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Jens Titze - One of the best experts on this subject based on the ideXlab platform.
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a different view on Sodium Balance
2015Co-Authors: Jens TitzeAbstract:Purpose of reviewTextbook theory holds that extracellular fluids readily equilibrate, electrolyte concentrations in the extracellular fluid compartments are constant, and the kidney is solely responsible for controlling the body Sodium content.Recent findingsInvestigation of salt and water Balance t
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Sodium Balance is not just a renal affair
2014Co-Authors: Jens TitzeAbstract:Purpose of review The equilibration theory of extracellular body fluids is tightly linked to Sodium (Na+) metabolism. Accepted is the notion that with changes in salt intake, renal Sodium elimination will prevent any change in interstitial Na+ content and concentration. This review summarizes recent anomalous findings in salt and water homeostasis that are inconsistent with current assumptions.
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Spooky Sodium Balance
2013Co-Authors: Jens Titze, Kathrin Lerchl, Natalia Rakova, Christoph W Kopp, Anke Dahlmann, Agnes Schröder, Friedrich C LuftAbstract:Current teaching states that when Sodium intake is increased from low to high levels, total-body Sodium (TBNa) and water increase until daily Sodium excretion again equals intake. When Sodium intake is reduced, Sodium excretion briefly exceeds intake until the excess TBNa and water are eliminated, at which point Sodium excretion again equals intake. However, careful Balance studies oftentimes conflict with this view and long-term studies suggest that TBNa fluctuates independent of intake or body weight. We recently performed the opposite experiment in that we fixed Sodium intake for several weeks at three levels of Sodium intake and collected all urine made. We found weekly (circaseptan) patterns in Sodium excretion that were inversely related to aldosterone and directly to cortisol. TBNa was not dependent on Sodium intake but instead exhibited far longer (≥monthly) infradian rhythms independent of extracellular water, body weight, or blood pressure. The findings are consistent with our ideas on tissue Sodium storage and its regulation that we developed on the basis of animal research. We are implementing 23 Na-magnetic resonance imaging (MRI) to pursue open questions on Sodium Balance in patients. Our findings could be relevant to therapeutic strategies for hypertension and target-organ damage.
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internal Sodium Balance in doca salt rats a body composition study
2005Co-Authors: Jens Titze, Friedrich C Luft, Rainer Lang, Katharina Bauer, Markus Schafflhuber, Peter Dietsch, Karl H Schwind, Kaiuwe Eckardt, Karl F HilgersAbstract:The idea that Na+ retention inevitably leads to water retention is compelling; however, were Na+ accumulation in part osmotically inactive, regulatory alternatives would be available. We speculated...
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long term Sodium Balance in humans in a terrestrial space station simulation study
2002Co-Authors: Jens Titze, Alain Maillet, Rainer Lang, Hannschristian Gunga, Bernd Johannes, Guillemette Gauquelinkoch, Emanuelle Kihm, I M Larina, C Gharib, K KirschAbstract:Abstract Background: Sodium accumulation has been considered to take place in the extracellular space, leading to water retention and weight gain. This traditional view has been questioned by recent studies that showed Sodium accumulation in humans without expansion of the extracellular volume. We investigated Sodium Balance and its impact on body weight (BW) during a long-term Balance study. Methods: Three healthy subjects were confined to a terrestrial MIR simulator for 135 days under conditions simulating a long-term spaceflight. During the entire isolation period, we meticulously measured daily Sodium Balance and its contribution to BW. Results: During the study period, subjects accumulated between 2,973 and 7,324 mmol of Sodium and gained between 5.1 and 9.3 kg in weight. In all subjects, there was a positive correlation between changes in total-body Sodium (ΔTBS) content and BW, reflecting Sodium-associated volume expansion. However, toward the end of isolation, Sodium gain exceeded weight gain, suggesting that Sodium accumulated in an osmotically inactive form. Especially at the onset of the experiment, two subjects showed inverse correlations between ΔTBS and BW. Conclusion: The finding of Sodium gain without weight gain is in contradiction to the widely accepted theory that changes in TBS levels are accompanied by changes in extracellular volume. We suggest the existence of a Sodium reservoir with the ability to store significant amounts of Sodium in an osmotically inactive form. This reservoir might be located in bone, dense connective tissue, or cartilage. © 2002 by the National Kidney Foundation, Inc.
Andrew D Bersten - One of the best experts on this subject based on the ideXlab platform.
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Sodium Balance not fluid Balance is associated with respiratory dysfunction in mechanically ventilated patients a prospective multicentre study
2015Co-Authors: Shailesh Bihari, Sandra L Peake, Shiroman Prakash, Manoj Saxena, Victoria Campbell, Andrew D BerstenAbstract:Background: Large positive Sodium Balances, independent of fluid Balance, may lead to expanded extracellular fluid volumes and adverse clinical outcomes in the critically ill, including impaired oxygenation. Objectives: To estimate Sodium and fluid Balances in critically ill patients needing invasive mechanical ventilation (MV) for more than 48 hours and to evaluate the relationship between fluid Balance, Sodium Balance and respiratory function (PaO2/FiO2 ratio and length of MV). Design and setting: A prospective, observational study of 50 patients on MV in four tertiary intensive care units. Main outcome measures: Daily Sodium and fluid input and output, biochemistry, haemodynamic variables, oxygenation (PaO2/FiO2) and steroid and vasopressor administration were recorded for 3 days after study enrolment. Outcome data included the duration of invasive MV, ICU and hospital mortality and ICU and hospital lengths of stay. Results: Fifty patients (33 men [66%]) with a mean age of 62.8 years (standard deviation, 14.6 years) and a median admission Acute Physiology and Chronic Health Evaluation III score of 82 (interquartile range [IQR], 61-99) were studied. By Day 3 after enrolment, the median cumulative fluid Balance was 2668mL (IQR, 875-3507mL) and the cumulative Sodium Balance was +717mmol (IQR, +422 to +958mmol). Intravenous steroids and the presence of shock led to a lower daily Sodium excretion (P=0.004 and P = 0.01, respectively). A positive Sodium Balance was associated with a reduction in the next day's PaO2/FiO2 ratio (P=-0.36, P = 0.001) and an increased length of MV (linear regression analysis, P< 0.01). The cumulative fluid Balance was not associated with either parameter. Conclusions: The cumulative positive Sodium Balance, not the cumulative positive fluid Balance, is associated with respiratory dysfunction and an increased length of MV.
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fluid Balance does not predict estimated Sodium Balance in critically ill mechanically ventilated patients
2013Co-Authors: Shailesh Bihari, Claire E Baldwin, Andrew D BerstenAbstract:Background: Distribution of total body water (TBW) depends on local and systemic factors including osmolality, relative Sodium content and permeability. Although positive fluid Balance has been associated with increased morbidity and mortality in critically ill patients, the mechanisms and relative roles of Sodium Balance and water distribution are uncertain. Objective: To track changes in Sodium and fluid Balance, respiratory function and body composition in patients who required mechanical ventilation for >= 48 hours. Design, setting and participants: Prospective observational study, set in a tertiary intensive care unit, of 10 patients (seven men) with a mean age of 60 years (standard deviation [SD],12 years) and mean admission Acute Physiology and Chronic Health Evaluation (APACHE) III score of 71 (SD, 26). Methods: Sodium and fluid Balances were estimated daily for up to 5 days, following institution of mechanical ventilation on Day 0. Serum Sodium level, oxygenation (PaO2/FIO2), body weight, intracellular and extracellular fluid (ECF) distribution (bioelectrical impedance spectroscopy), and blinded chest x-ray oedema scores were performed daily. Results: After 5 days of mechanical ventilation, the cumulative fluid Balance was - 954 mL (SD, 3181 mL) and estimated cumulative Sodium Balance was 253 mmol (SD, 346 mmol). Serum Sodium had increased from 140mmol/L (SD, 4mmol/L) to 147 mmol/L (SD, 5mmol/L). Cumulative Sodium Balance was weakly correlated with worsening chest x-ray score (r = 0.35, P = 0.004), a reduction in PaO2/ FIO2 ratio (r = - 0.52, P = 0.001) and 24-hour urinary Sodium (r = - 0.24, P = 0.02). Between Days 1 and 5, body weight decreased (- 2.7 kg; SD, 1.4 kg) and TBW decreased (- 3.4 L; SD, 1.3 L), despite a rise in ECF distribution (1.4% of TBW; SD, 1.9% of TBW). Conclusions: Fluid Balance may not reflect Sodium Balance in critically ill patients. As Sodium Balance correlates with respiratory dysfunction and increased extracellular volume, further studies examining Sodium Balance and morbidity seem warranted.
Bernard C Rossier - One of the best experts on this subject based on the ideXlab platform.
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epithelial Sodium channel enac and the control of blood pressure
2014Co-Authors: Bernard C RossierAbstract:The amiloride-sensitive epithelial Sodium channel (ENaC) constitutes the rate-limiting step for Sodium reabsorption in epithelial cells that line the distal part of the renal tubule, the distal colon, the duct of several exocrine glands, and the lung. The activity of this channel is regulated by aldosterone and hormones involved in the maintenance of Sodium Balance, blood volume and blood pressure. In this review, we discuss recent advances in our understanding of ENaC function and regulation relevant to the control of Sodium Balance and blood pressure. The identification of novel drug targets should help in the development of the next generation of diuretics and of new therapies for the treatment of hypertension.
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epithelial Sodium channel and the control of Sodium Balance interaction between genetic and environmental factors
2002Co-Authors: Bernard C Rossier, Sylvain Pradervand, Laurent Schild, Edith HummlerAbstract:▪ Abstract The epithelial Sodium channel (ENaC) expressed in aldosterone-responsive epithelial cells of the kidney and colon plays a critical role in the control of Sodium Balance, blood volume, and blood pressure. In lung, ENaC has a distinct role in controlling the ionic composition of the air-liquid interface and thus the rate of mucociliary transport. Loss-of-function mutations in ENaC cause a severe salt-wasting syndrome in human pseudohypoaldosteronism type 1 (PHA-1). Gain-of-function mutations in ENaC β and γ subunits cause pseudoaldosteronism (Liddle's syndrome), a severe form of salt-sensitive hypertension. This review discusses genetically defined forms of a salt sensitivity and salt resistance in human monogenic diseases and in animal models mimicking PHA-1 or Liddle's syndrome. The complex interaction between genetic factors (ENaC mutations) and the risk factor (salt intake) can now be studied experimentally. The role of single-nucleotide polymorphisms (SNPs) in determining salt sensitivity or...
Carina Aparecida Fabrício De ,andrade - One of the best experts on this subject based on the ideXlab platform.
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importance of the lateral parabrachial nucleus to Sodium Balance in fluid depleted rats
2016Co-Authors: K A Cabral, Carina Aparecida Fabrício De ,andradeAbstract:Abstract The lateral parabrachial nucleus (LPBN) exerts an important inhibitory influence for the control of Sodium and water intake. However, the importance of LPBN on renal responses and cardiovascular changes during extracellular dehydration are still unknown. Here we investigated the effects of bilateral injections of moxonidine (alpha 2 -adrenergic and imidazoline receptor agonist) on renal and cardiovascular changes in fluid-depleted rats. Male Wistar rats ( n = 4–8 per group) with bilateral stainless steel guide-cannulas implanted into the LPBN were treated with subcutaneous furosemide (10 mg/kg) + captopril (5 mg/kg) to induce fluid depletion. Forty-five min later vehicle or moxonidine (0.5 nmol/0.2 μl) were bilaterally injected into the LPBN. In fluid-depleted rats, moxonidine produced strong 0.3 M NaCl and water intake without noticeable changes in cardiovascular parameters. Moxonidine did not change Sodium excretion (488 ± 135, vs. vehicle: 376 ± 75 μEq/1 h) or urinary volume (2.5 ± 0.7, vs. vehicle: 2.5 ± 0.3 ml/1 h) in fluid-depleted rats without access to fluids for rehydration. However, moxonidine decreased natriuresis (462 ± 127, vs. vehicle: 888 ± 122 μEq/1 h) and diuresis (2.5 ± 0.5, vs. vehicle: 4.5 ± 0.5 ml/1 h) in fluid-depleted rats submitted to i.g. rehydration. These data suggest that alpha 2 -adrenergic mechanism of the LPBN facilitates Sodium/water retention and body fluid volume expansion during extracellular dehydration.
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Moxonidine into the lateral parabrachial nucleus reduces renal and hormonal responses to cell dehydration
2012Co-Authors: Carina Aparecida Fabrício De ,andrade, Margatho L. O., Andrade-franze G. M. F., De Luca L. A., Antunes-rodrigues J., Menani, José VanderleiAbstract:The deactivation of the inhibitory mechanisms with injections of moxonidine (alpha(2)-adrenoceptor/imidazoline receptor agonist) into the lateral parabrachial nucleus (LPBN) increases hypertonic NaCl intake by intra- or extracellular dehydrated rats. In the present study, we investigated the changes in the urinary Sodium and volume, Sodium Balance, and plasma vasopressin and oxytocin in rats treated with intragastric (i.g.) 2 M NaCl load (2 ml/rat) combined with injections of moxonidine into the LPBN. Male Holtzman rats (n=5-12/group) with stainless steel cannulas implanted bilaterally into LPBN were used. Bilateral injections of moxonidine (0.5 nmol/0.2 mu l) into the LPBN decreased i.g. 2 M NaCIinduced diuresis (4.6 +/- 0.7 vs. vehicle: 7.4 +/- 0.6 ml/120 min) and natriuresis (1.65 +/- 0.29 vs. vehicle: 2.53 +/- 0.17 mEq/120 min), whereas the previous injection of the alpha(2)-adrenoceptor antagonist RX 821002 (10 nmol/0.2 mu l) into the LPBN abolished the effects of moxonidline. Moxonidine injected into the LPBN reduced i.g. 2 M NaCl-induced increase in plasma oxytocin and vasopressin (14.6 +/- 2.8 and 2.2 +/- 0.3 vs. vehicle: 25.7 +/- 7 and 4.3 +/- 0.7 pg/ml, respectively). Moxonidine injected into the LPBN combined with i.g. 2 M NaCl also increased 0.3 M NaCl intake (7.5 +/- 1.7 vs. vehicle: 0.5 +/- 0.2 mEq/2 h) and produced positive Sodium Balance (2.3 +/- 1.4 vs. vehicle: -1.2 +/- 0.4 mEq/2 h) in rats that had access to water and NaCl. The present results show that LPBN alpha(2)-adrenoceptor activation reduces renal and hormonal responses to intracellular dehydration and increases Sodium and water intake, which facilitates Sodium retention and body fluid volume expansion. (C) 2012 IBRO. Published by Elsevier Ltd. All rights reserved.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq
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moxonidine into the lateral parabrachial nucleus reduces renal and hormonal responses to cell dehydration
2012Co-Authors: Carina Aparecida Fabrício De ,andrade, Jose Antunesrodrigues, L. A. De Luca, G M F Andradefranze, Lisandra Oliveira Margatho, José Vanderlei MenaniAbstract:The deactivation of the inhibitory mechanisms with injections of moxonidine (α2-adrenoceptor/imidazoline receptor agonist) into the lateral parabrachial nucleus (LPBN) increases hypertonic NaCl intake by intra- or extracellular dehydrated rats. In the present study, we investigated the changes in the urinary Sodium and volume, Sodium Balance, and plasma vasopressin and oxytocin in rats treated with intragastric (i.g.) 2 M NaCl load (2 ml/rat) combined with injections of moxonidine into the LPBN. Male Holtzman rats (n=5-12/group) with stainless steel cannulas implanted bilaterally into LPBN were used. Bilateral injections of moxonidine (0.5 nmol/0.2 μl) into the LPBN decreased i.g. 2 M NaCl-induced diuresis (4.6±0.7 vs. vehicle: 7.4±0.6 ml/120 min) and natriuresis (1.65±0.29 vs. vehicle: 2.53±0.17 mEq/120 min), whereas the previous injection of the α2-adrenoceptor antagonist RX 821002 (10 nmol/0.2 μl) into the LPBN abolished the effects of moxonidine. Moxonidine injected into the LPBN reduced i.g. 2 M NaCl-induced increase in plasma oxytocin and vasopressin (14.6±2.8 and 2.2±0.3 vs. vehicle: 25.7±7 and 4.3±0.7 pg/ml, respectively). Moxonidine injected into the LPBN combined with i.g. 2 M NaCl also increased 0.3 M NaCl intake (7.5±1.7 vs. vehicle: 0.5±0.2 mEq/2 h) and produced positive Sodium Balance (2.3±1.4 vs. vehicle: -1.2±0.4 mEq/2 h) in rats that had access to water and NaCl. The present results show that LPBN α2-adrenoceptor activation reduces renal and hormonal responses to intracellular dehydration and increases Sodium and water intake, which facilitates Sodium retention and body fluid volume expansion.
Shailesh Bihari - One of the best experts on this subject based on the ideXlab platform.
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Sodium Balance not fluid Balance is associated with respiratory dysfunction in mechanically ventilated patients a prospective multicentre study
2015Co-Authors: Shailesh Bihari, Sandra L Peake, Shiroman Prakash, Manoj Saxena, Victoria Campbell, Andrew D BerstenAbstract:Background: Large positive Sodium Balances, independent of fluid Balance, may lead to expanded extracellular fluid volumes and adverse clinical outcomes in the critically ill, including impaired oxygenation. Objectives: To estimate Sodium and fluid Balances in critically ill patients needing invasive mechanical ventilation (MV) for more than 48 hours and to evaluate the relationship between fluid Balance, Sodium Balance and respiratory function (PaO2/FiO2 ratio and length of MV). Design and setting: A prospective, observational study of 50 patients on MV in four tertiary intensive care units. Main outcome measures: Daily Sodium and fluid input and output, biochemistry, haemodynamic variables, oxygenation (PaO2/FiO2) and steroid and vasopressor administration were recorded for 3 days after study enrolment. Outcome data included the duration of invasive MV, ICU and hospital mortality and ICU and hospital lengths of stay. Results: Fifty patients (33 men [66%]) with a mean age of 62.8 years (standard deviation, 14.6 years) and a median admission Acute Physiology and Chronic Health Evaluation III score of 82 (interquartile range [IQR], 61-99) were studied. By Day 3 after enrolment, the median cumulative fluid Balance was 2668mL (IQR, 875-3507mL) and the cumulative Sodium Balance was +717mmol (IQR, +422 to +958mmol). Intravenous steroids and the presence of shock led to a lower daily Sodium excretion (P=0.004 and P = 0.01, respectively). A positive Sodium Balance was associated with a reduction in the next day's PaO2/FiO2 ratio (P=-0.36, P = 0.001) and an increased length of MV (linear regression analysis, P< 0.01). The cumulative fluid Balance was not associated with either parameter. Conclusions: The cumulative positive Sodium Balance, not the cumulative positive fluid Balance, is associated with respiratory dysfunction and an increased length of MV.
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fluid Balance does not predict estimated Sodium Balance in critically ill mechanically ventilated patients
2013Co-Authors: Shailesh Bihari, Claire E Baldwin, Andrew D BerstenAbstract:Background: Distribution of total body water (TBW) depends on local and systemic factors including osmolality, relative Sodium content and permeability. Although positive fluid Balance has been associated with increased morbidity and mortality in critically ill patients, the mechanisms and relative roles of Sodium Balance and water distribution are uncertain. Objective: To track changes in Sodium and fluid Balance, respiratory function and body composition in patients who required mechanical ventilation for >= 48 hours. Design, setting and participants: Prospective observational study, set in a tertiary intensive care unit, of 10 patients (seven men) with a mean age of 60 years (standard deviation [SD],12 years) and mean admission Acute Physiology and Chronic Health Evaluation (APACHE) III score of 71 (SD, 26). Methods: Sodium and fluid Balances were estimated daily for up to 5 days, following institution of mechanical ventilation on Day 0. Serum Sodium level, oxygenation (PaO2/FIO2), body weight, intracellular and extracellular fluid (ECF) distribution (bioelectrical impedance spectroscopy), and blinded chest x-ray oedema scores were performed daily. Results: After 5 days of mechanical ventilation, the cumulative fluid Balance was - 954 mL (SD, 3181 mL) and estimated cumulative Sodium Balance was 253 mmol (SD, 346 mmol). Serum Sodium had increased from 140mmol/L (SD, 4mmol/L) to 147 mmol/L (SD, 5mmol/L). Cumulative Sodium Balance was weakly correlated with worsening chest x-ray score (r = 0.35, P = 0.004), a reduction in PaO2/ FIO2 ratio (r = - 0.52, P = 0.001) and 24-hour urinary Sodium (r = - 0.24, P = 0.02). Between Days 1 and 5, body weight decreased (- 2.7 kg; SD, 1.4 kg) and TBW decreased (- 3.4 L; SD, 1.3 L), despite a rise in ECF distribution (1.4% of TBW; SD, 1.9% of TBW). Conclusions: Fluid Balance may not reflect Sodium Balance in critically ill patients. As Sodium Balance correlates with respiratory dysfunction and increased extracellular volume, further studies examining Sodium Balance and morbidity seem warranted.