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PubMed1989

Measurement of cation transport in vivo in healthy volunteers after the oral administration of lithium carbonate.

1. We have measured cation transport in vivo in seven healthy volunteers under control conditions and after they had taken lithium carbonate for 21 days in doses which maintained the serum lithium concentration in the range 0.6-0.8 mmol/l. 2. We have measured cation transport in vivo after the administration of an oral load of rubidium chloride, and have found that, although intra-erythrocytic concentrations of rubidium were significantly lower 1 h after the administration of rubidium when the subjects were taking lithium, there was a significant increase in the rate of uptake of rubidium into the erythrocytes over the subsequent period of the test, suggesting a direct stimulation of sodium, potassium-activated adenosine triphosphatase by lithium. 3. Lithium administration did not affect the plasma concentration versus time profile of rubidium after the rubidium load, implying that the lithium-stimulated uptake of rubidium which occurs in erythrocytes does not necessarily occur in other cell types. 4. These results suggest that previous studies of cation transport using peripheral cells and assay systems in vitro do not necessarily reflect changes in cation transport in vivo in excitable tissues.

Administration, Oral↗
PubMed1993

Effects of haemodialysis and continuous ambulatory peritoneal dialysis on abnormalities of ion transport in vivo in patients with chronic renal failure.

1. We have studied Na+/K+ pump activity in vivo in three groups of subjects: patients with chronic renal failure not receiving maintenance dialysis, patients being treated by either haemodialysis or continuous ambulatory peritoneal dialysis, and matched control subjects. 2. To do this we have measured the changes in plasma and intraerythrocytic rubidium concentrations after an oral load of rubidium chloride, having previously shown that changes in the disposition of rubidium measured in this way reflect changes in the activity of the Na+/K+ pump in vivo. 3. Erythrocyte rubidium uptake was significantly reduced both in ten patients with chronic renal failure not receiving maintenance dialysis and in 12 patients being treated by haemodialysis, when compared with 31 healthy control subjects. In contrast, erythrocyte rubidium uptake was not altered in 13 patients treated by continuous ambulatory peritoneal dialysis. There was also a significantly reduced rate constant for erythrocyte rubidium uptake in patients with undialysed chronic renal failure (0.66 h-1) and in those treated by haemodialysis (0.78 h-1), whereas in patients treated by continuous ambulatory peritoneal dialysis the rate constant for erythrocyte rubidium uptake was not significantly different from control values (1.36 h-1 and 1.41 h-1, respectively). 4. These findings are consistent with a reversal of the inhibition of erythrocyte Na+/K+ pump activity in vivo found in chronic renal failure by continuous ambulatory peritoneal dialysis, but not by haemodialysis. This difference may be due to the failure of haemodialysis to clear a circulating inhibitor of Na+, K(+)-ATPase or to the rapid re-accumulation of such an inhibitor after haemodialysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Effects of alterations in cell phenotype and hypokalemia on sodium-potassium pump activity in rabbit vascular smooth muscle.

We investigated in cell culture, how alterations in phenotype accompanying proliferation of rabbit aortic smooth muscle and chronic hypokalemia could affect the Na,K pump. Total rubidium-86 uptake as well as ouabain and frusemide-sensitive uptake into cells was measured in physiological salts solution (PSS), PSS containing 5% foetal calf serum and PSS containing foetal calf serum plus 15 microM monensin. In physiological salts solution 90% of the rubidium-86 uptake into contractile or synthetic state cells was frusemide-sensitive and less than 8% ouabain-sensitive. Total and frusemide-sensitive rubidium-86 uptakes, measured in PSS or PSS containing foetal calf serum were similar in cells cultured and maintained in the contractile phenotype, cells in the synthetic phenotype and those which had recently reverted from the synthetic to contractile phenotype. When cells were sodium loaded in the presence of monensin and foetal calf serum, ouabain-sensitive rubidium-86 uptake was 50% higher in cells which were maintained in culture in the contractile phenotype. Frusemide-sensitive rubidium-86 uptake was similar in each cell phenotype. To examine how cell culture in hypokalemic media would affect the Na,K pump, we determined ouabain-sensitive rubidium-86 uptake in the presence of monensin plus foetal calf serum in cells incubated for 24 hours in low and normal potassium containing culture media. Ouabain-sensitive uptake was 20% higher in cells cultured in a 0.76 mM potassium medium than in those cultured in 5.4 mM potassium medium. Frusemide-sensitive rubidium-86 uptake was unaffected. These results demonstrate that 'maximal' Na,K pump activity in sodium-loaded cells is reduced when cells change from the contractile to synthetic phenotype. This reduction appears only very slowly reversible when cells revert from the synthetic to contractile phenotype. Prolonged hypokalemia increases 'maximal' activity of the Na,K pump.

Animals↗
PubMed1992

[Interactions between lithium/rubidium and six muscle relaxants. A study on the rat phrenic nerve-hemidiaphragm preparation].

The cumulative concentration-response curves for alcuronium, metocurine, d-tubocurarine, suxamethonium, pancuronium and vecuronium alone or in combination with lithium or rubidium were measured using indirectly evoked twitch tension in the isolated rat phrenic nerve-hemidiaphragm preparation. In the experiments with lithium and rubidium, 10% and 2% of the sodium ions (118 mmol/l) of Krebs solution were replaced by lithium (11.8 mmol/l = 0.082 g/l) or rubidium (2.36 mmol/l = 0.202 g/l) ions, respectively. At these concentrations, neither lithium nor rubidium alone affected twitch tension. Lithium led to a statistically significant enhancement of the myoneural blocking effects of suxamethonium, pancuronium and vecuronium, but not of the other myoneural blocking drugs. Rubidium behaved similarly to lithium, except that enhancement of the effect of vecuronium was not statistically significant. At higher concentrations, lithium and rubidium alone depressed twitch tension in a dose-dependent manner. Neither myoneural blocking drugs nor lithium and rubidium affected the directly evoked twitch tension. It is concluded that myoneural blocking drugs, especially the newer ones, should be used with caution in patients receiving lithium or other alkali metal therapy as it is not known what interactions may arise.

Animals↗
PubMed1977

Ouabain-insensitive salt and water movements in duck red cells. II. Norepinephrine stimulation of sodium plus potassium cotransport.

Catecholamines induce net salt and water movements in duck red cells incubated in isotonic solutions. The rate of this response is approximately three times greater than a comparable effect observed in 400 mosmol hypertonic solutions in the absence of hormone (W.F. Schmidt and T. J. McManus. 1977 a.J. Gen. Physiol. 70:59-79. Otherwise, these two systems share a great many similarities. In both cases, net water and salt movements have a marked dependence on external cation concentrations, are sensitive to furosemide and insensitive to ouabain, and allow the substitution of rubidium for external potassium. In the presence of ouabain, but the absence of external potassium (or rubidium), a furosemide-sensitive net extrusion of sodium against a large electrochemical gradient can be demonstrated. When norepinephrine-treated cells are incubated with ouabain and sufficient external sodium, the furosemide-sensitive, unidirectional influxes of both sodium and rubidium are half- maximally saturated at similar rubidium concentrations; with saturating external rubidium, the same fluxes are half-maximal at comparable levels of external sodium. In the absence of sodium, a catecholamine-stimulated, furosemide-sensitive influx of rubidium persists. In the absence of rubidium, a similar but smaller component of sodium influx can be seen. We interpret these results in terms of a cotransport model for sodium plus potassium which is activated by hypertonicity or norepinephrine. When either ion is absent from the incubation medium, the system promotes an exchange-diffusion type of movement of the co-ion into the cells. In the absence of external potassium, net movement of potassium out of the cell leads to a coupled extrusion of sodium against its electrochemical gradient.

Animals↗
PubMed1983

Presence of a sodium-potassium chloride cotransport system in the rectal gland of Squalus acanthias.

In order to investigate whether the loop diuretic sensitive, sodium-chloride cotransport system described previously in shark rectal gland is in fact a sodium-potassium chloride cotransport system, plasma membrane vesicles were isolated from rectal glands of Squalus acanthias and sodium and rubidium uptake were measured by a rapid filtration technique. In addition, the binding of N-methylfurosemide to the membranes was investigated. Sodium uptake into the vesicles in the presence of a 170 mM KCl gradient was initially about five-fold higher than in the presence of a 170 mM KNO3 gradient. In the presence of chloride, sodium uptake was inhibited 56% by 0.4 mM bumetanide and 40% by 0.8 mM N-methylfurosemide. When potassium chloride was replaced by choline chloride or lithium chloride, sodium uptake decreased to the values observed in the presence of potassium nitrate. Replacement of potassium chloride by rubidium chloride, however, did not change sodium uptake. Initial rubidium uptake into the membrane vesicles was about 2.5-fold higher in the presence of a 170 mM NaCl gradient than in the presence of a 170 mM NaNO3 gradient. The effect of chloride was completely abolished by 0.4 mM bumetanide. Replacement of the sodium chloride gradient by a lithium chloride gradient decreased rubidium uptake by about 40%; replacement by a choline chloride gradient reduced the uptake even further. Rubidium uptake was also strongly inhibited by potassium. Sodium chloride dependence and bumetanide inhibition of rubidium flux were also found in tracer exchange experiments in the absence of salt gradients. The isolated plasma membranes bound 3[H]-N-methylfurosemide in a dose-dependent manner. In Scatchard plots, one saturable component could be detected with an apparent KD of 3.5 x 10(-6) M and a number of sites n of 104 pmol/mg protein. At 0.8 microM, N-methylfurosemide binding decreased 51% when sodium-free or low-potassium media were used. The same decrease was observed when the chloride concentration was increased from 200 to 600 mM or when 600 1 mM bumetanide or furosemide was added to the incubation medium. These studies indicate that the sodium-chloride cotransport system described previously in the rectal gland is in fact a sodium-potassium chloride cotransport system. It is postulated that this transport system plays an essential role in the secondary active chloride secretion of the rectal gland.

Animals↗
PubMed1988

Potassium efflux enhancement by cromakalim (BRL 34915) in rabbit mesenteric artery: an indirect effect independent of calcium?

Experiments have been performed in order to investigate the calcium and exposure time dependency of cromakalim (BRL 34915)-stimulated rubidium efflux in rabbit isolated mesenteric artery. Removal of calcium from the bathing medium prolonged the effects of cromakalim on rubidium efflux. Lanthanum was without effect on cromakalim-induced efflux whilst high concentrations of nifedipine were required to produce a significant inhibitory effect. Decreasing the exposure time to cromakalim, either in the presence or absence of calcium, led to a progressive loss of the response. However, significant increases in rubidium efflux rate were observed after very short exposures (15 sec) to the drug. In normal medium, exposure to cromakalim resulted in an inhibition of a second response when the drug was reapplied. Blockade by tetraethylammonium of the initial rubidium efflux response to cromakalim did not reverse the inhibition of the second response. These results suggest that the stimulation by cromakalim of rubidium efflux in rabbit isolated mesenteric artery is independent of calcium influx and requires only a short initial exposure to the drug in order to develop a response. The development and maintenance of the response after the removal of the drug suggest that cromakalim does not directly interact with the potassium channel through which rubidium efflux enhancement is observed.

Animals↗
PubMed1986

In vivo cation transport during short-term and long-term digoxin therapy.

We have studied the effects of digoxin on cation transport in vivo by measuring the changes in plasma and red cell rubidium concentrations following an oral load of rubidium chloride. In eight patients who had been taking digoxin for 7 to 10 days (mean plasma digoxin concentration 1.3 ng ml-1) the rise in plasma rubidium concentrations was enhanced and the rise in red cell rubidium concentrations was attenuated following the oral load of rubidium chloride, by comparison with the changes in well-matched controls. In contrast, the disposition of rubidium was not altered in 12 patients who had been taking digoxin for more than 3 months (mean plasma digoxin concentration 1.1 ng ml-1). These results suggest that the inhibitory effects of digoxin on cation transport are detectable in vivo during short-term therapy, but not during long-term therapy, and confirm our previous in vitro findings.

Adult↗
PubMed1984

An in vivo study of cation transport in essential hypertension.

In order to study cation transport in vivo the changes in plasma and red cell rubidium concentrations were measured following an oral load of rubidium chloride. Eight patients receiving short-term digoxin therapy, 10 patients with chronic renal failure and 22 patients with untreated essential hypertension were studied, and the findings were compared with those in healthy control subjects matched for age, sex, race, obesity index, and plasma and red cell potassium concentrations. In patients receiving short-term digoxin therapy, and in patients with chronic renal failure, the increases in plasma rubidium concentrations after the oral load of rubidium chloride were significantly enhanced and the increases in red cell rubidium concentrations were significantly attenuated. These findings are consistent with a generalized reduction in Na+, K+-ATPase activity in vivo. In contrast, in patients with untreated essential hypertension the increases in both plasma and red cell rubidium concentrations following the oral load were significantly enhanced. These data do not support the hypothesis that essential hypertension is associated with reduced Na+, K+-ATPase activity in vivo, at least in the red cell.

Adult↗
PubMed1983

[Cation flux in erythrocytes of patients with essential hypertension].

86Rubidium influx and Na--K-cotransport have been investigated in erythrocytes of mild essential hypertensives and normotensives devoid of familial hypertension. For measurement of cotransport Na-loaded/K-depleted erythrocytes were used while rubidium influx (with and without ouabain) was determined under physiological conditions. Both transport systems were linear in time, the interassay variances in a range of about 10%. The patients with essential hypertension exhibited a decreased rubidium influx compared to the normotensive controls. Ouabain-sensitive fluxes were not significantly different between the two groups, whereas ouabain-resistent rubidium influx was diminished in the group of the patients. Na--K-cotransport was also found to be decreased in essential hypertension. There was no correlation between cotransport and Rb-influx. The results indicate changes in cation fluxes in erythrocytes of essential hypertensives, the Na--K-cotransport being rather more altered than rubidium influx. It is speculated that hypertensive persons with reduced rubidium flux rates may represent a subpopulation of essential hypertension and that their high blood pressure may be additionally influenced by exogeneous factors e.g. enhanced sodium uptake.

Adult↗
PubMed1990

Progressive failure of coronary flow during reperfusion of myocardial infarction: documentation of the no reflow phenomenon with positron emission tomography.

During reperfusion of a myocardial infarct, development of microvascular occlusion may result in regional hypoperfusion ("no reflow") despite a patent infarct-related artery. This study examined the extent and time course of no reflow with use of rubidium-82 positron emission tomography. In 12 anesthetized dogs, the left anterior descending coronary artery was occluded for 90 min and then freely reperfused. Regional myocardial perfusion was imaged by serial rubidium-82 positron emission tomography during coronary occlusion and every 30 min during reperfusion. After 4 h of reperfusion, infarct size and no reflow zone were measured postmortem by triphenyltetrazolium and thioflavin staining, respectively. Perfusion defects evident on rubidium-82 images during coronary occlusion rapidly resolved during the early reflow period. However, a recurrent perfusion defect appeared after 1 to 2 h of reflow in all dogs. The severity of recurrent perfusion defects progressed with time; after 5 min of reflow, relative perfusion in the left anterior descending artery territory was 97 +/- 6% of that in the normal circumflex artery region, but perfusion decreased progressively to 68 +/- 5% after 2 h (p less than 0.05) and to 55 +/- 4% after 4 h of reperfusion (p less than 0.05 versus 2 h). As measured by radioactive tracer microspheres, endocardial blood flow decreased similarly in the postischemic left anterior descending artery region from 1.2 +/- 0.2 ml/min per g after 5 min of reflow to 0.4 +/- 0.1 ml/min per g after 3 h of reflow (p less than 0.01). Residual infarct perfusion, measured by rubidium-82 after 4 h of reflow, was related to both infarct size (r = -0.88) and the extent of the no reflow zone (r = -0.84) in the postmortem left ventricular sections. Thus, serial positron emission tomography with rubidium-82 demonstrates a progressive loss of infarct perfusion, beginning 1 to 2 h after initial restoration of blood flow despite patency of the infarct-related artery. This phenomenon is probably a manifestation of progressive microvascular occlusion within the reperfused myocardium.

Animals↗
PubMed1997

Inhibition of angiotensin-converting enzyme modulates structural and functional adaptation to loop diuretic-induced diuresis.

The roles of elevated cell sodium concentrations and the angiotensin-aldosterone system (AAS) in the structural and functional adaptation of the distal tubule and collecting duct system to a chronic increase of sodium delivery were examined using electron microprobe and quantitative morphologic/stereologic analyses. Studies were performed on rats given the loop diuretic torasemide acutely (20 min) or chronically (12 days), either alone or in combination with the angiotensin-converting enzyme (ACE) inhibitor, enalapril. In the sodium-absorbing cells of the distal tubule and cortical collecting duct-that is, in distal convoluted tubule (DCT), connecting tubule (CNT) and principal cells-an acute increase in sodium delivery caused a significant rise in intracellular sodium concentration and rubidium uptake, the latter an index of in vivo Na,K(Rb)-ATPase activity. The elevated cell sodium concentrations returned to, or close to, control values during chronic torasemide treatment. Intracellular rubidium concentrations, measured after a 30-second rubidium exposure, were not different from controls in DCT and CNT cells but were still higher in principal cells. Since, however, the distribution space for rubidium was significantly increased in chronic torasemide animals, rubidium uptake, and hence Na,K-ATPase activity, must have increased in proportion to cell volume in DCT and CNT cells, but more than proportionately in principal cells. When ACE was inhibited during chronic torasemide, the epithelial volume of DCT and cortical collecting duct (CCD) was increased mainly by lengthening and not, as was the case in rats given torasemide alone, by thickening of the tubule wall. Adaptation of the proximal tubule exclusively by lengthening was not affected by inhibition of the ACE. These data indicate that changes in cell ion composition may participate in initiating cell processes leading to adaptation of distal nephron segments to chronically increased salt delivery. Inhibition of the ACE reverses the torasemide-induced increase in apparent Na pump density in principal cells and seems to shift the relationship between hypertrophy and hyperplasia noted in DCT and CCD after chronic torasemide in favor of hyperplasia.

Aldosterone↗
PubMed1980

The effects of vanadate on the fluxes of sodium and potassium ions through the sodium pump.

1. The effects of sodium orthovanadate on the fluxes of sodium and potassium (or rubidium) ions through the sodium pump have been investigated in intact human red cells and in resealed ghosts prepared from them. Sodium-potassium exchange, potassium-potassium exchange, pump reversal, sodium-sodium exchange and uncoupled sodium efflux have each been studied.2. When intact human red cells were incubated in high-sodium media containing vanadate in low concentrations, inhibition of potassium or rubidium influx was marked only if the potassium or rubidium concentration in the medium was sufficiently high to cause nearly maximal influx in the absence of vanadate. The absence of inhibition at lower potassium or rubidium concentrations cannot be explained by supposing that the onset of inhibition by vanadate is slower in these conditions.3. Lowering the extracellular sodium concentration, or raising the vanadate concentration, decreased the minimum concentration of extracellular potassium or rubidium at which inhibition by vanadate was detected.4. Experiments on potassium influx into intact red cells treated with the ionophore A23187 showed that magnesium ions act at intracellular sites to promote inhibition by vanadate.5. Measurements of potassium efflux from intact red cells incubated in high-sodium media, with or without potassium, showed that potassium-potassium exchange was inhibited by vanadate at low concentrations whereas reversal of the pump was not.6. Measurements of sodium efflux from intact red cells or resealed ghosts incubated in high-sodium media, with or without potassium, showed that vanadate had little or no effect on sodium-sodium exchange at concentrations at which sodium-potassium exchange was markedly reduced. Much higher concentrations of vanadate did cause partial inhibition of sodium-sodium exchange.7. Experiments to determine whether vanadate in low concentrations inhibited uncoupled sodium efflux were inconclusive, but suggested that the flux was inhibited. Measurements of the ATP hydrolysis that is thought to be associated with the uncoupled sodium efflux showed that this hydrolysis was strongly inhibited.8. The different effects of vanadate on the different fluxes are discussed, and related to the way in which vanadate is thought to act on the sodium pump.

Biological Transport, Active↗
PubMed1988

Na+-K+ pump activities of high- and low-potassium sheep red cells with internal magnesium and calcium altered by A23187.

1. Sheep erythrocytes were treated with the divalent metal ionophore A23187 to alter the cellular magnesium (Mgi) and calcium (Cai) composition. Ouabain-sensitive Na+-K+ pump fluxes were measured using rubidium as a potassium congener in media where Cl- was replaced by NO3-. 2. A23187, per se, had no effect on ouabain-sensitive rubidium influx. However, lowering the concentration of cellular magnesium [( Mg]i) and increasing that of calcium [( Ca]i) decreased Na+-K+ pump flux. 3. Ouabain-sensitive rubidium influx was found to be a saturating function of [Mg]i in high-potassium (HK) red cells with a Hill coefficient of about 1.8 and an apparent half-activation constant (K0.5) of 0.46 mmol/(l original cells). In low-potassium (LK) cells, in the absence and presence of the Na+-K+ pump stimulatory L-antibody, ouabain-sensitive rubidium influx was also saturated with Mgi yielding Hill coefficients of close to 1.8 and K0.5 values of 0.20 and 0.30 mmol/(l original cells), respectively. 4. When [Ca]i was raised at constant [Mg]i ouabain-sensitive rubidium influx was inhibited at about 700 mumol/(l cells) in both HK, and in anti-L-treated LK red cells. 5. These data exclude the possibility that the Na+-K+ pump turnover, known to be different in HK red cells, and in LK red cells in the absence and presence of anti-L (Joiner & Lauf, 1978b), is based on differences in the activation by MgATP, and that Cai interacts with the Na+-K+ pump cycle differently in the two red cell cation types.

Animals↗
PubMed1984

Myocardial monovalent cation transport during the quinidine-digoxin interaction in dogs.

To study the relationship of the serum digoxin concentration to the digoxin effect on monovalent cation transport during the quinidine-digoxin interaction, we used radiolabeled rubidium to measure monovalent cation active transport in myocardial biopsy samples from dogs. In a preliminary study, we showed that quinidine did not affect rubidium uptake by myocardial samples from intact dogs. Then, we studied four groups, each consisting of 13 dogs, which received either saline, low dose digoxin, high dose digoxin, or low dose digoxin plus quinidine treatment. In these groups of dogs, the following steady state serum digoxin concentrations were achieved: saline-treated, 0 ng/ml; low dose digoxin, 1.2 +/- 0.2 ng/ml (mean +/- SD); high dose digoxin, 2.4 +/- 0.4 ng/ml; and low-dose digoxin plus quinidine treated, 2.3 +/- 1.1 ng/ml. Compared to control values, rubidium uptake was decreased by 17% in dogs treated with low dose digoxin (P less than 0.05) and by 38% in dogs treated with high dose digoxin (P less than 0.01 vs. saline-treated, P less than 0.01 vs. low dose digoxin). Although low dose digoxin plus quinidine-treated dogs had the same mean serum digoxin concentration as the high dose digoxin-treated dogs, rubidium uptake in low dose digoxin plus quinidine-treated dogs was decreased by only 17% compared to control (P less than 0.05 vs. saline-treated, (P less than 0.01 vs. high dose digoxin). During the quinidine-digoxin interaction in the intact dog, the reduction in myocardial rubidium uptake is less than expected from the increase in serum digoxin concentration.

Animals↗
PubMed1997

Increased hepatocyte permeability surface area product for 86Rb with increase in blood flow.

Liver cell recruitment (the equivalent of capillary recruitment in other organs) was explored by carrying out multiple indicator dilution experiments with labeled rubidium across the liver of the anesthetized dog under basal conditions and after bleeding with saline replacement infusion, which increases liver blood flow. A mixture of 51Cr-labeled red blood cells (a vascular reference), 22Na (which immediately equilibrates in the extracellular space, the sum of the sinusoidal plasma and Disse or interstitial spaces, the expected distribution space for labeled rubidium in the absence of cellular entry), and 86Rb was injected into the portal vein, and normalized outflow patterns, expressed as outflowing fractions of each injected tracer per milliliter versus time, were obtained. In relation to the labeled red blood cell curve, the labeled sodium curve is displaced by flow-limited distribution into the Disse or interstitial space; it is lower on the upslope, reaches a lower and delayed peak, and decays more slowly. The early part of the labeled rubidium curve lies within the labeled sodium curve; it reaches a much reduced peak, and the later return of tracer entering cells is so slow that it is obscured by recirculation. Modeling of the concentrative cellular uptake of rubidium from the Disse space provided an influx permeability surface area product for labeled rubidium. This increases with flow over the observed flow range, demonstrating that sinusoidal recruitment occurs with increase in hepatic blood flow.

Animals↗
PubMed1985

Red-cell sodium-potassium pump and sodium-lithium countertransport in human obesity. Re-evaluation of the methods and association in a Finnish population.

Specific ouabain binding, active rubidium transport and sodium-lithium countertransport were studied in erythrocytes of 55 normal weight (BMI less than 27), 10 overweight (27 less than or equal to BMI less than 32) and 27 obese (BMI greater than or equal to 32) Finnish subjects after re-examination of the methods. Intra-assay variation coefficients for these three determinations were 6 percent, 6 percent and 12 percent, respectively. When samples from the same subjects were analyzed again after one month interval no significant differences were obtained between the measurements. However, storing of the cells at +4 degrees C increased Na-K-ATPase mediated rubidium transport about 1.5-fold within one day which may partly account for the discrepancies between the previously reported results. Specific ouabain binding of the overweight group appeared to be slightly lower (13.4 percent, P less than 0.05) whereas that of the obese subjects was slightly higher (8.7 percent, P less than 0.05) in comparison with normal weight subjects. Also in active rubidium transport and sodium-lithium countertransport the values of the obese subjects were significantly higher (P less than 0.01, and P less than 0.05, respectively) than those of the normal weight subjects. Furthermore, there existed a significant correlation between active rubidium transport and body mass index (r = 0.34; P less than 0.001) and also between active rubidium transport and specific ouabain binding (r = 0.67; P less than 0.001). In spite of these differences between obese and normal weight subjects there existed considerable overlapping between the groups, and these changes cannot be used as diagnostic tools in screening persons metabolically susceptible to obesity.

Adult↗
PubMed1984

Comparison between concentrations of trace elements in normal and neoplastic human breast tissue.

Histologically normal and neoplastic human breast tissues obtained from 25 patients at the time of mastectomy were homogenized (200 mg/ml) in distilled water and 5-microliter aliquots dried on Formvar films for trace element analysis by energy-dispersive X-ray fluorescence. The elements measured were calcium, vanadium, copper, zinc, iron, chromium, manganese, nickel, selenium, molybdenum, bromine, rubidium, strontium, mercury, arsenic, and lead. In general, significantly large increases (p less than 0.001) in calcium, vanadium, copper, zinc, selenium, and rubidium were found in breast tumors, with a less significant increase (p less than 0.05) for nickel. When a comparison was made between histologically normal and neoplastic tissues from the same individual, zinc and rubidium were found to be consistently higher in the tumor, whereas calcium, copper, and vanadium levels varied from normal to high. In no instance were the tissue changes in calcium, copper, zinc, or rubidium reflected in the blood levels, which were within normal limits. The distribution of calcium, copper, and zinc in urine varied among individuals with primary tumors; however, rubidium levels tended to be consistently elevated. An attempt is being made to correlate these various differences with the extent of the primary disease at the time of surgery, the postoperative tumor-free interval, and subsequent therapy.

Breast↗