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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↗
PubMed1992

Intracellular fluid of waybread (Plantago major) as a prophylactic for mammary cancer in mice.

The investigations were performed on female mice of the strain C3H Strong. Only the breeders were used in the experiments. A number of mice were given intracellular fluid of way-bread in subcutaneous injections. The controls received no treatment. The age at which mammary cancer appeared was noted and also how often the tumors occurred. The frequency of tumor formation was 93.3% in the controls and 18.2% in the treated mice. The difference is significant.

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↗
PubMed1991

Relative expansion of extracellular fluid in obese vs. nonobese women.

There is a conflict in previous studies with regard to the relation between adipose tissue mass and total body fluid distribution. This study tested the hypothesis that obesity is accompanied by an increase in the extracellular-to-intracellular fluid ratio above that observed in nonobese subjects. Extracellular fluid was evaluated in obese (n = 39) and nonobese (n = 26) healthy women, using two different dilution volumes, 35SO4 [extracellular water (ECW)] and 24NaCl [exchangeable sodium (Nae)]. Intracellular water (ICW = 3H2O dilution volume-ECW) and total body potassium (TBK; 40K whole body counting) were assumed to represent intracellular fluid. Two independent markers of relative fluid distribution were formulated as ECW/ICW and Nae/TBK. Obese and nonobese women were of similar age and height but differed in body weight and TBW by 67.7 kg and 12.9 liters, respectively. The obese women had significantly larger absolute ECW, Nae, ICW, and TBK compared with the nonobese women (all P less than 0.001). The ratios ECW/ICW and Nae/TBK were significantly higher in obese vs. nonobese women and were highly correlated with each other (r = 0.54, P less than 0.001) in the pooled group of subjects. Fluid volumes are thus increased in obese women, and the expansion is relatively greater for the extracellular compartment. These results have implications in the study of human body composition and may also account in part for the fluid-overload states that often accompany severe obesity.

Adult↗
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↗
PubMed1986

A pharmacological explanation of the use-dependency of the verapamil (and D-600) block of slow calcium channels.

Contractures of the toe muscles of frogs produced by 123 mM K+ were reduced or blocked by verapamil (or D-600) when applied in concentrations of 10(-7) M or more. In concentrations between 10(-7) and 3 X 10(-5) M or less, little or no reduction was produced in the first test with high K+ after drug application. When tests were repeated at 10- to 15-min intervals, block was produced. This block decreased and eventually disappeared if the muscles were kept in the drug solution without testing for 25 min or more. In contrast, at 10(-4) M verapamil, the first contracture in response to high K+ was reduced or blocked. If exposure to 10(-4) M verapamil was limited to 0.5 hr, then recovery occurred in drug-free solution, but if the muscles were exposed to this concentration of verapamil for 2.5 hr or longer, the K+ contracture remained blocked, even in drug-free solution. These results provided an explanation for the frequency- and use-dependency effects of verapamil and D-600. Briefly, this explanation is that the drug receptor is inside the calcium channel which is closed to the extracellular fluid in the resting or in the inactivated state but open to the intracellular fluid at all times. The drug receptors will be effectively occupied and a block produced when lower drug concentrations are used if the calcium channels are opened, but verapamil will leave its receptor and diffuse into the intracellular fluid when the extracellular channel openings are closed. Further details of this mechanism are given in the paper.

Animals↗
PubMedDate not supplied

Control of ventilation in the hypercapnic skate Raja ocellata: II. Cerebrospinal fluid and intracellular pH in the brain and other tissues.

This study examined the possible role(s) of central acid-base stimuli in the increase in ventilation induced by hypercapnia in the skate, a response that is not due to an O2 signal (Graham et al., Respir. Physiol., 1990, 80: 251-270). Skate were sampled for cerebrospinal fluid (CSF) acid-base status, intracellular pH of the brain (14C-DMO method), and pHi in other tissues throughout 24 h of exposure to PICO2 = 7.5 Torr. CSF PCO2 rapidly equilibrated with the elevated PaCO2. Despite the much lower non-HCO3- buffer capacity in the CSF, CSF pH was not depressed to the same extent as blood pHa. CSF pH was also regulated rapidly, returning to control levels by 8-10 h, whereas pHa remained significantly depressed at 24 h. Similarly, the pHis of the weakly buffered brain and heart ventricle were initially compensated more rapidly than those of more strongly buffered white muscle and red blood cells. However, brain pHi adjustment slowed markedly after 4 h and stabilized at only 70% compensation by 20-24 h, suggesting that brain intracellular acidosis may play a role in the long-term increase in ventilation. CSF and brain were the only compartments which did not exhibit an apparent compounding metabolic acidosis during the initial stages of hypercapnic exposure. While these results illustrate the primacy of central acid-base regulation, they do not support a role for CSF pH in the long-term elevation of ventilation in response to hypercapnia. Depressions in pHa and brain pHi appear the two most likely candidates for proximate stimuli.

Acid-Base Equilibrium↗
PubMed1990

In vivo measurement of intra- and extracellular space of brain tissue by electrical impedance method.

An impedance method was applied to evaluate transcellular fluid shifts in ischaemic brain oedema. The admittances (apparent electrical conductivities) of tissues were measured at varied frequencies based on a simple model of an electrical equivalent circuit for tissues, which consisted of Re (resistivity of extracellular fluid), Ri (resistivity of intracellular fluid) and Cm (capacitance of cell membrane). Calculated were Re, Ri, Rinf (resistivity of total fluid), Re/Ri and alpha (Cole-Cole distribution index) of brain tissue by Cole-Cole an arc of a circle. During ischaemia induced by cat middle cerebral artery occlusion (MCAO), the parameters were examined continuously. After MCAO, cerebral blood flow (CBF) decreased to under 10 ml/100 g/min. Then Re and Re/Ri increased, but Ri decreased. These results indicated that fluid shift from extracellular (EC) to intracellular (IC) space occurred after ischaemic insult. Rinf showed no changes during ischaemia of 30 min, which demonstrated no changes of total fluid volume. Using this impedance technique, fluid accumulation and shift may be examined by changes of Re, Ri, Re/Ri and Rinf in various types of brain oedema in vivo.

Animals↗
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↗