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At least 19 recordsLinked to original sources
PubMed1979

Potassium, sodium, and the intracellular fluid space of cells from bone.

Cells enzymatically dispersed from fetal rat calvaria were analyzed for sodium and potassium content and intracellular fluid space (ICF). Even when obtained in comparatively high yield, the cells are damaged by the isolation procedure as evidenced by high sodium and low potassium content immediately after isolation. During a post-incubation period potassium is accumulated and sodium extruded to steady-state levels. Although electrolyte content of cells after recovery did not vary as a function of cell yield, ICF was increased in cells obtained in lower yield, suggesting cell swelling as a result of membrane damage. The weighted mean values obtained for the best cell preparations were 117 mM K+ and 27 mM Na+. Based on DNA assay of isolated cells and the whole tissue, 20- to 21-day calvaria were found to have an average of 8.1 x 10(6) cells/calvarium. Combining cell data with analysis of total tissue sodium, potassium, and water, it was concluded that the tissue extracellular sodium is in equilibrium with blood but that the potassium concentraiton is approximately 5-fold higher than blood levels.

Animals↗
PubMed1977

Enhancement of K transfer to intracellular fluid by cerebral artery K-loading.

Intact, UL, and pancreatectomized UL dogs were loaded with K by administration of 2 mEq KCl/kg/hr through a cerebral (vertebral) artery. K transfer to ICF was calculated and compared with that computed in control animals K-loaded through a PV. At the same rate of K administration, the change of route from PV to VA markedly increased transmembrane K transfer, even in the absence of insulin; the increase seems a specific response to K. KCl administration via a VA, with a resulting abrupt rise in the serum K concentration of cerebral blood, activates a K transfer mechanism (possibly by stimulation of a K-sensitive CNS receptor) that is strikingly unlike the insulin-mediated one stimulated by intravenous KCl. Hyperkalemic dogs may have more than one mechanism for maintaining K homeostasis, depending on the rate at which K enters the circulation.

Animals↗
PubMed1978

Osmotic behaviour of human red blood cells: an interpretation in terms of negative intracellular fluid pressure.

1. The observation that human red blood cells do not shrink in hypertonic media as much as expected for ideal osmometers has previously been explained in terms of either a marked increase in the osmotic coefficient of the cell contents or an increase in the chloride content of the cells.2. Changes in suspension pH and haematocrit have been observed when the concentration of the unbuffered NaCl medium was doubled. The small increases in external pH, and the size of the volume decreases, are inconsistent with variations in the Cl content as a significant factor in the non-ideal osmotic responses.3. Membrane potentials of red cells in buffered media were followed using the fluorescent dye, diS-C(3)-(5). On shrinking at pH 7.4, the cells hyperpolarized ca. 5 mV as predicted if changes in the osmotic coefficient rather than in Cl content explained the osmotic behaviour.4. Regarding haemoglobin in concentrated solution as a solute with high osmotic coefficient is formally correct but is little help in understanding the properties of the solution. We have found it useful to consider separately haemoglobin and the rest of the contents of the cell. The haemoglobin then supports part of the total hydrostatic pressure on the cell leaving the crystalloid solution to experience a reduced fluid pressure. In greatly shrunken cells the contents act like a gel with the matrix of haemoglobin under compression and the fluid which fills the spaces within the matrix under tension.

Erythrocytes↗
PubMed1975

Distribution characteristics of methyl-hydrazine in the plasma and cerebrospinal fluid of monkeys.

A Lumped parameter mathmatical model including extracellular fluid, intracellular fluid, and cerebrospinal fluid compartments has been applied to describe methylhydrazine (MMH) distribution kinetics in the blood and cerebrospinal fluid of Rhesus monkeys. Ten monkeys average weight 5.5 kg, were given intravenous infusions of MMH while blood and cerebrospinal fluid samples were periodically collected and analyzed for MMH. The mathematical model was used to simulate the infusions and the simulations were compared with experimental data to validate the model and to evaluate the mass transfer parameters required by the model.

Aerospace Medicine↗
PubMed1977

Lithium in depression: a biochemical study.

Two groups of depressed subjects, one with a history of recurrent depression, the other with a history of persistent apathy, were given lithium carbonate 1,200 mg q.i.d. and supplementart potassium 1,200 mg t.d.s. for 1 week. Measurements were made before and after the lithium treatment of total body water (tritium space), extracellular fluid (sulphate space), total exchangeable sodium (Nae) and total exchangeable potassium (Ke) using sodium-24 and potassium-42 multiple isotope dilution techniques. Prior to treatment when compared with a group of normal subjects, both depressed groups showed changes in body fluid volumes and electrolyte levels. Total body water, intracellular fluid and intracellular potassium were lowered, while electrolyte levels. Total body water, intracellular fluid and intracellular potassium were lowered, while intracellular sodium was raised. After treatment with lithium the values in the apathetic group showed little change but the group with recurrent depression showed a significant increase in intracellular fluid (p less than 0.025), Ke (p less than 0.001), intracellular potassium (p less than 0.025) and a significant decrease in Nae (p less than 0.05). There was a marked increase in mood in the group with recurrent depression but not in the apathetic group following lithium treatment. These findings suggest that recurrent depression, both in clinical improvement, mood and also correction of water and also correction of water and electrolyte disturbances arise, but not in patients with long-standing apathy.

Aged↗
PubMed1977

Body fluid compartments.

The terms mole, molality, molarity, osmole, osmolality, osmolarity, osmolar gap and anion gap are defined and their clinical usefulness indicated. The following body fluid compartments are described: total body water (TBW), extracellular fluid (ECF), intracellular fluid (ICF), transcellular fluid TCF), plasma volume, red cell volume and interstitial fluid volume. Isotope-dilution techniques are briefly discussed and representative normal values for the various compartments according to sex and age are indicated. The physiological mechanisms that maintain the distinctive ionic compositions of the various fluid spaces are briefly outlined. New concepts of the function of the gel matrix and of the lymph drainage of the interstitium are presented. Opposing models to the sodium-potassium membrane pump are briefly described.

Body Fluid Compartments↗
PubMed1975

Kaluresis and diuresis after administration of antidiuretic hormone to hyperkalemic dogs.

Dogs infused with 2 meq KCl/kg per h exhibit electrocardiographic evidence of prelethal cardiotoxicity in about 3 h when serum potassium reaches a level between 10.2-10.5 meq/liter. During this time, their urine output of 30 ml/h is equal to the volume of KCl infused. Studies of the potassium distribution in these animals indicate that 20 percent of the infused ion is added to the extracellular fluid and red blood cell mass, 20 percent is excreted in the urine, while the remaining 60 percent is unaccounted for and presumably transferred to intracellular fluid. Dogs treated with moderately large doses of antidiuretic hormone intramuscularly before and during KCl infusion delay development of prelethal cardiotoxicity for about 5 h, with serum potassium levels comparable to those of untreated dogs. In addition, treated animals display a considerable diuresis and kaluresis with urine volumes nearly 4 times that of the volume infused. The potassium ion distribution in animals given antidiuretic hormone is much different from that of untreated dogs, with 55 percent of the infused ion found in the urine, about 15 percent in extracellular fluid and red blood cell mass, and only 30 percent presumably transferred to intracellular fluid. Transfer of potassium to intracellular fluid was calculated to be 3.1 plus or minus 0.7 meq/kg in antidiuretic-hormone-treated animals and 3.8 plus or minus 0.7 meq/kg in untreated (control) animals. Since these values are, within experimental error, quite comparable, it is possible that antidiuretic-hormone-induced kaluresis and diuresis are involved in protecting some animals from the effects of hyperkalemia by delaying the attainment of cardiotoxic blood levels.

Animals↗
PubMed1975

Relationship between absolute body-fluid deficits and fluid intake in the rat.

Acute absolute body-fluid deficits were induced in rats by injection of the diuretic drug furosemide, which caused up to 20% reduction of extracellular fluid volume and up to 2% reduction of intracellular fluid volume. Water and .3 M NaCl were subsequently made available to allow the rats to replace their body fluids by drinking. The rats increased their intake of both fluids, but replaced less than half of the total deficit, thereby tolerating larger and larger voluntary body-fluid deficits as the size of the diuretic fluid loss increased. Plasma measures showed that the rats sustained hypovolemia after drinking, while intracellular fluid volume was apparently restored. Fluid-depleted rats drank normally in response to intracellular dehydration induced by a sodium chloride load. Incomplete restoration of body-fluid balance after body-fluid depletion is due to a failure to drink in response to extracellular dehydration.

Animals↗
PubMed1979

Volume studies in men with mild to moderate hypertension.

The importance of salt and water in the pathophysiology of the hypertensive state is well recognized. The current study is the first to report simultaneous measurements of red blood cell mass, plasma volume, extracellular fluid and total body water levels. Studies were performed in 82 white men, 14 with normal blood pressure and 16 with low renin and 52 with normal renin hypertension. The results indicate that subjects with normal renin hypertension compared with age-matched controls are characterized by an absolute increase (1.5 liter/m2) in intracellular fluid (total body water minus extracellular fluid). Furthermore, the ratio of extracellular fluid to total body water is decreased (0.43 to 0.38). No volume differences were found between subjects with low renin hypertension and age-matched subjects with normal renin hypertension. We conclude that subjects with normal renin hypertension compared with age-matched peers are characterized by an expanded intracellular fluid and that subjects with low renin hypertension do not exhibit a unique volume disorder.

Adult↗
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↗
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↗
PubMed1975

Saturable binding of dihydromorphine and naloxone to rat brain tissue in vitro.

The binding in vitro of an opiate agonist, 3H-dihydromorphine, was studied using a particulate fraction obtained from rat brain homogenates and compared with that of an opiate antagonist, 3H-naloxone. The binding of 3H-dihydromorphine may be separated into two components: one a saturable component and the other nonsaturable. The saturable binding may be calculated from the differences in binding observed in the absence and presence of high concentrations of levorphanol. The use of dextrorphan results in an artifactual separation of this component, although relative stereospecificity was observed for levorphanol and dextrorphan. There were marked regional differences in the distribution of saturable 3H-dihydromorphine binding in the brain. These were primarily due to the difference in the concentration of the saturable binding sites within various brain regions. It appeared that the saturable binding sites from various brain regions had similar affinities for dihydromorphine except for the binding site from cerebral cortex which had a higher affinity. In contrast, saturable binding sites for naloxone in various brain regions had different affinities for naloxone. It appears that naloxone has at least two types of saturable binding sites, one of which is not available to dihydromorphine. This is based on observations 1) that the total concentration of saturable binding sites for naloxone was greater than that for dihydromorphine in each brain region studied irrespective of the assay medium used and 2) that unlabeled dihydromorphine inhibited the 3H-naloxone binding in striatum but failed to alter it significantly in cerebellum, whereas unlabeled naloxone reduced 3H-naloxone binding significantly in both brain regions. The difference in concentrations of saturable binding sites for naloxone and dihydromorphine was relatively small in striatum but larger in cerebellum, indicating that the saturable binding sites in cerebellum are predominantly naloxone-specific, whereas those in striatum are capable of binding both naloxone and dihydromorphine. In cerebrospinal fluid or in simulated intracellular fluid, the apparent affinity for dihydromorphine was lower and that for naloxone was higher than in Tris-HCl buffer. It is concluded that naloxone binds to dihydromorphine binding site and to another site, which has a different affinity for naloxone and is not available to dihydromorphine. Studies in which opiate receptor binding was assayed in Tris-HCl buffer may need to be re-evaluated. Further, in studies where opiate binding in vitro is assessed following pharmacologic intervention, such binding should be estimated in a relevant physiological medium rather than in Tris-HCl buffer.

Animals↗
PubMed1992

Regulation of solute and water balance and cell volume in the central nervous system.

The mammalian brain is composed of four distinct fluid compartments: blood, cerebral spinal fluid, interstitial fluid surrounding glial cells and neurons, and intracellular fluid. Maintenance of the ionic and osmotic composition and volume of these fluids is crucial for the normal functioning of the brain. Small changes in intracellular or extracellular solute composition can dramatically alter neuronal signaling and information processing. Because of the rigid confines of the skull and complex brain architecture, changes in total brain volume can cause devastating neurological damage. As a result, it is not surprising to find that the composition and volume of brain intracellular and extracellular fluids are controlled tightly under both normal conditions and in various disease states. Osmotic and ionic balance in the central nervous system is regulated by solute and water transport across the blood-brain barrier, the choroid plexus, and the plasma membrane of glial cells and neurons. Despite its clinical and physiological significance, however, little is known about the underlying cellular and molecular mechanisms by which the central nervous system's osmotic and ionic balance is maintained. In this review, the current understanding of osmoregulation in the mammalian brain and its role in various disease processes such as hyponatremia, renal failure, and hypernatremia will be summarized. A detailed understanding of brain osmoregulatory processes represents a fundamental physiological problem and is required for the treatment of numerous disease states, particularly those encountered in the practice of nephrology.

Acute Kidney Injury↗
PubMed1979

Studies on the reaction between pyridine nucleotides and mercury compounds in artificial intracellular and extracellular fluids.

The strong complex formations of pyridine nucleotides with mercury compounds were demonstrated in artificial intracellular fluid containing oxianions (HPO42-, HCO3-), while those in artificial extracellular fluid were considerably weaker. Dissociation constants (K) of the complexes of [MC.NADP], [MC.NADPH], [MC.NAD], [MC.NADH], [MC.adenine], and [MC.nicotinamide mononucleotide] were found to be 1.0 x 10(-4), 2.6 x 10(-5), 1.2 x 10(-4), 2.9 x 10(-5), 7.2 x 10(-6), and 3.8 x 10(-3), respectively in phosphate buffer (43 mM, pH 8.0).

Extracellular Space↗
PubMed1979

Transmembrane potential and ionic content of rat alveolar macrophages.

The cell volume, cell water, intracellular ionic concentrations, and transmembrane potential of rat alveolar macrophages were determined. The measurements were made on cells which had been separated from the medium by centrifugation through dibutyl phthalate in order to greatly reduce the trapped extracellular space. The mean cell volume of the alveolar macrophages is 1,525 cubic microns and 72% of this volume is water. The intracellular fluid is high in Na+ (97 mM) and lower in K+ (50 mM) and the intracellular Cl- concentration in 64 mM. The transmembrane potential, as measured from the equilibrium distribution of tritiated triphenylmethyl phosphonium and by using the fluorescent probe, Di-S-C3(5), is approximately -37 millivolts. Neither Na+, K+, nor Cl- is distributed at equilibrium. However, the K+ permeability of alveolar macrophage membranes appears to be greater than Na+ permeability.

Animals↗