Changes In Plasma Sodium Concentration Research Articles

#2707 Prediction of plasma sodium changes in hypernatremic patients: the role of tissue sodium content

Abstract Background and Aims Hypo- and hypernatremia are frequently encountered electrolyte disturbances in clinical practice. Rapid correction of these dysnatremias can result in severe neurological complications. Therefore, various formulas have been developed to predict changes in plasma sodium concentration ([Na+]) after treatment. However, these kidney-centered formulas have been shown to be inaccurate. A potential explanation for the discrepancy between predicted and measured plasma [Na+] is the accumulation of sodium in the skin, which is not explicitly taken into account in these formulas. The purpose of this post-hoc analysis is to evaluate the association between factors related to tissue sodium accumulation and the discrepancy between measured and predicted plasma [Na+]. Method We used data from a hypernatremic intensive care unit (ICU) cohort with 66 patients and 1,034 ICU days with complete data on sodium, potassium and water balance. We excluded ICU days with incomplete balances, dialysis and severe diarrhea. The predicted plasma [Na+] was calculated using the Barsoum-Levine (BL) and the Nguyen-Kurtz (NK) formula. Then, we calculated the discrepancy between predicted and measured plasma [Na+] (∆[Na+]). We fitted a linear mixed-effect model to investigate the association between factors related to tissue sodium content and ∆[Na+]. Age, sex, blood pressure, eGFR, CRP, plasma albumin, total body water (TBW), baseline plasma [Na+] and changes in plasma [Na+] were incorporated as fixed effects in the model, while the subjects were introduced as a random effect. TBW was estimated as 60% of body weight for males and 50% of body weight for females, corrected for fluid balances on subsequent ICU days. Results A total of 613 ICU days of 66 patients were included in our analysis. The mean age was 58 ± 15 years and 38% was female. The mean plasma [Na+] at inclusion day was 145 ± 9 mmol/L and mean eGFR CKD-EPI was 52 ± 28 ml/min/1.73 m2. On average, the deviation between predicted and measured plasma [Na+] was 3.8 ± 3.3 mmol/L for the BL formula and 3.9 ± 3.4 mmol/L for the NK formula. For both formulas, TBW (p = 0.01), baseline plasma [Na+] (p < 0.001) and plasma [Na+] change (p < 0.001) were significantly associated with the discrepancy between predicted and measured plasma [Na+] (Table 1). Plasma albumin (p = 0.02) was also significantly associated with this discrepancy when the NK formula was used. Conclusion In a hypernatremic ICU cohort, baseline plasma [Na+], estimated TBW and plasma [Na+] changes are associated with the inaccurateness of plasma [Na+] prediction. As baseline plasma [Na+] and estimated TBW are available when initiating treatment, incorporation of these variables in the currently available formulas may improve the prediction of plasma [Na+].

#6844 MONITOR SWITCHING-INDUCED VARIATIONS IN CONDUCTIVITY AND PLASMA SODIUM DURING HEMODIALYSIS SESSIONS

Abstract Background and Aims Until the advent of the new monitors with sodium modules, the differences between prescribed and actual sodium have been little studied. And most dialysis centers have a fixed sodium prescription. However, the sodium gradient during sessions is one of the key factors in its balance in hemodialysis patients. Predialysis plasma sodium has an important interindividual but not intraindividual variability, which supports the hypothesis of reference sodium (setpoint). This work aimed to compare the impact of switching from the 5008 Cordiax monitor to the new 6008 Cordiax monitor on the actually measured conductivity and initial and final plasma sodium. Method A total of 106 hemodialysis patients were included. Each patient received two dialysis sessions in which only the monitor was varied. The variables collected were: concentrate, prescribed sodium and bicarbonate, real conductivity, initial and final plasma sodium measured by ionic dialysance, and the change in plasma sodium concentration during treatment (ΔPNa), which has been related to mortality when it exceeds 4 mmol/L, was calculated. The clinical research ethics committee of Hospital Clínic de Barcelona approved the present study. Results The change of dialysis monitor showed small, although significant, differences in initial (138.14 mmol/L with 5008 vs. 138.81 mmol/L with 6008) and final plasma sodium (139.58 mmol/L vs. 140.97 mmol/L), as well as in the actual conductivity obtained (13.97 vs. 14.1 mS/cm). The ΔPNa also increased significantly, with the percentage of patients with a ΔPNa greater than 4 mmol/L going from 6 to 22% with the monitor change. All these differences were statistically significant regardless of the concentrate used. All sessions were performed without notable clinical incidents, hypotension, cramps or thirst episodes. Conclusion The ultimate goal of hemodialysis should be to achieve isonatremia that allows complete elimination of interdialytic sodium gain and avoid intradialytic sodium loading. The change from 5008 to 6008 monitor is associated with an increase in conductivity, higher plasma sodium, and an increase in ΔPNa. Knowing and confirming this change will allow us to individualize the sodium prescription to find adequate isonatremic dialysis and, thus, avoid possible adverse effects.

A first proof-of-concept for the non-invasive, time-efficient measurement of the plasma sodium concentration for individualized dialysis.

Dialysis-induced changes in plasma sodium concentration may cause undesirable side effects. To prevent these, the sodium content in dialysis fluid has to be individualized based on the patient's plasma sodium concentration. In this paper, we describe a simple conductivity based method for measuring the plasma sodium concentration. The method is based on performing a bypass during which the residual volume on the dialysate side of the dialyzer at least partially adopts the sodium concentration on the blood side. The conductivity at dialysate outlet of the dialyzer after the end of bypass corresponds to the sodium concentration. We show that already 14 s of bypass are sufficient to subsequently measure a conductivity that correlates with the blood-side sodium concentration. Thus, the short bypass method allows a time saving of 88% compared to the long bypass of 120 s. In vitro experiments with bovine blood show that plasma sodium concentration can be non-invasively and time-efficiently measured during dialysis. Bland Altman analysis reveals a bias of 0.28 mmol/l and limits of agreement of -3.17 and 3.74 mmol/l for the long bypass. For the short bypass, bias is 0.09 mmol/l and limits are -3.90 and 4.08 mmol/l. Since the method presented is based on established conductivity cells, no additional sensors are required, so that the method could be easily implemented in dialysis machines. In future, performing a bypass at the beginning of a treatment may be used to adjust the composition of dialysis fluid individually for each patient.

Fluid Restriction Therapy for Chronic SIAD; Results of a Prospective Randomized Controlled Trial.

Fluid restriction (FR) is the recommended first-line treatment for syndrome of inappropriate antidiuresis (SIAD), despite the lack of prospective data to support its efficacy. A prospective nonblinded randomized controlled trial of FR versus no treatment in chronic SIAD. A total of 46 patients with chronic asymptomatic SIAD were randomized to either FR (1 liter/day) or no specific hyponatremia treatment (NoTx) for 1 month. The primary endpoints were change in plasma sodium concentration (pNa) at days 4 and 30. Median baseline pNa was similar in the 2 groups [127 mmol/L (interquartile range [IQR] 126-129) FR and 128 mmol/L (IQR 126-129) NoTx, P = 0.36]. PNa rose by 3 mmol/L (IQR 2-4) after 3 days FR, compared with 1 mmol/L (IQR 0-3) NoTx, P = 0.005. There was minimal additional rise in pNa by day 30; median pNa increased from baseline by 4 mmol/L (IQR 2-6) in FR, compared with 1 mmol/L (IQR 0-1) NoTx, P = 0.04. After 3 days, 17% of FR had a rise in pNa of ≥5 mmol/L, compared with 4% NoTx, RR 4.0 (95% CI 0.66-25.69), P = 0.35. After 3 days, 61% of FR corrected pNa to ≥130 mmol/L, compared with 39% of NoTx, RR 1.56 (95% CI 0.87-2.94), P = 0.24. FR induces a modest early rise in pNa in patients with chronic SIAD, with minimal additional rise thereafter, and it is well-tolerated. More than one-third of patients fail to reach a pNa ≥130 mmol/L after 3 days of FR, emphasizing the clinical need for additional therapies for SIAD in some patients.

A Randomized Trial of Empagliflozin to Increase Plasma Sodium Levels in Patients with the Syndrome of Inappropriate Antidiuresis.

Treatment options to address the hyponatremia induced by the syndrome of inappropriate antidiuresis (SIAD) are inadequate. The sodium glucose cotransporter 2 (SGLT2) inhibitor empagliflozin promotes osmotic diuresis via urinary glucose excretion and therefore, might offer a novel treatment option for SIAD. In this double-blind, randomized trial, we recruited 88 hospitalized patients with SIAD-induced hyponatremia <130 mmol/L at the University Hospital Basel from September 2016 until January 2019 and assigned patients to receive, in addition to standard fluid restriction of <1000 ml/24 h, a once-daily dose of oral empagliflozin or placebo for 4 days. The primary end point was the absolute change in plasma sodium concentration after 4 days of treatment. Secondary end points included predisposing factors for treatment response and safety of the intervention. Of the 87 patients who completed the trial, 43 (49%) received treatment with empagliflozin, and 44 (51%) received placebo. Baseline plasma sodium concentrations were similar for the two groups (median 125.5 mmol/L for the empaflozin group and median 126 mmol/L for the placebo group). Patients treated with empagliflozin had a significantly higher increase of median plasma sodium concentration compared with those receiving placebo (10 versus 7 mmol/L, respectively; P=0.04). Profound hyponatremia (<125 mmol/L) and lower baseline osmolality levels increased the likelihood of response to treatment with empagliflozin. Treatment was well tolerated, and no events of hypoglycemia or hypotension occurred among those receiving empagliflozin. Among hospitalized patients with SIAD treated with fluid restriction, those who received empagliflozin had a larger increase in plasma sodium levels compared with those who received placebo. This finding indicates that empagliflozin warrants further study as a treatment for the disorder.

Adjusted Plasma Chloride and Bicarbonate Concentrations: An Approach to Identifying Acid–Base Disorders

Chloride disorders (hypochloremia, hyperchloremia) and bicarbonate disorders (hypobicarbonatemia, hyperbicarbonatemia) are common in clinical medicine and indicate metabolic and/or respiratory acid-base disorders. The normally inverse relationship between chloride and bicarbonate concentrations in the blood is altered, however, by changes in fluid balance, i.e., water excess or deficit, with resulting changes in sodium and other electrolyte concentrations and by anion gap metabolic acidosis, which lowers bicarbonate concentrations but not the chloride concentrations. We used formulas derived over a decade ago that utilize dry slide laboratory technology to adjust plasma chloride and bicarbonate concentrations for changes in water balance, as reflected in changes in plasma sodium concentrations and in the plasma anion gap. We then prospectively validated these formulas in 736 consecutive adults, 499 having abnormal basic metabolic panel results and 237 having normal panel results, using modern wet laboratory technology. Plasma chloride and bicarbonate concentrations were inversely correlated (2-tailed P-value <0.0001), but the correlations were only modest (Spearman r: -0.48 for the abnormal group and -0.41 for the normal group). After adjusting the plasma chloride and bicarbonate concentrations using the 2 prior formulas, the inverse correlations were very high, with Spearman r: -0.998 for the abnormal group and -0.999 for the normal group. Adjusting plasma chloride and bicarbonate concentrations for any water imbalance and anion gap alterations leads to very high inverse correlations between these 2 anions, allowing accurate assessment of either subtle or overt acid-base disorders.

Associations between dialysate sodium concentration and plasma sodium concentration of dogs receiving intermittent hemodialysis treatments.

OBJECTIVE To compare dialysate sodium concentration and patient plasma sodium concentration of dogs during intermittent hemodialysis treatments. SAMPLE 211 intermittent hemodialysis treatments performed on 40 client-owned dogs for the management of dialysis-dependent uremia. PROCEDURES Medical records were reviewed to determine the plasma sodium concentration of each dog before and after routine hemodialysis treatments. Associations between detected changes in plasma sodium concentration and dialysate sodium concentration were evaluated by use of Spearman rank correlations and linear regression analysis. RESULTS Significant linear correlations were found between the dialysate sodium concentration and patient sodium concentration. The starting dialysate-to-patient sodium gradient was associated with the strongest correlation to the change in patient sodium concentration at the end of the dialysis session. Modest correlations existed between the dialysate sodium concentration and postdialysis patient sodium concentration as well as between the predialysis dialysate-to-patient sodium gradient and postdialysis dialysate-to-patient sodium gradient. CONCLUSIONS AND CLINICAL RELEVANCE The dialysate sodium concentration was correlated with the patient sodium concentration in dogs, and the dialysate-to-patient sodium gradient could be used to further refine this association to predict the postdialysis patient sodium concentration and potentially manage dysnatremia during hemodialysis. Prospective studies should be performed to determine how these associations can be used to correct aberrations as well as to avoid unwanted alterations in patient sodium concentrations.

Extracellular volume depletion and resultant hypotonic hyponatremia: A novel translational approach

Although several methods currently exist to determine that a person is hypovolemic, it often remains very challenging to accurately estimate the effective circulating volume or amount of intravascular volume depletion in a non-controlled setting. This depletion of intravascular volume can have many causes and is frequently accompanied by hypotonic hyponatremia as a result of hypovolemia-induced release of arginine vasopressin (AVP) from the posterior pituitary gland. Here, we derive a novel, comprehensible equation that provides a theoretical insight into the complex interrelationship between the degree of isotonic volume depletion and the resultant change in plasma sodium concentration. We believe that the presented model can prove to be a valuable tool for the analysis of fluid and electrolyte imbalances.

Neuronal circuits involved in osmotic challenges.

The maintenance of plasma sodium concentration within a narrow limit is crucial to life. When it differs from normal physiological patterns, several mechanisms are activated in order to restore body fluid homeostasis. Such mechanisms may be vegetative and/or behavioral, and several regions of the central nervous system (CNS) are involved in their triggering. Some of these are responsible for sensory pathways that perceive a disturbance of the body fluid homeostasis and transmit information to other regions. These regions, in turn, initiate adequate adjustments in order to restore homeostasis. The main cardiovascular and autonomic responses to a change in plasma sodium concentration are: i) changes in arterial blood pressure and heart rate; ii) changes in sympathetic activity to the renal system in order to ensure adequate renal sodium excretion/absorption, and iii) the secretion of compounds involved in sodium ion homeostasis (ANP, Ang-II, and ADH, for example). Due to their cardiovascular effects, hypertonic saline solutions have been used to promote resuscitation in hemorrhagic patients, thereby increasing survival rates following trauma. In the present review, we expose and discuss the role of several CNS regions involved in body fluid homeostasis and the effects of acute and chronic hyperosmotic challenges.

Quantification of nonosmotic sodium storage capacity following acute hypertonic saline infusion in healthy individuals

The assumption that sodium accumulation in the human body is always accompanied by water retention has been challenged by data showing that sodium can be stored nonosmotically. Here we investigated the contribution of nonosmotic sodium storage to short-term sodium homeostasis after hypertonic saline infusion in healthy individuals on a low-sodium diet. During four hours after infusion, we compared the observed changes in plasma sodium concentration and urinary cation excretion with changes that were calculated with the Adrogue-Madias and Nguyen-Kurtz formula, formulations widely implemented to guide the treatment of dysnatremias. We included 12 healthy non-smoking male individuals with normal blood pressure, body mass index, and kidney function. Right after infusion, the average observed plasma sodium change from baseline (3.5 mmol/L) was similar to the predicted changes by the Adrogue-Madias (3.3 mmol/L) and Nguyen-Kurtz formula (3.1mmol/L). However, the observed plasma sodium concentration change after four hours (-1.8 mmol/L) was very different from the changes as predicted by the Adrogue-Madias (0.4 mmol/L) and the Nguyen-Kurtz formula (-0.9 mmol/L). Moreover, only 47% and 55%, respectively, of the expected sodium and potassium excretion were retrieved in the urine. Thus, healthy individuals are able to osmotically inactivate significant amounts of sodium after hypertonic saline infusion. Further research is needed to uncover factors that determine nonosmotic sodium storage.

Adipsic diabetes insipidus in adult patients.

Adipsic diabetes insipidus (ADI) is a very rare disorder, characterized by hypotonic polyuria due to arginine vasopressin (AVP) deficiency and failure to generate the sensation of thirst in response to hypernatraemia. As the sensation of thirst is the key homeostatic mechanism that prevents hypernatraemic dehydration in patients with untreated diabetes insipidus (DI), adipsia leads to failure to respond to aquaresis with appropriate fluid intake. This predisposes to the development of significant hypernatraemia, which is the typical biochemical manifestation of adipsic DI. A literature search was performed to review the background, etiology, management and associated complications of this rare condition. ADI has been reported to occur in association with clipping of an anterior communicating artery aneurysm following subarachnoid haemorrhage, major hypothalamic surgery, traumatic brain injury and toluene exposure among other conditions. Management is very difficult and patients are prone to marked changes in plasma sodium concentration, in particular to the development of severe hypernatraemia. Associated hypothalamic disorders, such as severe obesity, sleep apnoea and thermoregulatory disorders are often observed in patients with ADI. The management of ADI is challenging and is associated with significant morbidity and mortality. Prognosis is variable; hypothalamic complications lead to early death in some patients, but recent reports highlight the possibility of recovery of thirst.

Bone: An Acute Buffer of Plasma Sodium During Exhaustive Exercise?

Both hyponatremia and osteopenia separately have been well documented in endurance athletes. Although bone has been shown to act as a "sodium reservoir" to buffer severe plasma sodium derangements in animals, recent data have suggested a similar function in humans. We aimed to explore if acute changes in bone mineral content were associated with changes in plasma sodium concentration in runners participating in a 161 km mountain footrace. Eighteen runners were recruited. Runners were tested immediately pre- and post-race for the following main outcome measures: bone mineral content (BMC) and density (BMD) via dual-energy X-ray absorptiometry (DEXA); plasma sodium concentration ([Na+]p), plasma arginine vasopressin ([AVP]p), serum aldosterone concentration ([aldosterone]s), and total sodium intake. Six subjects finished the race in a mean time of 27.0±2.3 h. All subjects started and finished the race with [Na+]p within the normal range (137.7±2.3 and 136.7±1.6 mEq/l, pre- and post-race, respectively). Positive correlations were noted between change (Δ; post-race minus pre-race) in total BMC (grams) and [Na+]p (mEq/l) (r=0.99; p<0.0001), and between total sodium intake (mEq/kg) and %Δ lumbar spine BMD (r=0.94; p<0.001). Change in [aldosterone]s was positively correlated with: rate of total sodium intake (r=0.84; p<0.05); Δ total BMC (r=0.82; p<0.05); and Δ [Na+]p (r=0.88; p<0.05). No significant pre- to post-race mean differences were noted in BMC or BMD. Robust associations between Δ BMC and Δ [Na+]p suggest that sodium status and bone density may be inter-related during endurance exercise and should be considered in future investigations of athletic osteopenia.

Altering plasma sodium concentration rapidly changes blood pressure during haemodialysis

Plasma sodium is increased following each meal containing salt. There is an increasing interest in the effects of plasma sodium concentration, and it has been suggested that it may have direct effects on blood pressure (BP) and possibly influences endothelial function. Experimental increases of plasma sodium concentration rapidly raise BP even when extracellular volume falls. Ten patients with end-stage renal failure established on haemodialysis were studied during the first 2 h of dialysis without fluid removal during this period. They were randomized to receive haemodialysis with (i) dialysate sodium concentration prescribed to 135 mmol/L and (ii) 145 mmol/L in random order in a prospective, single-blinded crossover study. BP measurements and blood samples were taken every 30 min. Pre-dialysis sitting BP was 137/76 ± 7/3 mmHg. Lower dialysate sodium concentration (135 mmol/L) reduced plasma sodium concentration [139.49 ± 0.67 to 135.94 ± 0.52 mmol/L (P < 0.001)], whereas plasma sodium concentration was not altered by higher dialysate sodium (145 mmol/L) (140.17 ± 0.66 mmol/L at baseline to 140.72 ± 0.43 mmol/L at 120 min). Systolic BP was lower with dialysate sodium concentration 135 mmol/L [area under the curve (AUC) 15823.50 ± 777.15 (mmHg)min] compared with 145 mmol/L [AUC 17018.20 ± 1102.17 (mmHg)min], mean difference 1194.70 ± 488.41 (mmHg)min, P < 0.05. There was a significant positive relationship between change in plasma sodium concentration and change in systolic BP. This direct relationship suggests that a fall of 1 mmol/L in plasma sodium concentration would be associated with a 1.7 mmHg reduction in systolic BP (P < 0.05). The potential mechanism for the increase in BP seen with salt intake may be through small but significant changes in plasma sodium concentration.

Sodium supplementation has no effect on endurance performance during a cycling time-trial in cool conditions: a randomised cross-over trial

BackgroundSodium ingestion during exercise may exert beneficial effects on endurance performance by either its ability to attenuate the decrease in plasma volume or reduce the risk of Exercise Associated Hyponatremia (EAH). This study aimed to investigate the effect of sodium supplements on endurance performance during a 72 km road cycling time-trial in cool conditions (13.8 ± 2.0°C).MethodsNine well-trained cyclists (5 male, 4 female) participated in this randomized, double-blinded cross-over study, receiving either a 700 mg.h-1 salt capsule, or a corn flour placebo during the time trial. Water was ingested ad-libitum throughout the time trial. Measurements were taken pre, post, and 40 min following time-trials, analysing blood, sweat, and urinary hydration and sodium concentration.ResultsSodium supplements had no effect on time-trial performance (overall time = 171 min sodium vs. 172 min placebo; p = 0.46). There was also no effect on the change in plasma sodium concentration from pre to post time trial between trials (relative plasma [Na+] change (pre-post): sodium = 0.56%, placebo = 0.47%; p = 0.60). The greatest difference observed was a significantly change in plasma volume from pre to post exercise between the salt and the placebo trial (p = 0.02), which corresponded with an increased thirst with sodium supplementation.ConclusionSodium supplements therefore do not improving performance during exercise of approximately 3 h duration in cool conditions.

An increased fluid intake leads to feet swelling in 100-km ultra-marathoners - an observational field study

BackgroundAn association between fluid intake and changes in volumes of the upper and lower limb has been described in 100-km ultra-marathoners. The purpose of the present study was (i) to investigate the association between fluid intake and a potential development of peripheral oedemas leading to an increase of the feet volume in 100-km ultra-marathoners and (ii) to evaluate a possible association between the changes in plasma sodium concentration ([Na+]) and changes in feet volume.MethodsIn seventy-six 100-km ultra-marathoners, body mass, plasma [Na+], haematocrit and urine specific gravity were determined pre- and post-race. Fluid intake and the changes of volume of the feet were measured where the changes of volume of the feet were estimated using plethysmography.ResultsBody mass decreased by 1.8 kg (2.4%) (p < 0.0001); plasma [Na+] increased by 1.2% (p < 0.0001). Haematocrit decreased (p = 0.0005). The volume of the feet remained unchanged (p > 0.05). Plasma volume and urine specific gravity increased (p < 0.0001). Fluid intake was positively related to the change in the volume of the feet (r = 0.54, p < 0.0001) and negatively to post-race plasma [Na+] (r = -0.28, p = 0.0142). Running speed was negatively related to both fluid intake (r = -0.33, p = 0.0036) and the change in feet volume (r = -0.23, p = 0.0236). The change in the volume of the feet was negatively related to the change in plasma [Na+] (r = -0.26, p = 0.0227). The change in body mass was negatively related to both post-race plasma [Na+] (r = -0.28, p = 0.0129) and running speed (r = -0.34, p = 0.0028).ConclusionsAn increase in feet volume after a 100-km ultra-marathon was due to an increased fluid intake.

Dietary salt influences postprandial plasma sodium concentration and systolic blood pressure

The plasma sodium concentration has a direct effect on blood pressure in addition to its effects on extracellular volume regulated through changes in the endothelium. The mechanism for elevated blood pressure seen with habitually increased salt intake is unclear, especially the effect of salt in a single meal on plasma sodium concentration and blood pressure. To resolve this we compared the effect of soup with or without 6 g of salt (an amount similar to that in a single meal) on the plasma sodium concentration and blood pressure in 10 normotensive volunteers using a randomized, crossover design. The plasma sodium concentration was significantly increased by 3.13±0.75 mmol/l with salted compared with unsalted soup. Blood pressure increased in volunteers ingesting soup with added salt, and there was a significant positive correlation between plasma sodium concentration and systolic blood pressure. A 1-mmol/l increase in plasma sodium was associated with a 1.91-mm Hg increase in systolic blood pressure by linear regression. Thus, changes in plasma sodium concentration occur each time a meal containing salt is consumed. A potential mechanism for the changes in blood pressure seen with salt intake may be through its effects on plasma sodium concentration.

Total Body Water Via Bioelectrical Impedance Analysis in Relationship to Plasma and Urine Sodium Concentrations

Research suggests that acute changes in plasma sodium concentration ([PNa]), especially a decrease, may negatively affect bioelectrical impedance analysis (BIA) by either increasing or decreasing an individual's resistance to the outputted frequency. While research is conflicting, there is limited research utilizing the more practical and cost-effective lower body BIA when determining relationships between sodium balance and total body water (TBW) calculations. PURPOSE: To examine the relationship of calculated percent hydration (%HY) by TBW measures to [PNa] and urine sodium concentration ([UNa]). METHODS: Participants included 16 male and female recreational athletes (age=28.13+6.82y, height=171.2+12.16cm, weight=73.81+15.21kg). As part of a larger study we collected pre and post-exercise measures of [PNa], [UNa] and TBW (measured by the Tanita TBF-300A, Tanita Corporation, Tokyo, Japan). TBW measures were used to calculate %HY using a previously developed formula and categorized as: 1) hyperhydrated, 2) euhydrated-well hydrated, and 3) slightly-extremely hypohydrated. [PNa] and [UNa] measures were categorized as: 1) hyponatremic/sodium conservation, 2) normonatremic/normal sodium, and 3) hypernatremic/excessive sodium. RESULTS: We found no relationship between %HY and [UNa]. There was a relationship between %HY and [PNa] overall χ24(n=157)=14.329, p=0.003 and at post-exercise χ24(n=65)=9.079, p=0.029, but not at pre-exercise. Overall 10.2% of the participants were hyponatremic and 2.5% of these were euhydrated-well hydrated and 5.1% were slightly-extremely hypohydrated. Percentages were similar at post exercise 16.9% were hyponatremic, 10.8% of those were slightly-extremely hypohydrated, and 3.1% were euhydrated-well hydrated. CONCLUSION: Regardless of hydration status, active individuals may present with low [PNa]. Our findings suggest that %HY calculations from TBW measures are affected by [PNa] and may not be accurate when an individual is either euhydrated or hyperhydrated. An increase in water content decreases impendence, which may skew TBW calculations taken by a lower body BIA.

Acute Effects of Sodium Ingestion on Thirst and Cardiovascular Function

Sweating during exercise, especially during exercise in the heat, leads to sodium and water losses, and the quantity of these losses depends upon the intensity and duration of the activity, genetic predisposition and conditioning of the individual, and environmental factors. In athletes, adequate sodium intake is necessary to maintain fluid balance during training and competition. To ensure the precise regulation of volume and osmolality of body fluids, a number of integrated neural and hormonal systems have evolved to control thirst and sodium appetite. These systems respond to stimuli that arise from a deficit of fluid arising in both the intracellular and extracellular fluid compartments or to systemic hypertonicity. Thirst is highly sensitive to increases in plasma sodium concentration and osmolality, requiring only a 2%-3% increase to induce feelings of thirst. A larger change in plasma volume (10%) is required to induce thirst if there is no concomitant change in plasma sodium concentration. If plain water is used to replenish body water, plasma volume is preferentially restored over the interstitial and intracellular fluid space, suppressing plasma sodium concentration and removing the dipsogenic drive long before total body fluid has been restored. During or after dehydrating exercise, sodium ingestion helps to maintain and restore plasma volume and osmolality by continuing thirst sensation (thus drinking) and also by increasing body fluid retention. A high sodium meal or intravascular hypertonic saline infusion may cause transient osmotically mediated blood pressure increases, but in healthy people, acute sodium ingestion does not cause sustained hypertension. The purpose of this review is to provide evidence that acute increases in sodium are an intrinsic part of the thirst response during and after exercise, and that blood pressure increases associated with hypertonicity appear to be short lived.

Effect of resuscitative fluids upon physical properties of blood perfusing the brain.

Acute physiologic changes induced by the infusion of resuscitative fluids may be harmful, resulting in the clinical sequelae of pulmonary and intraventricular hemorrhage. Using a chronically catheterized lamb model, changes in plasma sodium concentration, osmolality, hematocrit, glucose, colloid osmotic pressure, and arterial pressure were quantified in blood directly perfusing the brain, following distal infusions of fluids commonly used during neonatal resuscitation: molar and .5M NaHCO3, D10W and D25W, and whole blood. Distal infusion of hypertonic solutions resulted in acute alterations in electrolyte and osmotic equilibrium in the common carotid artery. All infused solutions caused a brief elevation in mean blood pressure; whole blood transfusion resulted in a sustained increase in blood pressure.

Mice lacking the transient receptor vanilloid potential 1 channel display normal thirst responses and central Fos activation to hypernatremia

Neurons of the organum vasculosum of the lamina terminalis (OVLT) are necessary for thirst and vasopressin secretion during hypersmolality in rodents. Recent evidence suggests the osmosensitivity of these neurons is mediated by a gene product encoding the transient receptor potential vanilloid-1 (TRPV1) channel. The purpose of the present study was to determine whether mice lacking the TRPV1 channel had blunted thirst responses and central Fos activation to acute and chronic hyperosmotic stimuli. Surprisingly, TRPV1-/- vs. wild-type mice ingested similar amounts of water after injection (0.5 ml sc) of 0.5 M NaCl and 1.0 M NaCl. Chronic increases in plasma osmolality produced by overnight water deprivation or sole access to a 2% NaCl solution for 48 h produced similar increases in water intake between wild-type and TRPV1-/- mice. There were no differences in cumulative water intakes in response to hypovolemia or isoproterenol. In addition, the number of Fos-positive cells along the lamina terminalis, including the OVLT, as well as the supraoptic nucleus and hypothalamic paraventricular nucleus, was similar between wild-type and TRPV1-/- mice after both acute and chronic osmotic stimulation. These findings indicate that TRPV1 channels are not necessary for osmotically driven thirst or central Fos activation, and thereby suggest that TRPV1 channels are not the primary ion channels that permit the brain to detect changes in plasma sodium concentration or osmolality.