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.

Relationship between the Maximum Velocity and Sodium Affinity of the Erythrocyte Sodium Pump and its Rate Constant in Blood

1990 ◽  
Vol 79 (6) ◽  
pp. 625-630 ◽  
Author(s):  
T. H. Thomas ◽  
S. MacPhail ◽  
V. Mott ◽  
R. Wilkinson
Keyword(s):  
Rate Constant ◽  
Whole Blood ◽  
Sodium Pump ◽  
Maximum Velocity ◽  
Normal Subjects ◽  
Affinity Constant ◽  
Pump Rate ◽  
Median Error ◽  
Data Points ◽  
Erythrocyte Sodium

1. Young and mature erythrocytes from 15 normal subjects were used to compare the sodium pump rate constant measured in whole blood with the more definitive sodium affinity constant and maximum velocity of the sodium pump measured in artificial media using sodium-loaded cells. 2. Similar values were obtained from both erythrocyte fractions for the sodium affinity constant and maximum velocity and also by using two different plots. The median error in the estimate of individual sodium affinity constants and maximum velocities from regression analysis was about 20% and the precision was not improved by combining the data points for the two erythrocyte fractions. 3. The rate constant in whole blood was closely related to the sodium affinity constant and maximum velocity of the sodium pump (r = 0.75), suggesting that it was a reasonable overall assessment of available sodium pump activity. 4. Differences in the rate constant between subjects were due to differences in both the maximum velocity and sodium affinity constant of the sodium pump so that the rate constant could not be used as a guide to the underlying sodium pump physiology.

A serial study of erythrocyte sodium pump kinetics and sodium content in the puerperium

1994 ◽  
Vol 170 (2) ◽  
pp. 693-698 ◽  
Author(s):  
Lesley M. Bolton ◽  
Trevor H. Thomas ◽  
Sheila Macphail ◽  
William Dunlop
Keyword(s):  
Sodium Pump ◽  
Sodium Content ◽  
Erythrocyte Sodium

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.

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.

Erythrocyte Sodium and Potassium in Patients with Hypokalaemia

1983 ◽  
Vol 64 (2) ◽  
pp. 167-176 ◽  
Author(s):  
M. Cumberbatch ◽  
D. B. Morgan
Keyword(s):  
Potassium Concentration ◽  
Sodium Content ◽  
Potassium Content ◽  
Extracellular Potassium ◽  
Moderate Degree ◽  
Sodium Efflux ◽  
Erythrocyte Sodium ◽  
Curvilinear Relation ◽  
Sodium And Potassium

1. The erythrocyte content of sodium and of potassium were measured in 231 unselected patients with hypokalaemia, and together with net ouabain-sensitive sodium efflux in patients with severe hypokalaemia, before (20 patients) and during potassium repletion (14 patients). 2. The erythrocytes of the patients with hypokalaemia compared with control subjects had on average an increase in sodium content, a decrease in potassium content and a reduction in the rate constant of ouabain-sensitive sodium efflux. All three changes had a similar curvilinear relation to the concentration of potassium in plasma with relatively little change in the measured variable unless the plasma potassium was very low. 3. There was a similar curvilinear relation between the final sodium and potassium content of normal erythrocytes and the potassium concentration of the medium in which they were incubated for 48 h in vitro. 4. These results suggest that the changes in the sodium and potassium content of erythrocytes in hypokalaemia are due to a direct inhibiting effect of the hypokalaemia on the activity of the sodium pump. 5. In many patients with hypokalaemia of moderate degree the increase in erythrocyte sodium content was less than expected from the effect in vitro of a low extracellular potassium concentration. This finding suggests that a compensatory change, presumably an increase in the number of sodium pumps, is a common event even in moderate hypokalaemia.

The Relation between Membrane Cholesterol and Phospholipid and Sodium Efflux in Erythrocytes from Healthy Subjects and Patients with Chronic Cholestasis

1982 ◽  
Vol 62 (1) ◽  
pp. 101-107 ◽  
Author(s):  
P. A. Jackson ◽  
D. B. Morgan
Keyword(s):  
Rate Constant ◽  
Healthy Subjects ◽  
Sodium Content ◽  
Molar Ratio ◽  
Phospholipid Content ◽  
Efflux Rate ◽  
Sodium Efflux ◽  
Chronic Cholestasis ◽  
Efflux Rate Constant ◽  
Erythrocyte Sodium

1. The cholesterol and phospholipid content of the cell membrane and the efflux of sodium were measured in the erythrocytes of patients with chronic cholestasis and in healthy subjects. 2. The membranes from the patients contained more cholesterol and phospholipid and had a higher cholesterol/phospholipid molar ratio than the membranes from the healthy subjects. 3. The sodium efflux rate constant was reduced in the patients and this was entirely due to a reduction in the frusemide-sensitive efflux rate constant. There was no difference in either the ouabain-sensitive or the ouabain plus frusemide-resistant rate constants. 4. This reduction in the frusemide-sensitive rate constant was associated with a reduction in the erythrocyte sodium content. 5. When erythrocytes were loaded with cholesterol in vitro the frusemide-sensitive efflux rate constant was reduced by an amount similar to that observed in the patients. In addition, however, there was a reduction in the ouabain-sensitive efflux rate constant and an increase in the erythrocyte sodium content; neither of these changes was observed in the patients in vivo.

The Effects of Chronic Hypokalaemia, Hyponatraemia, and Acid-Base Alterations on Erythrocyte Sodium Transport

1972 ◽  
Vol 43 (2) ◽  
pp. 251-263 ◽  
Author(s):  
M. L. Levin ◽  
F. C. Rector ◽  
D. W. Seldin
Keyword(s):  
Active Transport ◽  
Sodium Concentration ◽  
Sodium Content ◽  
Acid Base ◽  
Large Component ◽  
Sodium Influx ◽  
Membrane Function ◽  
Disease States ◽  
Erythrocyte Sodium

1. Erythrocyte sodium concentration and fluxes were measured in patients with acid-base disturbances, hypokalaemia and hyponatraemia. Results were similar to those obtained with normal erythrocytes exposed to artificial in vitro alterations. 2. Erythrocyte sodium content and influx varied directly with extracellular bicarbonate which appeared to influence membrane permeability. 3. Hypokalaemia increased the erythrocyte sodium content by decreasing active transport initially. When a new high erythrocyte steady-state sodium concentration was reached, active transport returned to normal but efflux and influx were increased considerably by the appearance of a large component of exchange diffusion in the hypokalaemic environment. 4. Hyponatraemia induced a decrease in sodium influx secondary to the decreased transmembrane sodium concentration gradient. A decrease in erythrocyte sodium content then ensued. 5. The results are discussed in relation to the assessment of cell membrane function in disease states.

Increased Sodium Content and Altered Sodium Transport in Thymocytes of Spontaneously Hypertensive Rats

1981 ◽  
Vol 61 (3) ◽  
pp. 313-316 ◽  
Author(s):  
R. B. Jones ◽  
J. Patrick ◽  
P. J. Hilton
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Rate Constant ◽  
Spontaneously Hypertensive Rats ◽  
Sodium Content ◽  
Strong Positive Correlation ◽  
Hypertensive Rats ◽  
Sodium Efflux ◽  
Spontaneously Hypertensive

1. The intracellular sodium content and the sodium efflux rate constant have been determined in vitro in thymocytes derived from the Okamato-Aoki strain of spontaneously hypertensive rats. 2. A strong positive correlation between the systolic blood pressure and the sodium content of thymocytes was observed (r = 0.59, n = 39, P < 0.001). 3. The rate constant for total sodium efflux was negatively correlated with systolic blood pressure (r = −0.43, n = 45, P < 0.005) and this was due to a fall in the ouabain-sensitive component of sodium efflux. 4. Sodium efflux, influx and the thymocyte potassium content were not related to the blood pressure.

Citrate Anticoagulant Artificially Masks the Hemostatic Effect of Recombinant Factor VIIA in Dilutional Coagulopathy.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 3160-3160
Author(s):  
Christian Fenger-Eriksen ◽  
Jørgen Ingerslev ◽  
Else Tønnesen ◽  
Benny Sørensen
Keyword(s):  
Whole Blood ◽  
Ex Vivo ◽  
Case Reports ◽  
Randomised Trial ◽  
Rabbit Model ◽  
Maximum Velocity ◽  
Clot Formation ◽  
Calcium Chelation ◽  
Dilutional Coagulopathy

Abstract Introduction: Dilutional coagulopathy may develop in massively bleeding patients who are substituted with synthetic colloid plasma expanders. A series of recent studies have demonstrated that synthetic colloids may induce abnormal function of fibrinogen by compromising fibrin polymerization and substitution with a fibrinogen concentrate appeared to reverse this coagulopathy and arrest traumatic bleeds. Clinical experiences, several case reports as well as a randomised trial point toward a beneficial effect of rFVIIa in control of massive bleeding associated with hemodilution caused by excessive volume substitution. Our haemostasis center recently put forward that rFVIIa, in vitro, was unsuccessful in correction of dilutional coagulopathy induced by HES 130/04. In addition, other investigations utilising a rabbit model have indicated that colloid hemodilution may attenuate the haemostatic potential of rFVIIa. For half a Century laboratory coagulation tests have been carried out using re-calcified citrated blood. However, recent experimental work has revealed that citrate dependent calcium chelation significantly changes the dynamic course of thrombin generation, suspectedly due to interference with the enzymatic properties of coagulation factors. In addition it has been documented that citrate and calcium chelation interferes with the metabolism in platelets. In the present study we aimed at investigating the haemostatic effect of rFVIIa in a laboratory whole blood model of colloid hemodilution using citrate as well as iso-citrate stabilized blood comparing to native whole blood and whole blood stabilized with corn trypsin inhibitor (CTI) that specifically blocks factor XIIa. Materials and Methods: Following informed consent 11 healthy male volunteers with a mean age of 30 years (range 26–38 years) delivered blood for study. Dynamic whole blood coagulation profiles were recorded using thrombelastography activated with minute amounts of tissue factor in a model of ex vivo hemodilution with HES 130/0.4 in a prospective approach. Analyses were evaluated at 30% dilution level, and following ex vivo addition of rFVIIa to whole blood collected into tubes containing citrate, iso-citrate, CTI, or no stabilizer. Results: Hemodilution with HES 130/0.4 induces a coagulopathy characterized by a reduced maximum rate of clot formation and a pronounced reduction in the final clot firmness. With all test mediums investigated, rFVIIa significantly shortened the clot initiation phase. In cases of native whole blood and CTI stabilized whole blood rFVIIa shortens the clotting time but also demonstrated an acceleration of the maximum velocity of clot formation. Conclusion: When citrate or iso-citrate is used as anticoagulants in thromboelastographic clotting assays, these anticoagulants may artificially mask the haemostatic effect of rFVIIa in colloid hemodilution blood. The effect in vitro of rFVIIa in citrated blood samples may significantly underestimate the haemostatic potential of rFVIIa. In cases where the hemostatic potential of rFVIIa is tested in vitro a potentially efficacious rescue treatment may be delayed or excluded.

Non-esterified fatty acids may regulate human leucocyte sodium pump activity

1986 ◽  
Vol 71 (6) ◽  
pp. 737-742 ◽  
Author(s):  
L. L. Ng ◽  
T. D. R. Hockaday
Keyword(s):  
Fatty Acids ◽  
Rate Constant ◽  
Acid Level ◽  
Sodium Pump ◽  
Efflux Rate ◽  
Fatty Acid Level ◽  
Esterified Fatty Acids ◽  
Pump Activity ◽  
Efflux Rate Constant

1. Human leucocyte sodium pump activity was studied in normal fasting subjects by measuring the ouabain-sensitive 22Na+ efflux rate constants. 2. This 22Na+ efflux rate constant was inversely related to the fasting plasma non-esterified fatty acid level (rs = −0.73, P < 0.0001). 3. An oral glucose load (40 g/m2 surface area) led to an increase in the leucocyte ouabain-sensitive 22Na+ efflux rate constant after 2 h (1.97 ± 0.25 to 2.44 ± 0.19 h−1, P < 0.0001, n = 11). There was a concomitant fall in the plasma non-esterified fatty acid level. 4. Incubation of leucocytes in vitro with 100 μmol/l linoleic acid inhibited the leucocyte ouabain-sensitive 22Na+ efflux rate constant (1.52 ± 0.27 vs 0.84 ± 0.24 h−1, P < 0.001, n = 8). 5. The leucocyte Na+,K+-dependent adenosine triphosphatase (Na+,K+-ATPase) activity was inhibited in vitro by long chain non-esterified fatty acids, especially when unsaturated. 6. Non-esterified fatty acids may account for some of the Na+,K+-ATPase inhibitory activity of plasma.

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