The use of this microfluidic perfusion system enables us to: 1) confine cells in a monolayer channel to prevent image ambiguity, 2) perform cell counting, 3) statistically study cell osmotic response and determine cell membrane transport properties, and (4) lower manufacturing costs.
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Crawford, N., M. Crook, J. Dawes, and C. R. W. Gray. "THE SOLE USE OF MAGNESIUM CHLORIDE FOR BLOOD ANTICOAGULATION: PRESERVATION OF PLATELET SURFACE-BOUND “PROTEINACEOUS HALO”!" In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643708.

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European Patent No. 83901336 [C.R.W. GRAY & N. CRAWFORD] refers to the use of bivalent cations for blood anticoagulationand the preparation of plasma and cellular products. Both CaCl2 and MgCl2 are effective as sole anticoagulants although the concentration of Ca+2 to maintain blood fluid for >7 days exceeds the osmolarity limits for good preservation of cellular integrity. With MgCl2 ,however, [at final concentrations 25-30 mM and suitable blood/MgCl2 volume ratios] red cells show good preservation, granulocytes phagocytose well and platelets are discoid and respond to all conventional agonists [although higher than normal doses are required]. The concentrations of 6 thromboglobulin (βTG) in “MgCl2-plasma” aresubstantially lower than with Cacomplexing anticoagulants containing theophylline and PGE . Thrombospondin [TSP]another major granule protein, unlike 6TG, binds after release to the activated platelet surface in the presence of physiological [Ca+2+]1 RIA assays of TSP has revealed that “Mg platelets” have 3 times more surface bound TSP than “CPD-platelets”. Subpopulation profiling by continuousflow electrophoresis shows that formol-fixed platelets from Mg2 anticoagulated blood are substantial>ly less electronegative than "CPD platelets" similarly processed. We believe that plateletsfrom blood in which the extracellular[Ca2+] is undisturbed carrya surface-associatd “halo”ofnonspecific [electrostatically-associated] and Ca2+-linked adsorbed proteins. Released TSP is an example of the latter association. Since plasma 0TG levels are influenced by kidney clearancekinetics and other factors, the measurement of surface bound TSP on platelets from MgCl2-anticoagulatedbloodmay have clinical value as an indexof invivo release events and particularly in vascular disorders accompanied by renal damage where the findings with 0TGhave been equivocal(2)
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Kim, Jung Hwan, Xiaoming Chen, Garrett W. Astary, Thomas H. Mareci, and Malisa Sarntinoranont. "Computational Model of Direct Injection Into the Spinal Cord Using in Vivo Diffusion Tensor Imaging." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193114.

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Local infusion, i.e., convection-enhanced delivery (CED), is increasingly being considered as a means to deliver therapeutic agents to nervous tissues. These infusion techniques bypass the blood-brain barrier and overcome problems associated with slow diffusion [1, 2]. Predictive models of extracellular fluid flow and transport during and following CED would be useful in treatment optimization and planning. To account for large infusion volumes, such infusion models should incorporate tissue boundaries and anisotropic tissue properties.
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Illarionov, Vladimir, Mikhail Solovev, Zafar Yuldashev, Rustam Khapaev, and Vadim Nimaev. "Three-frequency Bioimpedance Method of Evaluating Extracellular and Intracellular Fluid Volumes, Fat and Muscle Mass Parameters on Groups of Patients with Untypical Body Structure." In 2019 International Multi-Conference on Engineering, Computer and Information Sciences (SIBIRCON). IEEE, 2019. http://dx.doi.org/10.1109/sibircon48586.2019.8958288.

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