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Sodium in plasma

Seiler K., Wang K., Bakker E., Morf W.E., Rusterholz B., Spichiger U.E., Simon W., Characterization of sodium-selective optode membranes based on neutral ionophores and assay of sodium in plasma, Clinical Chemistry 1991 37 1350-1355. [Pg.321]

EN86 Boeyckens, A., Schots, J., Vandenplas, H., Senesael, F., Goedhuys, W. and Gorus, F.K. (1992). Ektachem slides for direct potentiometric determination of sodium in plasma Effect of natremia, blood pH, and type of electrolyte reference fluid on concordance with flame photometry and other potentiometric methods. Clin. Chem. 38, 114-118. [Pg.316]

C Dumouseaux, S Muramatsu, W Takasaki et al. Highly sensitive and specific determination of pravastatin sodium in plasma by high-performance liquid chromatography and laser-induced fluorescence detection after immobilized antibody extraction. J Pharm Sci 83 1630, 1994. [Pg.306]

Lee, H.S. Kim, E.J. Zee, O.P. Lee, Y.J. High performance liquid chromatographic determination of diclofenac sodium in plasma using column-switching technique for sample clean-up. Arch.Pharm. (Weinheim)., 1989, 322, 801-806... [Pg.499]

In parallel with these studies, other ligands were assessed for use in sodium-selective electrodes, including the methyl, butyl, and adamantyl ketone tetramers of p-f-butylcalix[4]arene. However, only the methyl ketone derivative produced satisfactory PVC membrane electrodes [6]. These were subsequently applied to the analysis of sodium in plasma samples [11]. Excellent correlations (r = 0.979, r = 0.987 and r = 0.951, n = 10) were found in comparative tests with three reference... [Pg.155]

The volume of extracellular fluid is direcdy related to the Na" concentration which is closely controlled by the kidneys. Homeostatic control of Na" concentration depends on the hormone aldosterone. The kidney secretes a proteolytic enzyme, rennin, which is essential in the first of a series of reactions leading to aldosterone. In response to a decrease in plasma volume and Na" concentration, the secretion of rennin stimulates the production of aldosterone resulting in increased sodium retention and increased volume of extracellular fluid (51,55). [Pg.380]

Sodium is the major extracellular cation. Because of its osmotic effects, changes in sodium content in the body have an important influence on extracellular fluid volume, including plasma volume. For example, excess sodium leads to the retention of water and an increase in plasma volume. Increased plasma volume then causes an increase in blood pressure. Conversely, sodium deficit leads to water loss and decreased plasma volume. A decrease in plasma volume then causes a decrease in blood pressure. Therefore, homeostatic mechanisms involved in the regulation of plasma volume and blood pressure involve regulation of sodium content, or sodium balance, in the body. [Pg.336]

Sodium reabsorption is also influenced by ANP. The original decrease in plasma volume leads to a decrease in atrial filling and a decrease in the release of ANP from the myocardium. Atrial natriuretic peptide, which acts on vascular smooth muscle, granular cells of the kidney, and the adrenal cortex, normally causes the following ... [Pg.338]

Taken together, the homeostatic responses elicited by the initial decrease in plasma volume serve to decrease sodium filtration, increase sodium reabsorption, and, consequently, decrease sodium excretion in the urine. This conservation of sodium leads to conservation of water and an expansion of plasma volume toward normal. [Pg.338]

Szathmary and Luhmann [50] described a sensitive and automated gas chromatographic method for the determination of miconazole in plasma samples. Plasma was mixed with internal standard l-[2,4-dichloro-2-(2,3,4-trichlorobenzyloxy) phenethyl]imidazole and 0.1 M sodium hydroxide and extracted with heptane-isoamyl alcohol (197 3) and the drug was back-extracted with 0.05 M sulfuric acid. The aqueous phase was adjusted to pH 10 and extracted with an identical organic phase, which was evaporated to dryness. The residue was dissolved in isopropanol and subjected to gas chromatography on a column (12 m x 0.2 mm) of OV-1 (0.1 pm) at 265 °C, with nitrogen phosphorous detection. Recovery of miconazole was 85% and the calibration graph was rectilinear for 0.25 250 ng/mL. [Pg.45]

The recovery of neurotransmitters from synaptic clefts and their storage in cytoplasmic vesicles is accomplished by the tandem actions of the secondary transporters in plasma and vesicular membranes. Sodium-dependent symporters mediate neurotransmitter reuptake from synaptic clefts into neurons and glia, whereas proton-dependent antiporters concentrate neurotransmitters from neuronal cytoplasm into synaptic vesicles (Fig. 5-13). [Pg.84]

SODIUM-DEPENDENT GLUTAMINE TRANSPORTERS IN PLASMA MEMBRANES MEDIATE THE TRANSFER OF GLUTAMINE FROM ASTROCYTES TO NEURONS 287... [Pg.267]

Abnormalities in either the renal or tissue autoregulatory processes for sodium excretion, plasma volume, and arteriolar constriction ... [Pg.124]

Acutely, diuretics lower BP by causing diuresis. The reduction in plasma volume and stroke volume associated with diuresis decreases cardiac output and, consequently, BP. The initial drop in cardiac output causes a compensatory increase in peripheral vascular resistance. With chronic diuretic therapy, the extracellular fluid volume and plasma volume return almost to pretreatment levels, and peripheral vascular resistance falls below its pretreatment baseline. The reduction in peripheral vascular resistance is responsible for the long-term hypotensive effects. Thiazides lower BP by mobilizing sodium and water from arteriolar walls, which may contribute to decreased peripheral vascular resistance. [Pg.131]

FIGURE 1.46 Effects of major experimental variables (A) extraction time, (B) pH, (C) sodium chloride concentration, and (D) temperature on the efficiency of direct SPME of anticonvulsants in plasma sample.1 7 (Reproduced with permission from the authors.)... [Pg.57]

Pretreatment of rats with chlorpromazine (10 mg/kg intramuscularly) and sodium thiosulfate (1,000 mg/kg intraperitoneally) greatly decreased or abolished the increase in plasma creatine kinase observed in rats exposed to hydrogen cyanide at 200 ppm for 12.5 minutes (O Flaherty and Thomas 1982). In an in vitro study, chlorpromazine and 4,4 -diisothiocyano-2,2 -stilbene disulfonic acid reduced cyanide-induced contractions in vascular smooth muscle (Robinson et al. 1985a). It was suggested that chlorpromazine prevents cyanide-induced calcium influx and reduces peroxidation of membrane lipids (Maduh et al. [Pg.115]

These results suggest acute renal failure (ARF) due to tubular necrosis caused by phenol. Plasma sodium is low due mainly to impaired reabsorption in the nephron, although the slightly low albumin suggests haemodilution possibly as a result of excessive i.v. fluids. Potassium is raised due to poor exchange with sodium in the distal tubule and the acidosis (low pH and low bicarbonate concentration) arises from defective acidification of the glomerular filtrate acidosis is often associated with hyperkalaemia (raised plasma... [Pg.280]


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The determination of sodium in plasma

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