The Response of the Human Leucocyte to Alterations in Extracellular Osmolality

1973 ◽  
Vol 44 (5) ◽  
pp. 457-465 ◽  
Author(s):  
J. Patrick ◽  
P. J. Hilton

1. The effect of variations in extracellular osmolality from 249 to 345 mosmol/kg upon the sodium, potassium and water content of human leucocytes has been studied. 2. Similar studies were performed using human erythrocytes. 3. Changes in the leucocyte water content were not explicable in terms of passive movement of water across an ‘ideal’ semi-permeable membrane. 4. Hypo-osmolal swelling was associated with a rise in intracellular sodium content and hyperosmolal shrinkage was associated with a fall in intracellular sodium content. 5. There were no significant changes in sodium and potassium content of the erythrocyte with altered external osmolality.

1965 ◽  
Vol 48 (3) ◽  
pp. 469-472 ◽  
Author(s):  
Genaro Palmieri ◽  
Denis Ikkos

ABSTRACT Measurements of the fat, water, sodium, potassium and chloride content of muscle were performed in biopsies obtained from nine unselected acromegalic patients. The water, sodium and chloride contents were normal, while the potassium content was significantly increased (P < 0.01) by eight per cent. These results were interpreted as showing that the intracellular sodium content of the muscle is normal in acromegaly and that there is no extracellular oedema in this disease.


1974 ◽  
Vol 46 (5) ◽  
pp. 583-590 ◽  
Author(s):  
J. Patrick ◽  
N. F. Jones

1. The leucocyte has been used as a model for the study of intracellular sodium, potassium and water in uraemia. The advantages of this cell are described. 2. In undialysed patients with advanced renal failure leucocyte sodium and water contents were significantly greater than normal. Leucocyte potassium content (mmol/kg of dry solids) and concentration (mmol/l of cell water) were reduced. 3. In patients receiving regular dialysis leucocyte water was significantly reduced. Leucocyte potassium content was also reduced in this group, but leucocyte potassium concentration in cell water had returned to normal. 4. In the normal subjects and also in the dialysed patients leucocyte water correlated better with potassium than with sodium content. In contrast, in the undialysed uraemic patients leucocyte water correlated better with sodium than with potassium content, indicating that the increased cell sodium was an important determinant of the increased cell water in this group.


1985 ◽  
Vol 69 (2) ◽  
pp. 223-226 ◽  
Author(s):  
G. A. Sagnella ◽  
D. A. Nolan ◽  
A. C. Shore ◽  
G. A. MacGregor

1. The effects of synthetic human and rat atrial peptides on sodium and potassium ion transport has been investigated in intact human erythrocytes. 2. The effects of these peptides have been tested on the active, sodium pump-dependent (ouabain-sensitive) and on the sodium-potassium cotransport system (bumetanide-sensitive) with 86Rb used as a tracer. 3. Human (α-ANP, 28 amino acids) or rat (atriopeptin III) atrial peptides, over a wide range of concentrations, did not influence the uptake of 86Rb in either the ouabain-sensitive or the bumetanide-sensitive transport system. 4. These results suggest that the natriuretic effect of the atrial peptides is not mediated through inhibition of the sodium pump or the loop-diuretic-sensitive Na-K cotransport.


1957 ◽  
Vol 189 (3) ◽  
pp. 451-454 ◽  
Author(s):  
Louis Tobian ◽  
Paul D. Redleaf

Administration of desoxycorticosterone and NaCl resulted in an increased sodium and potassium content of the aorta in rats becoming severely hypertensive. Equivocally hypertensive animals on this regimen showed smaller increases in sodium and a decrease in potassium. Sodium restriction prevented both hypertension and changes in arterial wall chemistry from occurring in rats receiving desoxycorticosterone. Hypertension per se may be fundamentally associated with an increased potassium and sodium content in artery, as experimental renal hypertension is characterized by a similar electrolyte alteration.


1958 ◽  
Vol 193 (3) ◽  
pp. 634-638 ◽  
Author(s):  
Yehia A. Habib ◽  
George C. Nichopoulos ◽  
Richard R. Overman

Following a 2-hour period of vividialysis against a potassium free fluid, the rate of loss of potassium from the blood of dogs was determined (using K42) as well as the electrolyte and water content of heart, liver and skeletal muscle. A significant increase in potassium content of cardiac muscle and in sodium content of liver was found. There was a definite decrease in the specific activity of muscle potassium as well as in the ratio of muscle to plasma specific activity. The rate of loss of blood potassium (K42 vascular slope) was diminished in animals in which an amount of potassium less than that originally present in the extracellular space was removed. The data exclude the heart, liver and skeletal muscle as the sites from which potassium removed in acute experiments was derived.


2013 ◽  
Vol 119 (1) ◽  
pp. 119-128 ◽  
Author(s):  
Brandon R. Esenther ◽  
Zhijun Ge ◽  
Fanli Meng ◽  
James E. Cottrell ◽  
Ira S. Kass

Abstract Background: Sevoflurane preconditioning improves recovery after hypoxia. Sevoflurane administered before and during hypoxia improved recovery and attenuated the changes in intracellular sodium, potassium, and adenosine triphosphate (ATP) levels during hypoxia. In this study, the authors examine the effects of sevoflurane applied only before hypoxia on sodium, potassium, and ATP. Methods: Hippocampal slices from adult male Sprague–Dawley rats were pretreated with 4% sevoflurane, washed, and then subjected to hypoxia (n ≥ 8 animals/group). The cornus ammonis 1 regions of the hippocampal slices were micro-dissected and sodium, potassium, and ATP concentrations measured. Results: Pretreatment with sevoflurane for 15 or 60 min did not attenuate the increase in intracellular sodium or the decrease in intracellular potassium during hypoxia. After 60 min of preconditioning and 5 min of hypoxia, sodium increased 57% (vs. nonpreconditioned hypoxia 54% increase) and potassium decreased 31% (vs. 26%). These changes were not statistically significant versus untreated hypoxia. The 60-min sevoflurane preconditioning group had statistically significant higher ATP levels at 5 min of hypoxia (3.8 nmol/mg dry wt.) when compared to untreated hypoxic tissue (2.1 nmol/mg). There was no significant difference in ATP levels between the sevoflurane preconditioned and the untreated tissue before hypoxia (8.9 vs. 8.5 nmoles/mg, respectively). Conclusion: Preconditioning with sevoflurane for 60 min before hypoxia does not alter changes in intracellular sodium and potassium during hypoxia but does attenuate the fall in intracellular ATP levels during hypoxia. Thus, there are differences between anesthetic preconditioning and when anesthetics are present before and during hypoxia.


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