Effect of varying amounts of polysal and/or dextrose intravenous fluids on the blood levels of sodium, potassium, chloride and blood sugar.
Explore the source record for details and available documents.
SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Hypokalemia plus elevated carbon dioxide (CO2) content usually indicates renal or gastrointestinal potassium (K+) loss. Hypokalemia plus decreased CO2 content usually means intestinal K+ loss. Hyperkalemia is common in metabolic acidosis and oliguric renal failure. With hemolysis or thrombocytosis, serum K+ concentration may be elevated while plasma concentration is normal. A CO2 value less than 18 mmole/liter suggests metabolic acidosis; a value greater than 30 mmole/liter suggests metabolic alkalosis.
Explore the source record for details and available documents.
It has been recognised that the sweat (extracellular area) excreted from those affected with psoriasis contains twice the amount of sodium and four times the amount of potassium in comparison to those not affected with psoriasis. According to Saalmann, after HUV therapy (SUP) there is a significant reduction of the saliva sodium content (intercellular area) not only with psoriasis patients, but with all other patients receiving radiation therapy as well. This result has never before been described in the literature. Therefore, on the one hand, completely new aspects of psoriasis and therapy can be recognized, and on the other hand, of the effects of SUP.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
cDNAs encoding the two major electroneutral sodium-chloride transporters present in the mammalian kidney, the bumetanide-sensitive Na(+)-K(+)-Cl- symporter and thiazide-sensitive Na(+)-Cl- cotransporter, were isolated and their functional activity characterized in Xenopus laevis oocytes [2]. Although they differ in sensitivities to bumetanide and thiazides and have different requirements for potassium, these approximately 115-kDa proteins share about 60% sequence similarity and exhibit a topology featuring 12 potential membrane-spanning helices flanked by large hydrophilic domains at the NH2- and COOH-termini. These molecules, together with the Na-Cl cotransporter from the flounder urinary bladder, which exhibits a significant homology suggestive of common ancestry, define a new family of electroneutral Na(+)-(K+)-Cl- cotransporters. Northern blot analysis and in situ hybridization indicate that these transporters are expressed predominantly in kidney with an intrarenal distribution consistent with their recognized functional localization. The kidney-specific distribution of transcripts encoding these cotransporters suggest that other, probably related, genes encode non-renal Na(+)-(K+)-Cl- cotransporters.
In the adult CNS, GABA is the predominant inhibitory neurotransmitter, mediating the hyperpolarization of membrane potential and regulating the glutamatergic activity. In the immature CNS, on the other hand, GABA mediates depolarization and is involved in controlling morphogenesis. This developmental shift in GABA actions from depolarization to hyperpolarization occurs as a result of decreasing the intracellular chloride ion (Cl(-)) concentration ([Cl(-)](i)) which is regulated by the potassium (K(+))-Cl(-) co-transporter 2 (KCC2). To clarify the time-course of changes in the GABA actions during development, we examined the developmental localization of the KCC2 in the granule cells of the postnatal mouse cerebellum using specific antibodies against KCC2. The granule cell precursors and migrating granule cells were devoid of immunoreactivity against KCC2 antibodies. At postnatal day 3 (P3), the KCC2-immunolabeling was negative in the internal granular layer, although synaptophysin-positive mossy fiber terminals were detected. At P5, we first detected the KCC2-immunolabeling at the somata of granule cells and their dendrites before granule cells received inhibitory input from Golgi cells. Almost all KCC2-positive dendrites (more than 98%) attached to and formed synapses with mossy fiber terminals. As development proceeded, the number of KCC2-positive granule cells increased, and all granule cells became positive by P21. These results suggested that GABAergic transmission on granule cells might shift from excitation to inhibition after the synapse formation, and the excitatory synapse-formation and related factors might be the triggers for the expression and localization of the KCC2 in the granule cells. Furthermore, it was also suggested that formation of the GABAergic synapses and GABAergic transmission were not necessary for the KCC2-expression in the mouse cerebellar granule cells in vivo.
Explore the source record for details and available documents.
Explore the source record for details and available documents.