1973
DOI: 10.1093/bja/45.9.976
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Hyponatraemia and Sick Cells

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Cited by 113 publications
(53 citation statements)
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“…We believe that our data support either (1) movement of water from the ECF into a hyperosmolal gut lumen, or (2) accumulation or generation of solutes within cells, as likely causes of the observed postprandial hyperosmolality and hypernatraemia. There need be no alterations in cell membrane permeability to account for our observations; hence there would not be a redistribution of normally constrained intracellular osmoles, such as organic phosphate (Flear & Singh 1973), and indeed this did not alter in our experiments (see Table 1). Percentage plasma water content, measured by refractometry, also did not change, probably because of a fall in plasma volume as well as water content after food.…”
Section: Discussionmentioning
confidence: 67%
“…We believe that our data support either (1) movement of water from the ECF into a hyperosmolal gut lumen, or (2) accumulation or generation of solutes within cells, as likely causes of the observed postprandial hyperosmolality and hypernatraemia. There need be no alterations in cell membrane permeability to account for our observations; hence there would not be a redistribution of normally constrained intracellular osmoles, such as organic phosphate (Flear & Singh 1973), and indeed this did not alter in our experiments (see Table 1). Percentage plasma water content, measured by refractometry, also did not change, probably because of a fall in plasma volume as well as water content after food.…”
Section: Discussionmentioning
confidence: 67%
“…The increased presence of certain cytokines (interleukine-1b and tumour necrosis factor-a) was found to be inversely correlated with the amount of FFM in patients with rheumatoid arthritis (Roubenoff & Rall, 1993) and the authors suggested that rheumatoid cachexia is at least partly driven by in¯ammation. Flear & Singh (1973) suggested that cell membrane function may be changed by disease, which may causē uid shifts. The pathogenesis of tissue injury in IBD involves an imbalance between increased reactive oxidative compounds production and reduced antioxidant defences, resulting in oxidative stress (Grisham, 1994;Lih-Brody et al, 1996).…”
Section: Discussionmentioning
confidence: 99%
“…The acute loss of solute, according to Flear,9. IO is categorized by a larger than normal osmolal gap, obtained by subtracting the calculated plasma osmolality from the measured plasma osmolality.…”
Section: Discussionmentioning
confidence: 99%
“…Suggested mechanisms include inappropriate secretion of ADH and potassium depletion, S-8 while Flear 9 • 10 has postulated a 'sick cell' syndrome in which damaged cell membranes allow the escape of unidentified organic solutes which are normally confined to the cell.…”
Section: Adh Secretionmentioning
confidence: 99%