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Results for “Intracellular Fluid”

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PubMed1989

[The effect of sodium levels in dialysis solutions on the distribution of total body water during hemodialysis].

Thirty-seven haemodialyses with ultrafiltration were performed (3000 ml/6 hours). using three sodium concentrations (140, 145 and 150 mmol/l) in the dialysate solution in 16 hyperhydrated patients during a long-term dialysis program. The amount of eliminated sodium during haemodialysis depended on the sodium concentration in the dialysate solution. The reduction of the volume of total body water corresponded to ultrafiltration. When a sodium concentration of 150 mmol/l in the dialysate solution was used, the smallest diminution of extracellular fluid and greatest diminution of intracellular fluid was observed. At the same time the greatest transport of water from the intracellular into the extracellular fluid was recorded. A sodium concentration of 145 and 150 mmol/l in the dialysate solution gave rise to positive values of sodium-free water and of sodium-free water clearance. Sodium-free water and of sodium-free water clearance correlated directly with the sodium concentration in the dialysate solution and inversely with the amount of eliminated sodium. The patients were free from complaints during haemodialyses and no significant blood pressure changes were found. The dialysate solution with the sodium concentrations used is suitable for a long-term dialysis programme; the authors recommend, however, to use individual sodium concentrations, depending on the patient's clinical condition.

Adult↗

PubMed2000

Effect of dialysate sodium concentration on interdialytic increase of potassium.

To evaluate the role of plasma tonicity in the postdialysis increment of plasma potassium (p[K(+)]), the outcome of two hemodiafiltration treatments that differed only in the Na(+) level in dialysate (Na(D))-143 mmol/L (high dialysate sodium concentration [H-Na(D)]) and 138 mmol/L (low dialysate sodium concentration [L-Na(D)])-were compared in the same group of uremic patients from the end of treatment (T0) to the subsequent 30 to 120 min and up to 68 h. Kt/V and intradialytic K(+) removal were comparable. At T0, plasma [Na(+)] was 145+/-1 and 137+/-1 mmol/L after H-Na(D) and L-Na(D), respectively (P<0.001). The difference in plasma tonicity persisted from T0 to T68 h. At T120, p[K(+)] was increased from the T0 value of 3.7+/-0.2 to 4.7+/-0.2 mmol/L (P<0.05) after H-Na(D), whereas it was unchanged after L-Na(D). The change of p[K(+)] was still different after 68 h (+76+/-10% and +50+/-7% in H-Na(D) and L-Na(D), respectively; P<0.05). Of note, in the first 2 h after the end of treatment, bioimpedance analysis revealed only in H-Na(D) a significant 11+/-3% decrement of phase angle that is compatible with a decrease of intracellular fluid volume at the expense of the extracellular volume. Similarly, within the same time frame, in H-Na(D), a significant reduction of mean corpuscular volume of red cells, associated with a 2 +/-1% decrease of the intracellular [K(+)], was observed. In contrast, mean corpuscular volume of red cells did not change and erythrocyte [K(+)] increased by 6+/-1% after L-Na(D) (P<0.005 versus H-Na(D)). Thus, hypertonicity significantly contributes to the increase of p[K(+)] throughout the whole interdialytic period by determining intracellular fluid volume/extracellular volume redistribution of water and K(+).

Adult↗

PubMed2003

GABAergic modulation of the ANG II-induced drinking response in the rat medial preoptic nucleus.

The present study was designed to examine the participation of gamma-aminobutyric acid (GABA) receptor mechanisms in the medial preoptic nucleus (MPO) in the drinking response caused by angiotensin II (ANG II) activation of the subfornical organ (SFO) in the awake rat. Local administration of ANG II (5 pmol, 50 nl) into the SFO elicited drinking. The water intake induced was significantly attenuated by previous injections (50 nl) into the MPO of the GABA(A) agonist muscimol (0.5, 5 and 50 pmol), but not by the GABA(B) agonist baclofen (0.5, 5 and 50 pmol) or vehicle, into the MPO. On the other hand, the ANG II-induced water intake was significantly enhanced by previous injections (50 nl) into the MPO of the GABA(A) antagonist bicuculline (0.5 and 5 pmol), but not the GABA(B) antagonist phaclofen (0.05, 0.5 and 5 pmol). Muscimol (50 nmol) injected into the MPO significantly reduced the water intake elicited by intracellular fluid depletion (i.e., hypertonic saline: 2 M, 2 ml/kg bw ip), whereas bicuculline (5 pmol) was without effect. These results show the involvement of the GABAergic system within the MPO in the dipsogenic responses induced by ANG II acting at the SFO and intracellular fluid depletion, and suggest that the system may serve to attenuate the ANG II-induced dipsogenic response through GABA(A) receptors.

Angiotensin II↗

PubMed1979

Influence of epinephrine and propranolol on transmembrane K transfer in anuric dogs with hyperkalemia.

In anuric dogs K loaded by infusion of 2 mEq of KCl per kg per hr the quantity of K transferred to intracellular fluid in ureter-ligated animals is considerably less than in nephrectomized ones; the combination of ureter ligation and hyperkalemia seems to suppress transmembrane K transfer. In the present investigation we found that treatment of K loaded ureter-ligated dogs with epinephrine markedly increased the animals' ability to transfer K to intracellular fluid, and that administration of propranolol (with and without epinephrine) reduced K transfer capacity below the control level. Further, we found that propranolol treatment of K-loaded nephrectomized dogs produced a striking diminution of K transfer ability. The data suggest that beta adrenergic receptors are importantly involved in the transmembrane K transfer of K-loaded anuric dogs, and that ureter ligation and hyperkalemia suppress K transfer capacity by blocking beta receptors.

Animals↗

PubMed1988

Effects of diltiazem on isoproterenol- or Ca-induced ventricular myocardial cell injuries in isolated perfused rabbit heart: an electron microscopic study.

The ultrastructural changes of isoproterenol- and those of Ca-induced ventricular cell injuries were compared in rabbits and the effect of diltiazem on these injuries was studied by electron microscopy. In comparison with the controls, the isoproterenol-treated (Group A), the Ca-treated (Group B), and the diltiazem-posttreated (Groups E and F) showed severe myocardial cell damage, such as sarcolemmal disruption, mitochondrial swelling, intramitochondrial electron-dense granules, membranous structures along mitochondrial cristae, thickening or close packing of the Z-lines, separation of cell junctions, frayed myofibrils, clumping of chromatin, and intracellular fluid accumulation. These ultrastructural changes were more pronounced in the Ca-treated (Groups B and F) than in the isoproterenol-treated (Groups A and E) animals. In contrast, the diltiazem-pretreated groups (Groups C and D) showed relatively intact myocardial ultrastructure. However, intramitochondrial electron-dense granules could be frequently found, and particularly the diltiazem-pretreated and Ca-treated group (Group D) showed intracellular fluid accumulation. The results of this study could suggest the following: 1) isoproterenol-induced myocardial cell damage is similar to Ca overload, 2) pretreatment with diltiazem could reduce the deleterious effects of isoproterenol-induced myocardial cell damage, but it could not prevent the effects of Ca overload completely, and 3) posttreatment with diltiazem could not provide any beneficial effect either on the isoproterenol-induced or on the Ca-overloaded myocardial cell damage, and 4) the beneficial effects of diltiazem are probably derived from the enhanced buffering function of mitochondria to cytosolic Ca or from selective inhibition of transsarcolemmal Ca influx.

Animals↗

PubMed1994

Physiological basis of the low calcium response in Yersinia pestis.

It is established that duplication in vitro of that amount of Ca2+ (2.5 mM) and Mg2+ (1.5 mM) present in blood permits vegetative growth of Yersinia pestis with repression of virulence factors encoded by the Lcr plasmid (Lcr+); similar simulation of intracellular fluid (no Ca2+ and 20 mM Mg2+) promotes bacteriostasis with induction of these virulence determinants. However, proliferation of yersiniae in mice occurs primarily within necrotic focal lesions (supplied by Ca(2+)-deficient host cell cytoplasm) within visceral organs rather than in Ca(2+)-sufficient blood. The present study addressed this enigma by defining conditions necessary for achieving vegetative growth of Lcr+ yersiniae at 37 degrees C in simulated intracellular fluid. Maximum optical densities were increased by substitution of K+ for Na+ and elimination of Cl-; the combination of Na+ plus L-glutamate was selectively toxic to Lcr+ cells. This phenomenon was attributed in part to the absence of aspartase in Y. pestis (a lesion known to facilitate massive accumulation of L-aspartate via transamination of the oxalacetate pool by L-glutamate). Replacement of L-glutamate by exogenous L-aspartate or alpha-ketoglutarate reversed this toxicity by favoring retention of oxalacetate. Proliferation of Lcr+ cells in a medium containing K+ and L-aspartate but lacking added Ca2+ and Na+ was markedly enhanced by increasing the concentration of fermentable carbohydrate. Accordingly, in the worst-case scenario (i.e., added Na+, Cl-, and L-glutamate), Lcr+ yersiniae underwent restriction of growth after one doubling, and in the best-case scenario (i.e., added K+ and L-aspartate), the organisms completed more than five doublings, thereby achieving full-scale growth. Both of these Ca(2+)-deficient media promoted maximum induction of Mg(2+)-induced V antigen, a virulence factor encoded by the Lcr plasmid.

Antigens, Bacterial↗

PubMed2002

Sodium and body fluid homeostasis in profiling hemodialysis treatment.

Acute adverse side-effects of hemodialysis such as hypotension, muscle cramps, osmotic imbalance and thirst are induced by the interference with fluid and electrolyte balance occurring during treatment. Changes in osmolarity due to alterations of plasma sodium concentration during hemodialysis strongly influence fluid distribution between extracellular and intracellular fluid volume. Increased sodium dialysate concentration induces fluid shift from the intracellular to the extracellular compartment. This shift leads to a more efficient ultrafiltration by increasing plasma refilling volume but also to an increased thirst. Treatment of hypotension, cramps and nausea with hypertonic saline solution leads also to a considerable retention of sodium. Profiling hemodialysis consists in deliberately changing ultrafiltration and dialysate. sodium in order to combine an efficient ultrafiltration with a balanced sodium handling and to prevent side-effects during treatment. Continuous measurement and control of blood volume seems to be the best method to prevent hypotensive episodes. Profiling of sodium should not be the cause of a positive sodium balance. The clinical benefits of sodium profiling to the patients have still to be proven.

Biological Transport↗

PubMed1982

Insulin and beta receptor modulation of K homeostasis in nephrectomized dogs with hyperkalemia.

In nephrectomized dogs infused with 2 mEq KCl/kg/hr a homeostatic mechanism retards the development of hyperkalemia by transferring about 70% of the K load to intracellular fluid. beta Adrenergic receptor activity is importantly involved in the transfer process; halting it with propranolol reduces the proportion transferred to less than 35%. The addition of pancreatectomy increases the involvement of beta receptor activity; propranolol treatment now reduces the proportion transferred to less than 20%. Insulin treatment, on the other hand, not only improves transfer of a K load, it also alters the response to propranolol. Nephrectomized dogs treated with 2 U insulin/kg/hr deposit some 80% of the infused K in intracellular fluid. After beta receptor blockade, nearly 90% is transferred. The results suggest that in the K homeostatic mechanism of nephrectomized dogs, insulin and beta receptors may be reciprocally related. K transfer mediated by beta receptors improves after pancreatectomy, and insulin mediated K transfer improves after beta receptors are inactivated.

Aldosterone↗

PubMed1984

Calcium out of control.

The accumulation of calcium during myocardial hypoxia or ischaemia followed by reoxygenation or reperfusion is related to the development of cell necrosis and may be an important causal mechanism. Influx of calcium is a late event during hypoxia but occurs abruptly on reoxygenation or reperfusion. On reoxygenation calcium influx is not altered by nifedipine or quiescence but can be prevented by nickel (3 mM), cyanide (5 mM) or FCCP (10(-6) M). The extracellular marker 51Cr-EDTA does not enter the intracellular fluid on reoxygenation but can when the cell membrane is disrupted by a detergent, Brij'35, or the calcium paradox. The results suggest that the uptake of calcium on reoxygenation or reperfusion is related to the reintroduction of oxygen and caused by an increased calcium influx down the concentration gradient. The flux is not through the slow calcium channel and is not due to disruption of the membrane. The effects of CN- and FCCP and the unaltered calcium efflux suggest that the major part of the calcium uptake is stored in intracellular compartments and is not located in the intracellular fluid.

Animals↗

PubMed1981

Effects of methandienone on the performance and body composition of men undergoing athletic training.

1. In a previous study of the effects of methandienone (Dianabol) on men undergoing athletic training, strength and performance increased, but not significantly more when the subjects were taking the drug than when they were taking placebo. The subjects did, however, gain more weight on the drug, with increases in total body potassium and muscle dimensions. It remained an open question whether the muscles had gained normal tissue or intracellular fluid. 2. In an attempt to distinguish between these possibilities the trial has been repeated, using as subjects seven male weight-lifters in regular training, and including measurements of total body nitrogen. As before, a dose of 100 mg of methandienone/day was given alternately with the placebo in a double-blind crossover experiment. The treatment periods lasted 6 weeks and were separated by an interval of 6 weeks. Body weight, potassium and nitrogen, muscle size, and leg performance and strength increased significantly during training on the drug, but not during the placebo period. 3. The finding of increased body nitrogen suggested that the weight gain was not only intracellular fluid. The increases in body potassium (436 +/- SEM 41 mmol) and nitrogen (255 +/- 69 g) were too large in proportion to the weight gain (2.3 +/- 0.4 kg) for this to be attributed to gain of normal muscle or other lean tissue, and imply gain of nitrogen-rich, phosphate-poor substance. Although this action of methandienone might be described as anabolic, the weight gain produced is not normal muscle.

Adult↗

PubMed1976

Inhibition of transmembrane K transfer in ureter-ligated dogs infused with KCl.

In anuric dogs loaded with K by infusion with 2 meq KCl/kg per h until prelethal hyperkalemic cardiotoxicity appears, the extent of transmembrane K transfer depends on the origin of the anuria. Animals with bilateral ureter ligation transfer a mean of 1.2 meq/kg to intracellular fluid, while those with bilateral nephrectomy transfer more than 2.5 times as much (3.1 meq/kg). Further, if dogs with functioning kidneys are ureter ligated or nephrectomized after approximately 45 min of K loading, K transfer ultimately falls as infusion continues. The fall is precipitate and over 90% in ligated animals; but it is gradual, and only 10% in those that are nephrectomized. Finally, K transfer, because of the absence of insulin, is negligible in K-loaded pancreatectomized dogs with bilateral ureter ligation, but fairly substantial in pancreatectomized animals with bilateral nephrectomy. The data suggest that ureter ligation and hyperkalemia activate a renal mechanism that interferes with the transfer of infused K to intracellular fluid. The mechanism may involve the renin-angiotensin II-aldosterone system to a limited degree.

Animals↗

PubMed2001

Physiological consequences of oxygen-dependent chloride binding to hemoglobin.

The PO(2)-dependent binding of chloride to Hb decreases the Cl(-) concentration of the red blood cell (RBC) intracellular fluid in venous blood to approximately 1-3 mmol/l less than that in arterial blood. This change is physiologically important because 1) Cl(-) is a negative heterotropic allosteric effector of Hb that competes for binding sites with 2,3-bisphosphoglycerate and CO(2) and decreases oxyhemoglobin affinity in several species; 2) it may help reconcile several longstanding problems with measured values of the Donnan ratios for Cl(-), HCO, and H(+) across the RBC membrane that are used to calculate total CO(2) carriage, ion flux rates, and membrane potentials; 3) it is a factor in the change in the dissociation constant for the combined nonvolatile weak acids of Hb associated with the Haldane effect; and 4) it diminishes the decrease in strong ion difference in the RBC intracellular fluid that would otherwise occur from the chloride shift and prevent the known increase of HCO concentration in that compartment.

Arteries↗

PubMed1981

Transmembrane K transfer in hyperkalemic dogs.

In a dog K loaded by infusion of 2 mEq KCl/kg/hr, kaluresis plays a relatively small part in slowing the development of hyperkalemia and cardiotoxicity. These are largely retarded by a non-renal mechanism that transfer most of the infused K from extracellular to intracellular fluid. Treatment with beta receptor blocking dosages of propranolol significantly reduces K transfer capacity, but it also markedly diminishes the KCl stimulated secretory response of insulin, a powerful mediator of K transfer. In dogs in which diminution of the insulin response is prevented by administration of exogenous hormone, beta receptor blockade has no effect on K transfer capacity. Thus, it appears that decreased insulin secretion is responsible for the observed fall of K transfer capacity in dogs with beta receptor blockade. However, other evidence suggests that our results can also mean that a K load elicits the secretion of enough insulin to mediate K transfer in the presence of beta receptor blockade; if the hormone response is absent or deficient, beta receptors may be importantly involved in mediation of K transfer to intracellular fluid.

Animals↗

PubMed1997

Acid-base regulation in tadpoles of Rana catesbeiana exposed to environmental hypercapnia.

Tadpoles of Rana catesbeiana were exposed to different levels of environmental hypercapnia. The acid-base regulatory response differed from that in adult amphibians in showing a high degree of pH compensation in the extracellular fluid (65-85%) and complete compensation in the intracellular fluid (tail muscle and liver) within 24 h. Hypercapnia induced a massive transfer of HCO3- equivalents and Ca2+ from the tadpoles to the environment, which lasted some 4-6 h. Bicarbonate accumulated in the body fluids came mainly from internal buffer sources (probably CaCO3 in lime sacs and/or skin deposits). It is suggested that the large bicarbonate efflux from the animal is a consequence of the dissolution of CaCO3 stores and the delayed adjustment of bicarbonate-retaining mechanisms. Re-exposure of tadpoles to hypercapnia after 1-3 weeks of normocapnic recovery only affected transepithelial fluxes of acid-base equivalents marginally, suggesting that mobilisable CaCO3 stores were depleted during the first exposure to hypercapnia and that they were not refilled. The CaCO3 stores may normally be mobilised during the slowly developing internal hypercapnia that occurs during metamorphosis.

Acid-Base Equilibrium↗

PubMed1988

Pharmacokinetics of iothalamate in endstage renal disease.

Some nephrologists make alterations in routine peritoneal and hemodialysis schedules after diagnostic studies that use radiographic contrast agents. A study to determine the pharmacokinetics of one contrast agent, iothalamate, is reported. The plasma (total body) clearance of iothalamate was measured in seven patients who had endstage renal disease (ESRD) and who received maintenance hemodialysis. During an interdialytic period, plasma clearance of iothalamate varied from 0.7 to 5.2 mL/min (3.1 +/- 1.8 mL/min, mean +/- SD) with an elimination rate constant (beta) of 0.0164 +/- 0.01 hr-1, a terminal half-life of 61 +/- 42 hours, and an estimated distribution volume of 11 +/- 3.9 L. Hemodialysis clearance of iothalamate was 104 +/- 54 mL/min. With the assumption that iothalamate is mainly distributed in the extracellular fluid (ECF) compartment, the theoretical fluid shift from the intracellular fluid (ICF) compartment to the ECF compartment was 323 mL after administration of the largest dose (2.1 mL/kg or 1.6 mmol/kg of body weight) of 60% meglumine iothalamate solution. The average maximum serum osmolarity change was less than expected, suggesting some type of internal buffering of meglumine iothalamate. In the first few hours after radiocontrast administration in four patients, the average change in serum osmolarity was 5 mmol/L; the average change in serum sodium concentration during this same time was a decrease of 0.5 mmol/L. The minor increase in ECF volume induced by hyperosmolar contrast agents does not require immediate dialysis in most patients. When needed, however, for contrast-related adverse effects, hemodialysis is efficient in rapidly removing iothalamate.

Aged↗

PubMed1972

Effect of changes in the osmolality of the luminal fluid on intracellular concentration of solutes in the hamster jejunum.

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Animals↗

PubMed2000

Total body water and ECFV measured using bioelectrical impedance analysis and indicator dilution in horses.

The purposes of this study were 1) to determine the compartmentation of body water in horses by using indicator dilution techniques and 2) to simultaneously measure bioelectrical impedance to current flow at impulse current frequencies of 5 and 200 kHz to formulate predictive equations that could be used to estimate total body water (TBW), extracellular fluid volume (ECFV), and intracellular fluid volume (ICFV). Eight horses and ponies weighing from 214 to 636 kg had catheters placed into the left and right jugular veins. Deuterium oxide, sodium thiocyanate, and Evans blue were infused for the measurement of TBW, ECFV, and plasma volume (PV), respectively. Bioelectrical impedance was measured by using a tetrapolar electrode configuration, with electrode pairs secured above the knee and hock. Measured TBW, ECFV, and PV were 0.677 +/- 0.022, 0.253 +/- 0.006, and 0.040 +/- 0.002 l/kg body mass, respectively. Strong linear correlations were determined among measured variables that allowed for the prediction of TBW, ECFV, ICFV, and PV from measures of horse length or height and impedance. It is concluded that bioelectrical impedance analysis (BIA) can be used to improve the predictive accuracy of noninvasive estimates of ECFV and PV in euhydrated horses at rest.

Algorithms↗

PubMed1994

Integrated responses to exhaustive exercise and recovery in rainbow trout white muscle: acid-base, phosphogen, carbohydrate, lipid, ammonia, fluid volume and electrolyte metabolism.

White muscle and arterial blood plasma were sampled at rest and during 4 h of recovery from exhaustive exercise in rainbow trout. A compound respiratory and metabolic acidosis in the blood was accompanied by increases in plasma lactate (in excess of the metabolic acid load), pyruvate, glucose, ammonia and inorganic phosphate levels, large elevations in haemoglobin concentration and haematocrit, red cell swelling, increases in the levels of most plasma electrolytes, but no shift of fluid out of the extracellular fluid (ECF) into the intracellular fluid (ICF) of white muscle. The decrease in white muscle pHi was comparable to that in pHe; both recovered by 4 h. Creatine phosphate and ATP levels were both reduced by 40% after exercise, the former recovering within 0.25 h, whereas the latter remained depressed until 4 h. Changes in creatine concentration mirrored those in creatine phosphate, whereas changes in IMP and ammonia concentration mirrored those in ATP. White muscle glycogen concentration was reduced 90% primarily by conversion to lactate; recovery was slow, to only 40% of resting glycogen levels by 4 h. During this period, most of the lactate and metabolic acid were retained in white muscle and there was excellent conservation of carbohydrate, suggesting that in situ glycogenesis rather than oxidation was the major fate of lactate. The redox state ([NAD+]/[NADH]) of the muscle cytoplasm, estimated from ICF lactate and pyruvate levels and pHi, remained unchanged from resting levels, challenging the traditional view of the 'anaerobic' production of lactate. Furthermore, the membrane potential, estimated from levels of ICF and ECF electrolytes using the Goldman equation, remained unchanged throughout, challenging the view that white muscle becomes depolarized after exhaustive exercise. Indeed, ICF K+ concentration was elevated. Lactate was distributed well out of electrochemical equilibrium with either the membrane potential (Em) or the pHe-pHi difference, supporting the view that lactate is actively retained in white muscle. In contrast, H+ was actively extruded. Ammonia was distributed passively according to Em rather than pHe-pHi throughout recovery, providing a mechanism for retaining high ICF ammonia levels for adenylate resynthesis in situ. Although lipid is not traditionally considered to be a fuel for burst exercise, substantial decreases in free carnitine and elevations in acyl-carnitines and acetyl-CoA concentrations indicated an important contribution of fatty acid oxidation by white muscle during both exercise and recovery.

Acid-Base Equilibrium↗