A Study In Vitro of the Sodium Pump in Fulminant Hepatic Failure

1978 ◽  
Vol 55 (4) ◽  
pp. 355-363 ◽  
Author(s):  
A. N. Alam ◽  
Lucilla Poston ◽  
S. P. Wilkinson ◽  
C. G. Golindano ◽  
R. Williams
Keyword(s):  
Fulminant Hepatic Failure ◽  
Hepatic Failure ◽  
Sodium Pump ◽  
Normal Subjects ◽  
Sodium Content ◽  
Atp Content ◽  
Efflux Rate ◽  
Sodium Efflux ◽  
Reduced Activity

1. The mechanism underlying the raised leucocyte sodium content in fulminant hepatic failure was studied by measurement of sodium fluxes, (Na+ + K+)-dependent adenosine triphosphatase activity, and leucocyte ATP content. 2. The rate constant for sodium efflux in the leucocytes was significantly reduced, and attributable to reduced activity of the enzyme (Na+ + K+)-ATPase. Leucocyte ATP content was not significantly different from that of control cells. 3. Incubation of cells from patients in the sera of normal subjects resulted in a reversal of these changes. Inhibition of the leucocyte sodium efflux rate constants and (Na+ + K+)-ATPase of normal cells was achieved by incubation in sera from patients. 4. We suggest that the raised sodium content of leucocytes in fulminant hepatic failure is attributable to a defective sodium pumping mechanism, possibly due to a circulating toxin.

Effects of Serum from Patients with Fulminant Hepatic Failure on Leucocyte Sodium Transport

1982 ◽  
Vol 63 (3) ◽  
pp. 237-242 ◽  
Author(s):  
R. B. Sewell ◽  
R. D. Hughes ◽  
Lucilla Poston ◽  
Roger Williams
Keyword(s):  
Fulminant Hepatic Failure ◽  
Sodium Transport ◽  
Hepatic Failure ◽  
Elution Profile ◽  
Sodium Efflux ◽  
Polyacrylonitrile Membrane ◽  
Normal Controls

1. Serum from patients with fulminant hepatic failure inhibits the ouabain-sensitive sodium efflux in leucocytes. A 1:100 dilution of the serum was necessary before the inhibition became undetectable. 2. Dialysates of the serum through cuprophane in vitro and polyacrylonitrile haemodialysis in vivo were inhibitory in small amounts. 3. Ultrafiltrates (<10 000 daltons) of serum were chromatographed on Sephadex G-25 and the elution profile obtained from patients with fulminant hepatic failure was both qualitatively and quantitatively different from that of normal controls. Material from peaks 3, 4, 5 and 7 in patients with fulminant hepatic failure inhibited leucocyte sodium transport. 4. The dialysate from haemodialysis with the polyacrylonitrile membrane contained most peaks, particularly peaks 4 and 5. Adsorption of serum with polymer coated charcoal in vitro largely removed peaks 5−8.

Observations on the Measurement and Regulation of the Sodium Content of Human Erythrocytes

1972 ◽  
Vol 42 (4) ◽  
pp. 447-453 ◽  
Author(s):  
E. K. M. Smith
Keyword(s):  
Linear Correlation ◽  
Sodium Pump ◽  
Potassium Concentration ◽  
Normal Subjects ◽  
Sodium Concentration ◽  
Sodium Content ◽  
Active Sodium ◽  
Sodium Efflux ◽  
Precise Control ◽  
A Cell

1. The sodium concentration within the erythrocytes of 159 subjects was found to be 7·35 ± 1·25 (SD) mmol/litre of cells. 2. In 157 normal subjects, the erythrocyte potassium concentration was 99·08 ± 5·3 (SD) mmol/litre of cells. 3. In the erythrocytes from twenty-seven normal subjects there was a striking linear correlation between the rate constant for active sodium efflux and resting sodium concentration. 4. It is concluded that these studies confirm the assumption that the resting concentration of sodium within a cell is determined by the activity of the sodium pump. What is not known is the mechanism by which this precise control is maintained.

Effect of the Calcium Antagonist Verapamil on Human Leucocyte Sodium Transport in vitro

1985 ◽  
Vol 68 (2) ◽  
pp. 239-241 ◽  
Author(s):  
H. H. Gray ◽  
L. Poston ◽  
V. E. Johnson ◽  
P. J. Hilton
Keyword(s):  
Essential Hypertension ◽  
Calcium Antagonist ◽  
Sodium Transport ◽  
Rate Constants ◽  
Sodium Pump ◽  
Efflux Rate ◽  
Sodium Efflux ◽  
Pump Activity ◽  
External Calcium

1. Sodium efflux rate constants and intracellular sodium were measured in leucocytes from healthy volunteers in the presence and absence of the calcium antagonist verapamil hydrochloride. 2. Verapamil stimulated sodium pump activity and this effect was dependent on the presence of external calcium. 3. Verapamil has been reported to reverse the abnormality of sodium transport seen in leucocytes from patients with essential hypertension and the present study demonstrates that sodium pump activity in leucocytes from control subjects is also stimulated by exposure to verapamil in vitro. This direct cellular effect appears to be due to the calcium antagonist properties of the drug.

Plasma Inhibitory Activity against Tumour Necrosis Factor in Fulminant Hepatic Failure

1996 ◽  
Vol 90 (1) ◽  
pp. 77-80 ◽  
Author(s):  
Helen M. Keane ◽  
Nick Sheron ◽  
John Goka ◽  
Robin D. Hughes ◽  
Roger Williams
Keyword(s):  
Tumour Necrosis Factor ◽  
Normal Control ◽  
Fulminant Hepatic Failure ◽  
Hepatic Failure ◽  
Tumour Necrosis ◽  
Neutralization Capacity ◽  
Control Subjects ◽  
Significant Difference ◽  
Necrosis Factor

1. Soluble tumour necrosis factor receptors released into the circulation inhibit the effects of excess tumour necrosis factor-α and represent an important protective response. 2. In this study we have measured the levels of tumour necrosis factor and soluble tumour necrosis factor receptors p55 and p75 in the plasma of 10 patients with fulminant hepatic failure and 10 healthy control subjects. The capacity of the plasmas at varying dilutions to inhibit the biological activity of 1000 pg/ml of recombinant tumour necrosis factor in a tumour necrosis factor cytotoxicity assay in vitro was also determined. 3. The mean plasma levels of tumour necrosis factor in patients with fulminant hepatic failure (48.4 ± 10.9 pg/ml) were significantly increased compared with normal control subjects (6.1 ± 1.04 pg/ml, P < 0.01). Plasma soluble tumour necrosis factor receptors p55 and p75 were also significantly elevated in patients with fulminant hepatic failure (18.16 ± 9.94 ng/ml and 16.06 ± 9.93 ng/ml respectively) when compared with normal control subjects (1.28 ± 0.24 ng/ml and 1.62 ± 0.91 ng/ml, P < 0.001). 4. Fulminant hepatic failure plasma had a much lower capacity to inhibit tumour necrosis factor bioactivity in vitro, with a statistically significant difference between the inhibitory capacity of the fulminant hepatic failure and normal plasma seen at plasma dilutions of 1:5 and 1:20 (P < 0.05). 5. The reduced tumour necrosis factor neutralization capacity observed in fulminant hepatic failure, despite the increased levels of soluble tumour necrosis factor receptors, suggests enhanced susceptibility to the potential deleterious effects of tumour necrosis factor in fulminant hepatic failure.

Leucocyte Electrolytes and Sodium Efflux Rate Constants in the Hypertension of Pre-Eclampsia

1980 ◽  
Vol 59 (s6) ◽  
pp. 199s-201s ◽  
Author(s):  
T. E. Forrester ◽  
G. A. O. Alleyne
Keyword(s):  
Blood Pressure ◽  
Rate Constant ◽  
Rate Constants ◽  
Sodium Pump ◽  
Efflux Rate ◽  
Sodium Efflux ◽  
Pump Activity

1. Leucocyte electrolytes were measured in pre-eclampsia and comparison was made with leucocytes from normal primigravidae and from the original pre-eclamptic subjects 6 months after delivery when blood pressure had returned to normal. 2. In pre-eclamptic subjects, leucocyte sodium was elevated and potassium depressed, and the rate constant for sodium efflux was depressed. 3. These changes returned to normal after delivery. 4. An increase in cellular sodium as a result of altered sodium pump activity may be the cause of hypertension in pre-eclampsia.

Effect of Zinc on Leucocyte Sodium Transport In Vitro

1978 ◽  
Vol 54 (5) ◽  
pp. 585-587 ◽  
Author(s):  
J. Patrick ◽  
J. Michael ◽  
M. N. Golden ◽  
B. E. Golden ◽  
P. J. Hilton
Keyword(s):  
Tissue Culture ◽  
Sodium Transport ◽  
Zinc Concentration ◽  
Culture Fluid ◽  
Sodium Content ◽  
Cell Water ◽  
Sodium Influx ◽  
Sodium Efflux

1. In a preparation of human leucocytes maintained in tissue culture fluid, increasing the extracellular zinc concentration leads to a significant increase in both ouabain-sensitive sodium efflux and in sodium influx. 2. Cell water and sodium content do not alter significantly with increasing extracellular zinc concentration. 3. A small increase in the ouabain-insensitive sodium efflux can be demonstrated when the external zinc concentration is raised from 0·75 μmol/l to 90 μmol/l.

Observations on the Measurement and Regulation of the Sodium Content of Rabbit Erythrocytes: Evidence for a Single Sodium Pump

1972 ◽  
Vol 50 (8) ◽  
pp. 791-797 ◽  
Author(s):  
E. K. M. Smith ◽  
D. Farrington ◽  
L. Sydiuk
Keyword(s):  
Rate Constant ◽  
Sodium Pump ◽  
Ethacrynic Acid ◽  
Sodium Content ◽  
Red Cells ◽  
Red Cell ◽  
Sodium Efflux ◽  
A Value ◽  
Active Transport Mechanism ◽  
Sodium Dependent

We have studied the cation content of rabbit erythrocytes; for a group of 40 animals red cell sodium was 9.2 ± 2.7 (S.D.) mmol/1 of cells, while potassium was 112 ± 8.6 mmol/1. Cell sodium content rose as the animals aged, but there was always a wide concentration gradient across the cell wall. This gradient was maintained by an active sodium pump, inhibited by ouabain (10−4 M) and comparable to pump I in the human red cell. The rate constant for this process in 16 rabbits was 0.313 ± 0.07 (S.D.) h−1, a value similar to that seen in man. Ethacrynic acid (10−3 M) inhibited a further component of sodium efflux, the rate constant being 0.259 ± 0.015 (S.D.) h−1. This was superficially comparable to pump II as previously described in the human; on further study, however, it was found to be sodium dependent, but able to function in the absence of adenosine triphosphate and incapable of net up-hill transport. These findings indicate that there is only one active transport mechanism in the red cells of the rabbit, which is a useful model for study in comparison to the red cells of man.

Sodium exchange and net movement in rat uteri at 25 °C

1970 ◽  
Vol 48 (9) ◽  
pp. 598-624 ◽  
Author(s):  
E. E. Daniel ◽  
Kathleen Robinson
Keyword(s):  
Diffusion Coefficient ◽  
Time Course ◽  
Sodium Content ◽  
Free Solution ◽  
Electrochemical Gradient ◽  
Efflux Rate ◽  
Fresh Tissue ◽  
Sodium Efflux ◽  
Na Efflux ◽  
Wet Weight

Sodium fluxes in fresh and Na-rich uterine horns were studied. The change in efflux rate was compared with that in a theoretical model and analyzed by a curve-peeling technique. In both fresh and Na-rich tissues, the time course of efflux could be described by the sum of three exponentials. There was also a nearly inexchangeable ('bound') fraction of labelled sodium and a fraction of unlabelled sodium. Analysis of efflux led to the following equations:[Formula: see text]for fresh tissue, and[Formula: see text]for Na-rich tissues, where Y = tissue 22Na in millimoles per kilogram. The unlabelled part of the 'bound' Na amounted to 4 to 6 mmoles/kg in fresh and 6 to 8 mmoles/kg in Na-rich tissues. The amounts of 22Na in cells were calculated to be 7 and 34 mmoles/kg wet weight in fresh and Na-rich tissues. One phase of influx was similar to the fastest fraction of efflux and had a diffusion coefficient which was consistent with diffusion in the extracellular space (1/10 of that in free solution). The sodium content of this compartment was somewhat greater than sodium in the 14C-sucrose spaces (430 and 480 ml/kg in fresh and Na-rich tissue respectively). The second fastest sodium fraction (observed during efflux) was much larger in Na-rich tissues, and evidence that it contained cellular sodium was presented. Sodium efflux from cells was 5.9 pmoles cm−2 s−1 for fresh tissues and 26 pmoles cm−2 s−1 for Na-rich tissues. Comparable but less accurate values for influx were 4.2 and 7.0 pmoles cm−2 s−1. Assuming all emerging sodium was pumped against the electrochemical gradient, the energy expenditure would be 0.11 kcal/kg per h in fresh tissue and 0.22 kcal/kg per h in Na-rich tissues. It was concluded that this kind of active transport provides an unsatisfactory explanation for 22Na efflux.

A Serial Study of Erythrocyte Sodium Content and Sodium Pump Kinetics in Pregnancy

1990 ◽  
Vol 79 (6) ◽  
pp. 631-638 ◽  
Author(s):  
S. MacPhail ◽  
T. H. Thomas ◽  
R. Wilkinson ◽  
J. M. Davison ◽  
W. Dunlop
Keyword(s):  
Rate Constant ◽  
Whole Blood ◽  
Sodium Pump ◽  
Maximum Velocity ◽  
Sodium Content ◽  
Affinity Constant ◽  
Pump Rate ◽  
Erythrocyte Sodium ◽  
Sodium Pump Inhibition

1. Normotensive primigravid pregnant women were studied longitudinally during pregnancy and 20 weeks after delivery. 2. Erythrocyte sodium content, ouabain-sensitive sodium flux and sodium pump rate constant were measured in whole blood, and the maximum velocity and sodium affinity of the sodium pump were measured in vitro. 3. Erythrocyte sodium content decreased and the sodium pump rate constant increased up to 26 weeks gestation. The increase in rate constant was due to an increase in the affinity of the sodium pump for sodium up to 20 weeks gestation. After 20 weeks gestation there was an increase in maximum velocity and a decrease in sodium affinity of the sodium pump but no further change in the sodium pump rate constant. 4. At 14 weeks gestation the sodium pump rate constant was correlated with both the maximum velocity and sodium affinity constant. After this time the relationship was much more variable and there was no correlation with the sodium affinity constant. The comparison of measurements of the sodium pump in whole blood and in vitro gave no evidence of sodium pump inhibition. 5. The erythrocyte sodium pump changed throughout gestation with different components to the change, but, overall, available sodium pump activity in blood increased and sodium content decreased.

scholarly journals Abnormal Platelet Ultrastructure in Fulminant Hepatic Failure

1977 ◽  
Author(s):  
G. Bullock ◽  
M.J. Weston ◽  
M.H. Rubin ◽  
J. Roberts ◽  
P.G. Langley ◽  
...  
Keyword(s):  
Liver Damage ◽  
Fulminant Hepatic Failure ◽  
Hepatic Failure ◽  
Platelet Rich Plasma ◽  
Recovery Period ◽  
Test Group ◽  
Normal Subjects ◽  
Clinical Disorder ◽  
Pharmacological Studies ◽  
Platelet Structure

Platelets obtained from eight patients with varying degrees of liver damage have been studied with respect to their ultrastructure. These platelets were isolated from platelet-rich plasma which had been utilised in the pharmacological studies described by Dr. Weston (previous abstract) and were compared with control platelets isolated from five normal subjects. The latter were chosen for normal bleeding times and response of their platelets to aggregation with ADP and collagen.Marked differences were seen between control platelets and those from the test group in that there was an alteration in the microtubular content and disposition. In addition, these changes were partially reversed during the recovery period suggesting that production of new normal platelets was taking place. This is one of the few conditions where platelet structure has been correlated with a clinical disorder.

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