The temporality between the mandated reduction of salt in processed food and the decrease of death from stroke and ischemic heart disease, the association of hypertension, and cardiovascular disease led many public health organizations to recommend reducing dietary sodium to a maximum of 2300 mg per day. It turns out that some nuances can be brought about to this universally shared belief.

Indeed, consideration of health outcomes instead of only blood pressure as a surrogate marker of cardiovascular disease and prognosis gave contradictory results whereas low sodium intake is associated to an excess of death and cardiovascular events.

Accordingly, sodium intake should be adapted to individual risk factors, and evidence is still clearly lacking to support indiscriminate recommendations in healthy people. By contrast, a restricted sodium diet is certainly useful in patients with chronic kidney disease exposed to salt retention, and by reciprocity, low sodium diet must be absolutely avoided in all patients presenting renal or extra renal sodium wasting where sodium depletion is a life-threatening condition.

The regulation of body fluid balance is a key concern in health and disease and comprises three concepts. The first concept pertains to the relationship between total body water (TBW) and total effective solute and is expressed in terms of the tonicity of the body fluids. Disturbances in tonicity are the main factor responsible for changes in cell volume, which can critically affect brain cell function and survival. Solutes distributed almost exclusively in the extracellular compartment (mainly sodium salts) and in the intracellular compartment (mainly potassium salts) contribute to tonicity, while solutes distributed in TBW have no effect on tonicity. The second body fluid balance concept relates to the regulation and measurement of abnormalities of sodium salt balance and extracellular volume. Estimation of extracellular volume is more complex and error prone than measurement of TBW. A key function of extracellular volume, which is defined as the effective arterial blood volume (EABV), is to ensure adequate perfusion of cells and organs. Other factors, including cardiac output, total and regional capacity of both arteries and veins, Starling forces in the capillaries, and gravity also affect the EABV. Collectively, these factors interact closely with extracellular volume and some of them undergo substantial changes in certain acute and chronic severe illnesses. Their changes result not only in extracellular volume expansion, but in the need for a larger extracellular volume compared with that of healthy individuals. Assessing extracellular volume in severe illness is challenging because the estimates of this volume by commonly used methods are prone to large errors in many illnesses. In addition, the optimal extracellular volume may vary from illness to illness, is only partially based on volume measurements by traditional methods, and has not been determined for each illness. Further research is needed to determine optimal extracellular volume levels in several illnesses. For these reasons, extracellular volume in severe illness merits a separate third concept of body fluid balance.

Canalicular fluid flow is acknowledged to play a major role in bone functioning, allowing bone cells' metabolism and activity and providing an efficient way for cell-to-cell communication. Bone canaliculi are small canals running through the bone solid matrix, hosting osteocyte's dendrites, and saturated by an interstitial fluid rich in ions. Because of the small size of these canals (few hundred nanometers in diameter), fluid flow is coupled with electrochemical phenomena. In our previous works, we developed a multi-scale model accounting for coupled hydraulic and chemical transport in the canalicular network. Unfortunately, most of the physical and geometrical information required by the model is hardly accessible by nowadays experimental techniques. The goal of this study was to numerically assess the influence of the physical and material parameters involved in the canalicular fluid flow. The focus was set on the electro-chemo-mechanical features of the canalicular milieu, hopefully covering any in vivo scenario. Two main results were obtained. First, the most relevant parameters affecting the canalicular fluid flow were identified and their effects quantified. Second, these findings were given a larger scope to cover also scenarios not considered in this study. Therefore, this study gives insight into the potential interactions between electrochemistry and mechanics in bone and provides the rational for further theoretical and experimental investigations.

Frusemide (Lasix) is commonly used diuretic in horse racing and equine clinical practice. While pharmacology, pharmacodynamics, renal and haematological effects of frusemide have been studied in horses, its effects on the distribution of fluid within the horse remain unknown.

To quantify the effects of frusemide on extracellular and intracellular fluid shifts.

Horses were infused with 1 mg/kg body mass (n = 7) or 2 mg/kg (n = 9) i.v. frusemide. Total body water (TBW), extracellular fluid volume (ECFV) and plasma volume (PV) were measured using D2O, NaSCN and Evans blue dilution. Change in ECFV was assessed from the change in plasma [protein] and from repeated infusion/dilution of NaSCN.

Frusemide resulted in a 0.020 +/- 0.002 l/kg decrease in TBW within 120 min. At 120 min after frusemide infusion the ECFV losses were nearly double the TBW losses, therefore ECFV loss in excess of TBW loss is seen as an increase in ICFV.

Frusemide resulted in a net shift of fluid (electrolytes and water) from the extracellular to intracellular fluid compartment.

The fluid shifts that occur within horses administered frusemide has not previously been characterised. The intracellular shift of fluid is of performance and clinical significance.

Hemorrhagic hypotension or operative trauma is believed to cause a contraction of the extracellular fluid volume (ECV) beyond the measured fluid losses. The aim of this review was to explore the evidence and implications of ECV loss.

We performed a systematic review of original trials measuring ECV changes during hemorrhage or operation. PubMed, relevant periodicals, and reference lists were searched until no further original articles appeared. The quality of both the scientific and the technical methods of the trials were evaluated.

A total of 61 original articles were found. The pattern appeared that all investigators reporting shock or operation to cause a disparate reduction of the ECV had measured the ECV with the same method. The ECV was calculated from very few blood samples that were withdrawn after 20 to 30 minutes of equilibration of a tracer (the (35)SO(4)-tracer). Trials calculating ECV from multiple blood samples, after longer equilibration times, or using other tracers did not find a contraction of the ECV. On the contrary, trials using a bromide tracer found the ECV to be expanded after operation.

The evidence supporting the idea that hemorrhage or operation cause a contraction of the ECV is weak, and probably a result of flawed methodology.

A method is described for simultaneous measurement of total body water, extracellular body water, plasma volume, exchangeable potassium pool employing radioactive tracers (3H2O, Na235SO4, 42KCl and 125I human serum albumin). Some suggestions are made that are particularly applicable to routine use in anuric and/or dialyzed patients. The observed values fit well with the values predicted for a reference subject.