A neural basis for tonic suppression of sodium appetite.

Sodium appetite is a powerful form of motivation that can drive ingestion of high, yet aversive concentrations of sodium in animals that are depleted of sodium. However, in normal conditions, sodium appetite is suppressed to prevent homeostatic deviations. Although molecular and neural mechanisms underlying the stimulation of sodium appetite have received much attention recently, mechanisms that inhibit sodium appetite remain largely obscure. Here we report that serotonin 2c receptor (Htr2c)-expressing neurons in the lateral parabrachial nucleus (LPBNHtr2c neurons) inhibit sodium appetite. Activity of these neurons is regulated by bodily sodium content, and their activation can rapidly suppress sodium intake. Conversely, inhibition of these neurons specifically drives sodium appetite, even during euvolemic conditions. Notably, the physiological role of Htr2c expressed by LPBN neurons is to disinhibit sodium appetite. Our results suggest that LPBNHtr2c neurons act as a brake against sodium appetite and that their alleviation is required for the full manifestation of sodium appetite.

Artificial Hydration at the End of Life.

Initiation or continuation of artificial hydration (AH) at the end of life requires unique considerations. A combination of ethical precedents and medical literature may provide clinical guidance on how to use AH at the end of life. The purpose of this review is to describe the ethical framework for and review current literature relating to the indications, benefits, and risks of AH at the end of life. Provider, patient, and family perspectives will also be discussed.

Haemodynamic parameters and cognitive function during modeled acute volume loss.

PURPOSE: The purpose of the present study was to find a noninvasive way of detecting even smaller volume loss which is easier to carry out and possibly more precise than the currently used (mostly sphygmomanometer-based) methods. Haemodynamic and EEG measurements were carried out in simulated volume loss, involving blood donation and orthostatic challenges to assess adaptive responses and cognitive performance. Cognitive performance was assessed in an oddball task and changes of the evoked potential P300 were analyzed. Both haemodynamic and cognitive parameters were recorded in 'pre-donation' and 'post-donation' conditions for purposes of comparison. RESULTS: Cognitive performance (as reflected by P300 changes) was found to be a poor marker of volume loss. Difference between the two conditions in none of the parameters reached the level of statistical significance (defined as p < 0.05) RR mean, baroreceptor sensitivity and pulse pressure were rather sensitive to the relatively mild volume loss (p < 0.01 between pre- and post-conditions). CONCLUSION: Our study indicates that traditional sphygmomanometer based values can safely be replaced by values yielded by finger plethysmography, combined with brief orthostatic challenges and that P300 as a cognitive marker cannot be used to assess volume loss.

Gastric emptying and intestinal absorption of ingested water and saline by hypovolemic rats.

Recent experiments showed that in a one-bottle test conducted 16h after sc injection of polyethylene glycol (PEG) solution, hypovolemic rats consumed water or 0.30 M NaCl in an initial drinking episode but did not empty the ingested fluid from the stomach or absorb it from the small intestine very rapidly, certainly not as rapidly as when 0.15M NaCl was consumed (Smith et al., Am J Physiol 292: R2089-R2099, 2007). The present experiments examined the patterns of water and 0.30 M NaCl ingestion and the movement of consumed fluid through the gastrointestinal tract when PEG-treated rats were given a two-bottle delayed-access test. We found that both fluids always were consumed in the first drinking episode, that the fluid mixture ingested was equivalent to 0.10-0.15M NaCl, and that gastric emptying rate and net fluid absorption from the small intestine usually were much faster than when PEG-treated rats drank either water or hypertonic saline alone. Thus, ingestion of water and 0.30 M NaCl by hypovolemic rats in the same episode adaptively facilitated the movement into the circulation of a near-isotonic fluid that is ideal for restoring plasma volume deficits.