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1 esuscitation results in smaller increases in plasma sodium.
3 tic patients, cachectic patients had reduced plasma sodium and increased norepinephrine, epinephrine
4 nel (ENaC) participates in the regulation of plasma sodium and volume, and gain of function mutations
6 of isosal on hemodynamics, brain edema, and plasma sodium concentration after head injury associated
7 the effects on the cerebellum of the rise of plasma sodium concentration and the emergence of thirst
9 1, we identified eight loci associated with plasma sodium concentration at P<5.0 x 10(-6) Of these,
10 nome-wide association study meta-analysis on plasma sodium concentration in 45,889 individuals of Eur
12 level as in the rats on solid chow; however, plasma sodium concentrations and plasma osmolality remai
18 (2.02 +/- 0.96 L) was FW loss, and increased plasma sodium from 139 (range: 135-143 mmol/L) to 143 (r
19 es did not correlate with either the initial plasma sodium level (r=0.05, P>.12) or the rate of corre
22 ean decrease (+/- one half of the 95% CI) in plasma sodium levels of 0.9 +/- 0.9 mmol/L from a mean o
23 restriction cycle, significant decreases in plasma sodium levels of 1.23 +/- 0.5 mmol/L (from values
24 m chloride before respiratory insufficiency, plasma sodium levels were increased by 22 (10) mmol/L in
25 ong patients who had fluid restriction only, plasma sodium levels were increased by 3 (2) mmol/L in 4
26 um chloride after respiratory insufficiency, plasma sodium levels were increased by 30 (6) mmol/L in
31 al positive psychotic symptoms (P < .09) and plasma sodium (P < .18) were even marginally associated
32 ases the strong ion difference by increasing plasma sodium, tris-hydroxymethyl aminomethane acts by i
33 ed from body composition (WD(4)), the actual plasma sodium (WD(5)), the substitution of plasma osmola
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