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PubMedDate not supplied

The effect of polyamines and dialysate fluid on extracellular matrix synthesis in VERO cell cultures.

BACKGROUND: Polyamines are involved in normal and pathological cell proliferation and differentiation. Like acid radicals, they play an important role in remodelling the extracellular matrix and are considered "uremic toxins". Proteins and glycosaminoglycans are essential components of the extracellular matrix, and contribute to normal mature organ functions. The aim of this study was to analyse the effects of free polyamines, dialysate fluid components and dialysis fluid on protein and extracellular glycosaminoglycan synthesis in VERO cell cultures. METHODS: The dialysate fluid components were separated with a Sephadex G15 column and the cultures were analysed after incorporation of 3H-leucine and 3H-glucosamine. Cultures were run at pH 7.0 and pH 7.4. The glycosaminoglycan classes were separated with a DEAE column, and polyamines were determined by high-performance liquid chromatography. Proteins and single glycosaminoglycan classes were quantified by a scintillator. DNA gel electrophoresis was done to detect chromatin fragmentation. RESULTS: Dialysate contained putrescine, spermidine and spermine, chromatography showing four peaks; only peaks I and II indicated polyamines at respectively Da 5000 and 1500. Polyamines are therefore linked to different carriers. There was an increase of protein and glycosaminoglycan synthesis with dialysis fluid and polyamines, but inhibition with peak II or dialysate. DNA gel electrophoresis showed no chromatin fragmentation. Findings at pH 7.0 and 7.4 were similar. CONCLUSIONS: It would appear that in uremic patients polyamines are conjugated to protein carriers of different molecular weights with different biological actions. As polyamines and dialysis fluid affect changes in extracellular matrix, they could be related to physiological organ functions. However, these in vitro data must be considered with the appropriate limitations when we try to extrapolate them to the in vivo situation.

Animals↗

PubMed1992

Push-pull cannula for localized application of drugs and sampling of medium, combined with electrophysiological recordings in an interface slice chamber.

These experiments combined electrophysiological recordings from hippocampal slices with application of drugs to and sampling of extracellular fluid from a restricted region of the slice using a push-pull cannula placed under the slice in an interface chamber. Stable and apparently normal extracellular and intracellular recordings could be obtained directly over the tip of the cannula and solutions changed without disturbing the recording. Relatively rapid effects (1-5 min) were observed when TTX, CNQX, or medium containing 50 mM K+ were applied via the cannula and recovery from these effects was achieved. In addition, effects were restricted to the immediate vicinity of the cannula; neurones recorded several hundred micrometers away were apparently unaffected. Samples of extracellular fluid obtained as minute fractions during the application of high K+ containing medium contained higher concentrations of GABA, aspartate and glutamate than control fractions but the same levels of other amino acids, e.g., isoleucine and leucine. With appropriate design of push-pull cannula and recording chamber, therefore, stable electrophysiological recordings can be combined with localized extracellular fluid sampling and rapid and localized application of test solutions in an interface slice chamber.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMed1997

Language guiding therapy: the case of dehydration versus volume depletion.

Indiscriminate use of the terms dehydration and volume depletion, so carefully crafted by our predecessors, risks confusion and therapeutic errors. These two conditions should be distinguished at the bedside and in how we speak to one another. Dehydration largely refers to intracellular water deficits stemming from hypertonicity and a disturbance in water metabolism. The diagnosis of dehydration cannot be established without laboratory analysis of p[Na +] or calculation of serum tonicity. In contrast, volume depletion describes the net loss of total body sodium and a reduction in intravascular volume and is best termed extracellular fluid volume depletion. The diagnosis of this condition relies principally on history, careful physical examination, and adjunctive data from laboratory studies. The pathophysiology of both dehydration and extracellular fluid volume depletion must be understood if these conditions are to be recognized and appropriately treated when they occur separately or together. There is no inclusive therapy for all situations. For example, indiscriminate treatment with 0.45% saline cannot be recommended when these conditions coexist because extracellular fluid volume depletion is often treated rapidly with 0.9% saline and dehydration is often treated more slowly with 5% dextrose.

Dehydration↗

PubMed2003

MR imaging in the diagnosis of denervated and reinnervated skeletal muscles: experimental study in rats.

PURPOSE: To describe the magnetic resonance (MR) imaging findings of denervation and reinnervation of skeletal muscles in rats. MATERIALS AND METHODS: The posterior tibial nerve was transected in 48 rats (nerve section group) and was repaired just after transection in another 48 rats (nerve repair group). At 2, 4, 6, and 8 weeks after surgery, changes in the area and signal intensity of the gastrocnemius muscle on T1- and T2-weighted MR images in vivo (four rats in each group) and T1s and T2s were analyzed in vitro in both groups (20 rats each) and compared with electromyographic findings. Water volume content and extracellular fluid space of the muscle in vitro were also examined in both groups (24 rats each). Four rats were used as controls for in vitro analysis. RESULTS: At T2-weighted MR imaging, the muscle showed continuously high signal intensity in the nerve section group. In the nerve repair group, the signal intensity was high until 4 weeks, when it recovered. Increases in signal intensity on T2-weighted MR images and T2s were seen in the nerve section group throughout the study period. In the nerve repair group, increased signal intensity on T2-weighted MR images was noted at 2 and 4 weeks and significantly returned to normal at 6 weeks (P <.014), just after the detection of the M wave at electromyography. T2 increased at 2 weeks, then decreased significantly at 4 weeks (P =.012). Extracellular fluid space significantly increased in the nerve section group at all measurement times and in the nerve repair group at 2 and 4 weeks, then it decreased after 6 weeks (P <.003), which is parallel to the change in signal intensity on T2-weighted MR images, although there was little change in total water volume content in either group. CONCLUSION: Changes in signal intensity on T2-weighted MR images that are related to denervation may result from an increase of extracellular fluid space. MR imaging clearly demonstrates that changes in rat skeletal muscle are reversed when the nerve heals and reinnervation proceeds.

Animals↗

PubMed1991

Effects of haloperidol administration on in vivo extracellular dopamine in striatum and prefrontal cortex after partial dopamine lesions.

The effects of haloperidol on striatal and prefrontal cortical extracellular fluid dopamine (DA) concentrations were examined in sham-operated control rats and in rats which had received partial lesions of their dopamine systems. In control rats haloperidol administration produced increases in extracellular fluid DA concentrations in both the striatum and prefrontal cortex. However, in rats which had been partially lesioned with intracerebroventricular 6-hydroxydopamine, haloperidol produced an increase in extracellular fluid DA concentration in the prefrontal cortex but failed to alter striatal DA release. These data suggest that nigrostriatal and mesocortical DA neurons have different response capabilities following partial DA lesions.

Animals↗

PubMed1994

[Role of blood-brain barrier in cerebral homeostasis].

By a variety of mechanisms, the cerebral endothelium isolates the extracellular fluid space in the central nervous system from the plasma. The combination of physical and enzymatic mechanisms which prevent macromolecules, polar solutes, neurotransmitters, peptides, and electrolytes from passively entering the brain has been termed the blood-brain barrier (BBB). Specific mechanisms provide facilitated transport across the BBB and active secretion of extracellular fluid and CSF maintain homeostasis for nutrients and for cation and H+ respectively. Consequently, interstitial fluid volume in the CNS does not increase when the total extracellular fluid volume is increased. Total tissue volume is sensitive to osmotic forces, while oncotic forces are relatively unimportant. Most anaesthetic drugs are sufficiently lipid soluble that they enter the CNS easily by passive diffusion. Differences in the rates of CNS penetration between drugs can be predicted from their lipid solubility. Anaesthetic drugs have little effect on BBB permeability and their effects on brain oedema formation derive principally from their haemodynamics effects.

Anesthetics↗

PubMedDate not supplied

Cell volume regulation in liver.

The maintenance of liver cell volume in isotonic extracellular fluid requires the continuous supply of energy: sodium is extruded in exchange for potassium by the sodium/potassium ATPase, conductive potassium efflux creates a cell-negative membrane potential, which expelles chloride through conductive pathways. Thus, the various organic substances accumulated within the cell are osmotically counterbalanced in large part by the large difference of chloride concentration across the cell membrane. Impairment of energy supply leads to dissipation of ion gradients, depolarization and cell swelling. However, even in the presence of ouabain the liver cell can extrude ions by furosemide-sensitive transport in intracellular vesicles and subsequent exocytosis. In isotonic extracellular fluid cell swelling may follow an increase in extracellular potassium concentration, which impairs potassium efflux and depolarizes the cell membrane leading to chloride accumulation. Replacement of extracellular chloride with impermeable anions leads to cell shrinkage. During excessive sodium-coupled entry of amino acids and subsequent stimulation of sodium/potassium-ATPase by increase in intracellular sodium activity, an increase in cell volume is blunted by activation of potassium channels, which maintain cell membrane potential and allow for loss of cellular potassium. Cell swelling induced by exposure of liver cells to hypotonic extracellular fluid is followed by regulatory volume decrease (RVD), cell shrinkage induced by reexposure to isotonic perfusate is followed by regulatory volume increase (RVI). Available evidence suggests that RVD is accomplished by activation of potassium channels, hyperpolarization and subsequent extrusion of chloride along with potassium, and that RVI depends on the activation of sodium hydrogen ion exchange with subsequent activation of sodium/potassium-ATPase leading to the respective accumulation of potassium and bicarbonate. In addition, exposure of liver to anisotonic perfusates alters glycogen degradation, glycolysis and probably urea formation, which are enhanced by exposure to hypertonic perfusates and depressed by hypotonic perfusates.

Animals↗

PubMed1990

Environmental stress increases extracellular dopamine in striatum of 6-hydroxydopamine-treated rats: in vivo microdialysis studies.

Bilateral intraventricular injections of 6-hydroxydopamine depleted dopamine (DA) in striatal tissue of rats by 88%. Tail shock increased DA in striatal extracellular fluid of these rats from 10 to 17 pg/20 microliters as measured by microdialysis, values less than half those seen in normal striatum. The increase was observed even in rats that were akinetic. DA in extracellular fluid after stress was negatively correlated with behavioral performance. Thus, residual nigrostriatal DA neurons are responsive to stress but do not produce normal DA levels in striatal extracellular fluid.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1998

An oral glutamine load enhances renal acid secretion and function.

In a recent study, a small oral glutamine load acutely elevated plasma bicarbonate concentrations in healthy adults (Am J Nutr 1995;61:1058-61). The present study was designed to elucidate the renal mechanism underlying the base-generating response to L-glutamine. Accordingly, vehicle (489 mL diet soda) or vehicle plus 2 g L-glutamine (28 mg/kg body wt) was ingested and the gain in extracellular fluid volume bicarbonate was compared with renal acid elimination as either ammonium excretion or tubular acid secretion (titratable acid plus bicarbonate reabsorption). Vehicle alone, which contained 27 mmol acid, did not increase extracellular fluid volume bicarbonate over the 90-min period. In contrast, L-glutamine increased plasma bicarbonate concentration (from 25.4+/-2 to 27.9+/-1 mmol/L, P < 0.05) and extracellular fluid volume bicarbonate by an estimated 39+/-10 mmol. When added to that required to neutralize the ingested acid, the combined total for new bicarbonate generated gave an estimated 66+/-10 mmol. Surprisingly, ammonium excretion accounted for < 2% of this newly generated bicarbonate. However, acid secreted and excreted as net acid (5.2+/-4.0 mmol/90 min) as well as that coupled to enhanced bicarbonate reabsorption (76+/-20 mmol/90 min) readily accounted for the estimated base gain (81+/-24 compared with 66+/-10 mmol/90 min). Concomitant with enhanced renal acid secretion, the oral glutamine load elicited an increase in glomerular filtration rate. These results rule out a role for L-glutamine as a direct precursor of bicarbonate and instead point to an indirect role in accelerating acid secretion, apparently coupled to increased glomerular filtration rate.

Adolescent↗

PubMed1995

Zeta potential of bone from particle electrophoresis: solution composition and kinetic effects.

The morphology of bone may be influenced by many factors, including electromechanical ones such as electric potentials, electric fields, or zeta potentials. Stress-generated potential studies in bone and particle electrophoresis studies using calcium-deficient hydroxyapatite have shown that the zeta potential depends on the composition of the steeping fluid and steeping time. To better quantify and understand these in situ potential changes in bovine cortical bone, the effects of alterations in calcium, phosphate, and fluoride concentrations in Neuman's Fluid (NF), which simulates in vivo bone extracellular fluid, were investigated using particle electrophoresis. The zeta potential increased in magnitude with increased calcium concentration in NF in as little as 17 min. Increasing phosphate concentration in NF also increased the zeta potential magnitude. These results provide support for a structural model of the bone matrix surface-bone fluid interface, which incorporates the bone surface proper (composed of collagen, mineral, and boundary regions), stationary layer (in which ions, ionic complexes, and proteins may be adsorbed), and bone extracellular fluid. These results, coupled with those of previous studies, indicate that the protein phase probably has an important role in the determination of the physiologic zeta potential; the role of the mineral phase may also be important.

Adsorption↗

PubMed2002

A case for strain-induced fluid flow as a regulator of BMU-coupling and osteonal alignment.

Throughout life, human bone is renewed continuously in a tightly controlled sequence of resorption and formation. This process of bone remodeling is remarkable because it involves cells from different lineages, collaborating in so-called basic multicellular units (BMUs) within small spatial and temporal boundaries. Moreover, the newly formed (secondary) osteons are aligned to the dominant load direction and have a density related to its magnitude, thus creating a globally optimized mechanical structure. Although the existence of BMUs is amply described, the cellular mechanisms driving bone remodeling-particularly the alignment process-are poorly understood. In this study we present a theory that explains bone remodelling as a self-organizing process of mechanical adaptation. Osteocytes thereby act as sensors of strain-induced fluid flow. Physiological loading produces stasis of extracellular fluid in front of the cutting cone of a tunneling osteon, which will lead to osteocytic disuse and (continued) attraction of osteoclasts. However, around the resting zone and the closing cone, enhanced extracellular fluid flow occurs, which will activate osteocytes to recruit osteoblasts. Thus, cellular activity at a bone remodeling site is well related to local fluid flow patterns, which may explain the coordinated progression of a BMU.

Bone Remodeling↗

PubMedDate not supplied

[Body fluids during 120-day anti-orthostatic hypokinesia].

Body fluid variations were examined during 120-day antiorthostatic (-5 degrees) hypokinesia in 21 test subjects, 9 of which comprised a control group (Group 1). The remaining 12 subjects formed three groups (four subjects each) who received drugs to normalize mineral and lipid metabolism (Group 2), or performed specially developed exercises (Group 3), or were on the combined treatment (Group 4). Total body water (TBW), intracellular fluid volume (IFV), extracellular fluid volume (EFV), and EFV composition were measured by nuclear physical methods. Measurements were taken prior to exposure, on head-down tilt days 1, 60 and 120, and on recovery day 15. Body composition and K40 content were investigated before and after head-down tilt. The controls showed body dehydration that began on tilt day 1 at the expense of vascular fluid and continued by day 60 at the expense of interstitial fluid and by day 120 at the expense of IFV. Group 2 subjects exhibited variations that were similar to those of controls. Group 3 subjects were in better shape due to the beneficial effect of exercise which diminished as head-down tilt continued. In the recovery period the above changes regressed.

Blood Volume↗

PubMed1985

Blood to interstitial fluid volume ratio in chronic hypokalaemic states.

The distribution of extracellular fluid over the intra- and extravascular spaces was determined in hypokalaemic and normokalaemic patients. In six patients with Bartter's syndrome, four with pseudo-Bartter's syndrome, and twenty with essential hypertension (EH) chronically treated with chlorthalidone, serum potassium (serum K+) and extracellular fluid volume (ECFV) were decreased, while plasma volume (PV) and blood volume (BV) were normal (see Table 1 for means, standard deviations, and levels of significance). Consequently, the ratio of BV to interstitial fluid volume (IFV) was increased. In ten patients with EH on long-term combined enalapril chlorthalidone therapy, eight EH patients on long-term spironolactone treatment, and twenty-three EH patients treated by short-term sodium restriction, PV, BV, and ECFV were decreased, but serum K+ and BV/IFV were normal. In six patients with primary hyperaldosteronism (PHA) serum K+ was decreased, while PV, BV, and BV/IFV were elevated. Significant negative correlations between sK and BV/IFV were found in the Bartter patients (r = -0.88) and the pooled data of all patients (r = -0.50). These findings suggest an association between chronic hypokalaemia and a fluid shift from the extra- into the intravascular space. The hypothesis that this phenomenon is due to a decreased venous resistance as a consequence of chronic hypokalaemia is discussed.

Bartter Syndrome↗

PubMed1983

Distribution of Pz-peptidase in bovine epididymal and ejaculated semen.

Bovine epididymal or ejaculated semen was fractionated by density gradient centrifugation in Percoll, and seminal components recovered from the gradients were subjected to additional separation and washing steps. This procedure resulted in isolation of four major seminal constituents: particle-free extracellular fluid, washed light particulates, washed cytoplasmic droplets, and washed spermatozoa. When assayed using the Pz-peptide substrate, all the isolated seminal fractions contained substantial Pz-peptidase activity. The extracellular fluid Pz-peptidase was present in soluble form, but Triton X-100 was required for complete extraction of the Pz-peptidase activity from the spermatozoa, cytoplasmic droplets, and light particulates. The greatest Pz-peptidase activities were observed in the cytoplasmic droplet and epididymal sperm extracts, whereas the activities in extracellular fluid, extracts of light particulates, and extracts of ejaculated spermatozoa were relatively low. Most of the Pz-peptidase activity in extracts of epididymal spermatozoa was attributable to cytoplasmic droplets. The specific Pz-peptidase activities found by regression analysis were 6.1 mU/billion attached cytoplasmic droplets and 1.1 mU/billion spermatozoa. These results established that in the bovine, cytoplasmic droplets were the major source of Pz-peptidase activity in semen and that Pz-peptidase was not primarily a spermatozoal enzyme.

Animals↗

PubMed1988

Extracellular lactic acid as an indicator of brain metabolism: continuous on-line measurement in conscious, freely moving rats with intrastriatal dialysis.

Lactic acid was measured continuously in the dialysis perfusate emerging from the striatum of conscious, freely moving rats. The continuous measurement utilized a specific enzymatic/fluorometric detector that provided temporal information about the changes in the concentration of lactate in extracellular fluid (ECF). The level of lactate in extracellular fluid was found to be directly linked to local cellular metabolism. Inhibition of glycolysis with 2-deoxyglucose decreased the ECF level of lactate, whereas increased lactate production was observed after uncoupling mitochondrial electron transport with 2,4-dinitrophenol. A transient increase in the extracellular level of lactate was found after neuronal stimulation (e.g., electroconvulsive shock or local administration of kainic acid). The response to electroconvulsive shock could be attenuated by inhibiting the electrical activity of neurons with tetrodotoxin. Thus, this system is capable of providing novel information about transient changes in the extracellular concentration of lactic acid in real time, and these changes can be related to changes in metabolism and neuronal activity.

2,4-Dinitrophenol↗

PubMed1990

Beta-lactoglobulin enhances the uptake of free palmitate by hepatocyte monolayers: the relative importance of diffusion and facilitated dissociation.

We compared the uptake of bound palmitate by rat hepatocytes to its uptake by polyethylene using beta-lactoglobulin (BLG) as the binding protein. The experiments were designed to supply a direct measure of the protein-dependent change in the diffusive conductance of extracellular fluid without determining the diffusion coefficients for free and bound fatty acid or the off-rate constant for protein binding. Rate-limiting dissociation in the stirred phase of extracellular fluid was excluded. The results obtained with BLG are strikingly similar to those previously obtained with albumin and provide additional circumstantial evidence that when the free fraction is small, palmitate uptake is partially driven by the concentration of bound fatty acid. Because this phenomenon is not specific for the binding protein, it may reflect direct exchange of ligand between the binding protein in extracellular fluid and the putative transport protein in the hepatocyte plasma membrane.

Animals↗

PubMed2006

[Effects of grape procyanidins on the concentration of intracellular calcium and the proliferation activity of the hepatoma cells].

OBJECTIVE: To investigate the effects of grape procyanidins (GPC) on concentration of intracellular calcium and the proliferation activity of normal hepatic cells and the hepatic cell injuried by alcohol. METHODS: Rat hepatic cells and the cell injuried by alcohol were cultured with different concentration of GPC. The proliferation activity and concentration of intracellular calcium of the hepatic cells were measured by MTT assay and Fura-2 fluorescence methods. RESULTS: (1) The concentration of intracellular calcium of the normal control group and alcohol injury group were (108.26 +/- 14.17) and (651.24 +/- 47.95) nmol/L respectively, and that of both the high and the medium dose GPC groups were lower than the alcohol injury group, all differences are significant (P < 0.05). (2) The concentration of intracellular calcium in the normal hepatic cells treated with GPC is the group with calcium of extracellular fluid > the group free from calcium of extracellular fluid > the normal control group. (3) The proliferation activity of the high and the medium dose GPC group of normal hepatic cell and the cell injuried by alcohol were higher than the normal control group and alcohol injury group, all differences are significant (P < 0.05). CONCLUSION: GPC can raise the intracellular calcium concentration of normal hepatic cell by increasing extracellular fluidca introaffluxion and release from calcium pool, and enhance the proliferation activity of hepatic cells. It also can inhibit the abnormal rise (overload) of intracellular calcium concentration and the proliferation activity injury of hepatic cell induced by alcohol.

Animals↗

PubMed1999

Hormonal control of calcium homeostasis.

Calcium homeostasis in the extracellular fluid is tightly controlled and defended physiologically. Hypercalcemia always represents considerable underlying pathology and occurs when the hormonal control of calcium homeostasis is overwhelmed. The major hormones that are responsible for normal calcium homeostasis are parathyroid hormone and 1,25-dihydroxyvitamin D; these hormones control extracellular fluid calcium on a chronic basis. Over- or underproduction of these hormones or the tumor peptide, parathyroid hormone-related peptide, are the major causes of aberrant extracellular fluid calcium concentrations. These hormonal defense mechanisms are reviewed here.

Animals↗