Cell Sodium Content Research Articles

Changes in surgar transport and in electrophysiological characteristics of intestinal preparations of temperature-acclimated goldfish (Carassius auratus L.)

1. Goldfish were acclimated to temperatures of 10°C and 30°C for at least 4 weeks. 2. Fish acclimated to 10°C have longer intestines with larger mucosal folds than fish acclimated to 30°C. 3. When fish acclimated to 10°C are compared with 30°C fish, the electrical resistance of intestinal mucosa, expressed in Ωcm2 of serosal area, from 10°C-acclimated fish is higher. However when related to mucosal area, the resistance in 30°C-acclimated fish is higher. 4. Mucosal glucose application evokes a change in the transepithelial potential difference. Although this effect is smaller in the intestines of 30°C-acclimated fish, a sustained change in potential difference due to the presence of glucose is observed in both cases. 5. Transepithelial sugar transport across in vitro intestinal preparations was measured using 3-oxy-methyl-d-glucose as a substrate. At 30°C the net flux, expressed in mmol·kg wet weight−1·h−1, is larger in intestinal mucosa of 30°C-acclimated fish than in mucosa of 10°C-fish. 6. Ion content was determined in both freshly isolated muscosa and mucosa incubated for 1 h at 20°C. The sodium concentration in intestinal cells from 30°C-acclimated fish was found to be higher. 7. Oxygen consumption by intestinal mucosa was determined at 20°C in the absence and presence of ouabain. The difference in ouabain-sensitive oxygen consumption between 10°C-fish or 30°C-fish is not significant.

Red blood cell sodium content and permeability changes in hemorrhagic shock

Recent studies of cellular function have demonstrated significant alterations of cell homeostasis during hemorrhagic shock. The progressive depolarization of cell membranes demonstrated in several organs has been attributed to failure of energy-dependent active ion transport. Similar changes in intracellular electrolyte composition have been observed in the red blood cells of some patients in late hemorrhagic shock and in other severely ill patients. The ready availability of isolated cells that do not require extracellular fluid space assessment makes the red blood cell an attractive model for investigating the factors controlling ion movements across the cell wall. It has been suggested that the red blood cell ion abnormalities may represent a generalized cellular response to severe illness. Red blood cell sodium concentration was measured in 145 patients during severe hemorrhagic shock. The direction and magnitude of changes in red blood sodium concentration was correlated with the time course of the shock state. The initial decrease in sodium content was a function of the diminished red blood cell membrane permeability due to a decrease in plasma bicarbonate levels. The subsequent red blood cell sodium uptake above the normal range, not associated with an increase in sodium influx, indicated an impairment of energy-dependent active transport. The observed high sodium concentrations associated with a potassium decrease in the red blood cell appeared to be only one manifestation of a generalized defect in cellular function and composition during severe hemorrhagic shock.

Zinc concentrations in plasma and erythrocytes in digitalized patients.

Determination of zinc, sodium, potassium and magnesium in plasma and red blood cells were performed in 31 controls and 63 patients treated with digitalis. In digitalized patients sodium and zinc concentrations in red blood cells were significantly increased. The intraerythrocyte magnesium and potassium levels as well as all investigated electrolytes in plasma remained within the normal range. There was a close relationship between the increase of sodium and zinc content in red blood cells, indicating alterations in transmembrane transport mechanisms induced by digitalis therapy.

Methodological assessment of assays for red cell sodium concentration and sodium-dependent lithium efflux

Assays for red cell sodium concentration and sodium-dependent lithium efflux were studied from a methodological point of view. The technical errors for sodium concentration—based on concurrent analysis of randomized blind duplicate samples —was 2.5% and for lithium efflux 6.4%. Based on repeated measures in the same individual, the assays were stable over time and reproducible; individual differences at a mean interval of 16 days were not significantly different. A wait of two hours from time of phlebotomy to analysis yielded a slight (3.8%) but significant fall in the sodium concentration; no further change was found at four hours. No change occurred in the lithium efflux over time. A standardized breakfast containing 664 mg sodium did not affect the measurements when fasting and three-hour postprandial levels were compared. The ratios of intra- to inter-individual variances were small—0.04 for red cell sodium concentration and 0.09 for sodium-stimulated lithium efflux. These assays appear to be reproducible and stable and can be applied in large scale field trials.

Red blood cell sodium and potassium after hydrochlorothiazide

In six of seven healthy males 6 days of hydrochlorothiazide (HCT), 50 mg twice daily, without potassium supplements resulted in a rise in red blood cell (RBC) sodium concentration. Serum potassium concentration fell in all subjects. Four days after discontinuing HCT, intracellular sodium and extracellular potassium concentrations had normalized. Throughout the evaluation period the course of mean relative intracellular sodium was almost a mirror image of mean relative extracellular potassium. Thus, either the decline of serum potassium or of HCT (because of its inhibitory effect on Na-K-ATPase activity) might have diminished Na-K-ATPase-dependent active RBC sodium efflux with a resultant rise in erythrocyte sodium concentration. RBC potassium and serum sodium concentrations were not affected by short-term exposure to HCT.

Defective genetic control of sodium-pump density in manic depressive psychosis.

SynopsisThe ability of lymphocytes from manic-depressive and normal subjects to produce new pump sites in response to increased cell sodium was compared in a series of experiments. Ethacrynate or different potassium concentrations were used to increase cell sodium concentration. The lymphocytes of manic depressives had a significantly reduced ability to produce new pump sites. It is suggested that this may be the genetic defect underlying manic depressive psychosis.

Pituitary resistance to thyroid hormone in cystinosis.

Eleven children with nephropathic cystinosis without clinical features of hyperthyroidism or hypothyroidism had elevated serum levels of immunoreactive TSH. The mean TSH level (+/- SE) was 37.4 +/- 12.3 microM/ml. Serial determinations of thyroid function during 1 yr were: mean (+/- SE) serum T4, 10.8 +/- 0.7 microgram/dl; free T4, 2.1 +/- 0.2 ng/dl; and T3, 239 +/- 6 ng/dl. After 500 microgram TRH iv, the peak TSH level exceeded 100 microU/ml in 6 of 10 patients, whereas T3 responses were variable. Studies of parameters influenced by thyroid hormone, including red cell sodium content, serum cholesterol, and 24-h urinary hydroxylysine excretion, were consistent with euthyroidism. On the other hand, the mean pulse wave arrival time was significantly reduced, consistent with hyperthyroidism. Three control patients, 2 with Lowe's syndrome and 1 with benign cystinosis, had normal thyroid studies. Eight of the patients were given either exogenous L-T4 or T3 in doses which were increased at weekly intervals. The serum TSH concentrations were suppressed to normal only after elevation of serum levels of thyroid hormones and with high exogenous thyroid replacement doses. The data suggest abnormal pituitary resistance to feedback by thyroid hormone in patients with cystinosis. We believe this to be the first description of the association of a heritable metabolic disease with such pituitary resistance.

Parathyroid hormone stimulates bone resorption via a Na-Ca exchange mechanism.

Parathyroid hormone (PTH) stimulates the release of calcium from bone and is thought to initiate its action by a direct effect on the plasma membrane of bone cells. Although specific membrane receptors for PTH have not yet been identified in bone, they have been characterized in kidney, and PTH does stimulate production of cyclic AMP in bone. However, the mechanism by which PTH causes the release of Ca from bone is not understood. We have determined that several agents that alter ion transport across biological membranes inhibit PTH-stimulated bone resorption in vitro. These agents include ouabain, veratridine and certain monovalent cation ionophores, which transport monovalent cations selectively. The inhibition of bone resorption is dose dependent and reversible within the first 24 h of treatment. All these compounds would be expected to increase intracellular sodium concentration in bone cells. Also, we find that decreasing the extracellular Na+ concentration prevents PTH-stimulated resorption. Therefore, we propose that PTH acts on bone to stimulate Ca release by means of a Na-Ca exchange mechanism. Decreasing the Na gradient across the bone cell plasma membrane would prevent the Na-Ca exchange and thus inhibit the physiological response to PTH.

Red cell sodium and potassium contents in liver cirrhosis

Red cell sodium and potassium contents were investigated in 57 patients with histologically proven liver cirrhosis and were compared with 13 controls without clinical evidence of liver disease. Patients with normal serum electrolytes (and without digoxin treatment) had normal red cell sodium content indicating no influence of the cirrhosis per se on the sodium-potassium pump or membrane permeability for sodium. Red cell potassium content was elevated, possibly as a consequence of subclinical hemolysis and a relatively young cell population. Hypokalemia was correlated to increased red cell sodium. Hyponatremia was correlated to low red cell sodium indicating reduced influx due to a decreased concentration gradient. According to the concept of the “sick cell syndrome,” membrane failure and cellular gain of sodium and loss of potassium can lead to hyponatremia. Our findings of normal or low red cell sodium contents provide evidence against this mechanism as explanation for the often severe hyponatremia in terminal liver failure. The abnormalities found in the red cells could be attributed to secondary complications to the cirrhosis.

Abnormal cation composition and transport in erythrocytes from hypertensive patients.

Red cell sodium and potassium were determined in 100 untreated subjects with uncomplicated essential hypertension and compared with the values from 908 healthy normotensive control subjects. Red cell sodium concentration (expressed as mmol/l of erythrocytes) was significantly higher in hypertensive than in normotensive subjects. Red cell potassium concentration (in mmol/l of erythrocytes) was not significantly different in the two groups. Passive efflux of red cell potassium into buffered isotonic sucrose solution determined in eight hypertensive and nine normotensive subjects showed a lower potassium efflux rate in the hypertensive subjects. Comparison of active sodium efflux in sixteen hypertensive and fourteen normotensive subjects showed that ouabain-sensitive active sodium efflux was higher in red cells of normotensive than in those of hypertensive subjects.

Distribution of non-electrolytes in halobacterium cells I. Halobacterium marismortui

Halobacterium marismortui is an obligatorily halophilic species isolated from the Dead Sea. When inulin, fructose or glycerol are added to suspensions of bacteria, the amounts of these substances recovered from centrifuges pellets are more than could have been present in the extracellular space. Thus a certain amount becomes associated with the bacteria, though not enough to equilibrate with all the cell water. The inulin or fructose concentration found after uptake of these substances was correlated with the cell sodium concentration. It is argued that inulin, fructose or glycerol is unlikely to be adsorbed on the outside of the bacteria and more probably crosses the plasma membrane. A possible scheme for explaining the data is presented.

Effect of chronic administration of aldosterone on bile secretion, on liver cytochrome P-450, and on red blood cell sodium content.

Male adult albino rabbits received, during a period of two weeks, a daily subcutaneous injection of aldosterone, 150 micrograms/kg body weight. Twenty-four hr after the last injection, bile was collected during two hr under anaestheia, then the liver was removed and submitted to cytochrome P-450 measurements and microscopic analyses. Red blood cell sodium content was measured before and after aldosterone treatment. In animals treated with aldosterone, compared with controls, we found: (1) a significant diminution (p less than 0.01) of bile flow rate, of sodium biliary excretion and of biliary bile acid output; (2) a significant increase (p less than 0.001) of liver cytochrome P-450; (3) hyaline modifications of hepatocytes without necrosis or steatosis; (4) a proliferation of liver smooth endoplasmic reticulum; (5) an increase (p less than 0.001) of red blood cell sodium content.

A simple technique for the measurement of ouabain-sensitive sodium transport in red cells

A new, simple and non-radioactive technique is described for the measurement of ouabain-sensitive sodium transport in red cells, which is an alternative to the more complex standard technique using radioactive sodium. The new technique is based on the observation that when excess ouabain is added to blood, the sodium content of the red cells rises, due to complete inhibition of ouabain-sensitive sodium efflux while influx remains unchanged. The rate of increase of red cell sodium is therefore a measure of ouabain-sensitive sodium efflux ( Einos). This estimate of Eos, when expressed as a fraction of the original red cell sodium concentration, gives a measure of the ouabain-sensitive, efflux rate constant (ERC os). In healthy persons, ERC os obtained with this new technique agrees closely with that obtained with the standard radioactive technique. In hypokalaemic patients the ERC os estimated by the new technique was less than that obtained with the standard technique, but this difference disappeared as the patients became normokalaemic. We suggest that this difference arises because the new technique measures only net ouabain-sensitive sodium transport whereas the standard technique also measures the ouabain-sensitive Na : Na exchange which is present in patients with hypokalaemia.

Effect of zinc on leucocyte sodium transport in vitro.

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 mumol/l to 90 mumol/l.

Red cell sodium concentration as an indicator of cellular injury in clinical shock.

Red cell sodium concentration has been found to be elevated in shock. The significance of this change relative to survival and the possible sources for this increase were examined. Twenty patients in shock had red cell sodium levels compared to shock-related variables and to conditions known to increase red cell sodium levels in vitro. There was no difference noted in red cell sodium elevations between survivors and nonsurvivors. There was a highly significant correlation with transfusions of banked blood and a significant correlation with the administration of digitalis. There was no correlation with the type, duration, or severity of shock. Changes in the sodium gradients across red cell membranes in clinical shock are not good indicators of the general cellular injury of shock.

The effect of mild hyperventilation on red cell sodium.

Control subjects voluntarily overbreathed to produce end-tidal PCO2 levels similar to those found in patients suffering from neurotic or endogenous non-retarded depression. Red cell sodium content was found to decrease during overbreathing in all the subjects. The changes were similar to those usually reported for depressed patients. The results imply that red cell sodium levels are in part dependent on respiratory behaviour. They suggest a need for considerable caution in interpreting red cell sodium values from psychiatric patients.

Age and sex differences of sodium and potassium concentration in red blood cells

Age and sex differences of sodium and potassium concentration in red blood cells

ABNORMAL LEUCOCYTE COMPOSITION AND SODIUM TRANSPORT IN ESSENTIAL HYPERTENSION

Cation transport and electrolyte composition were studied in leucocytes from 17 patients with uncomplicated essential hypertension. Significant increases in cell sodium and water contents, associated with a depression of the rate-constant for active sodium efflux, were found in the hypertensive patients. These abnormalities in cell sodium transport may possibly be related to mechanisms of hypertension.

Hereditary Stomatocytosis With Hemolytic Anemia in the Dog

Abstract An autosomal recessive mutant (symbol, dan) in the dog causes chondrodysplastic dwarfism and mild anemia as pleiotropic effects. The anemia is characterized by stomatocytosis, macrocytosis, low MCHC, increased osmotic fragility, shortened red cell survival, reticulocytosis, erythroid hyperplasia, and increased iron turnover. Minor changes can be detected in the red cells of heterozygous carriers of the dan gene, but red cell survival is normal and chondrodysplasia is not present. Red cell sodium concentration and water content are increased in anemic dogs and to a lesser degree in carriers. Glutathione deficiency is present. The disorder described here resembles a number of human hemolytic anemias with stomatocytosis, glutathione deficiency, and disordered red cell cation and water content, and further study of the dan mutant, together with investigations of the hereditary human conditions, will elucidate the maintenance of normal red cell cation balance.

A new method for the determination of sodium and potassium in human red blood cells, using indocyanine green as a marker for trapped plasma

A new method for the determination of trapped plasma in packed red cells, using Indocyanine green as a marker, is described. The method was applied to measure sodium and potassium content in human red blood cells. The means of the three parameters studied, calculated from duplicate determinations on 39 normal subjects, are included in the following ranges with a confidence coefficient of 95%: Trapped plasma % = 7.10 ± 2.47; Na + mequiv/10 13 cells = 7.45 ± 3.72; K + mequiv/10 13 cells = 91.15 ± 22.41. Statistical evaluation of the data confirmed the reliability of the method. The results were reproducible and agree well with those obtained by other authors who used radioactive markers. Furthermore the new technique is cheap and requires a short time to set up.