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At least 145 records · Page 8Linked to original sources
PubMed1998

Measurements of extracellular fluid volume in highly perfused organs and lung water in hypo- and hypervolaemic dogs.

The purpose of this study was to identify whether the central extracellular fluid volume status following hypo- and hypervolaemia can be measured by the initial distribution volume of glucose or by the extravascular lung water. These two estimates were compared with the initial distribution volume of sucrose which has been used as an indicator for the measurement of the extracellular fluid volume. The above three estimates were determined by the administration of glucose, chilled saline and sucrose solutions, before and after haemorrhage (30 mL kg-1), and subsequent fluid load (lactated Ringer's solution 90 mL kg-1). The distribution volumes of glucose and sucrose decreased after haemorrhage and increased after fluid load compared with normovolaemic values, and a linear correlation was obtained between these two distribution volumes (r = 0.93, P < 0.001, n = 36). However, the extravascular lung water remained statistically unchanged throughout the procedure, despite a weak linear correlation with the sucrose distribution volume (r = 0.38, n = 33, P < 0.05). These results indicate that the initial distribution volume of glucose is more useful as an indicator of the central extracellular fluid volume status than the extravascular lung water.

Animals↗
PubMedDate not supplied

[Possibilities of assessment of the volume of extracellular fluid in children by integral conductometry].

The aim of this research was to specify M. I. Tischenko's formula (1978) for the estimation of the volume of extracellular liquid on the basis of integral resistance so as to use it in children. Simultaneous assessment of the volume of extracellular fluid by thiosulfate dilution method and registration of the basal integral resistance with data processing helped correct the formula for use in practical pediatrics. The technique of assessment of the volume of extracellular fluid is simple, does not involve intravenous infusions of drugs or blood collection, rapid, and reproducible under any conditions. It may be used for assessment of the volume of extracellular fluid in children with the edematous syndrome associated with renal diseases (acute renal failure, glomerulonephritis), liver diseases, circulatory insufficiency. Repeated studies give valuable information about the state of water-salt metabolism in patients with hyper- or dehydration and help assess the therapy efficacy.

Adolescent↗
PubMedDate not supplied

Effects of short-term strict metabolic control on kidney function and extracellular fluid volume in incipient diabetic nephropathy.

The effects of strict metabolic control (multiple insulin injections for 1 week) on urinary albumin excretion, glomerular filtration rate and extracellular fluid volume was evaluated in long-term Type 1 diabetic patients with (n = 9) and without (n = 10) incipient nephropathy. Investigations were carried out in poor (blood glucose 15 (interquartile range, 13-18) mmol l-1) and good metabolic control (5 (4-8) mmol l-1). In patients with incipient nephropathy glomerular filtration rate was 125 (SD 26) (poor control) vs 125 (20) ml min-1 (good control), urinary albumin excretion 60 (range 37-247) vs 60 (13-359) mg 24 h-1, fractional albumin clearance 6.1 (0.9-67.6) vs 6.7 (2.1-65.4) x 10(-6), extracellular fluid volume 13.4 (2.3) vs 14.3 (2.8) l (p less than 0.10). Apart from an increase in extracellular fluid volume during improved metabolic control (12.2 (1.6) vs 13.6 (2.5) l, p less than 0.02) all the above mentioned variables remained unchanged in the patients with normal urinary albumin excretion. In conclusion, strict metabolic control for 2-7 days has no effect on urinary albumin excretion and glomerular filtration rate in long-term Type 1 diabetic patients with or without incipient diabetic nephropathy.

Adult↗
PubMed1977

Extravascular lung water after extracellular fluid volume expansion in dogs.

We have compared extravascular lung water after extracellular fluid volume expansion with that predicted from lung sucrose space measured in control dogs. In control lungs mean extravascular water:dry weight ratio was 3.81 +/- 0.16 (SD) (n = 5) and extravascular sucrose space/dry weight was 1.79 +/- 0.45 (n = 4). After acute expansion of extracellular fluid volume by 10% of body weight mean extravascular water:dry lung weight was 4.17 +/- 0.27 (m = 5), less than half the predicted increase to 4.63 +/- 0.19, suggesting some degree of protection. After 20% (n = 4), 30% (n = 2), and 40% (n = 1) expansion, no protection was demonstrated and there was considerable scatter of lung water at each infusion volume. When volume expansion increased pulmonary capillary intravascular forces (due to decreased protein osmotic pressure and increased hydrostatic pressure) by more than 20 cmH2O there was a linear increase in extravascular lung water with increasing intravascular forces. Three dogs did not conform to this relationship and had disproportionately large increases in lung water, possibly due to alveolar flooding.

Animals↗
PubMed2002

Microdialysis sampling of carbamazepine, phenytoin and phenobarbital in subcutaneous extracellular fluid and subdural cerebrospinal fluid in humans: an in vitro and in vivo study of adsorption to the sampling device.

The purpose of the study was to determine if binding of the drugs to the sampling equipment during microdialysis would influence the results for carbamazepine, phenytoin and phenobarbital. In vitro experiments with microdialysis catheters and separate parts of catheters were performed to estimate the degree of drug binding to the dialysis equipment. A mathematical model to calculate drug binding and recovery is proposed. In vivo protein unbound carbamazepine concentrations in subcutaneous extracellular fluid at different flow rates (6 patients), unbound carbamazepine (1 patient) and unbound phenobarbital (I patient) in subdural cerebrospinal fluid and subcutaneous extracellular fluid were estimated and the in vivo data were compared to the in vitro results and data generated by the mathematical model. Binding to the soft outlet polyurethane tubing was extensive and variable for phenytoin, which precluded in vivo testing, but limited and more predictable for carbamazepine and phenobarbital. None of the three compounds bound to the hard internaltubing. Phenytoin and phenobarbital did not bind to the dialysis membrane, while a small degree of binding may be present for carbamazepine. In vivo estimates of carbamazepine protein unbound subcutaneous extracellular concentrations by microdialysis, adjusted for binding to the plastic tubing, were 81% of protein unbound plasma concentrations. In single case studies, subdural cerebrospinal fluid and subcutaneous extracellular levels of carbamazepine and phenobarbital were similar and when corrected for binding to the plastic tubings they were also close to protein unbound plasma concentrations. Microdialysis can be used for reliable estimations of protein unbound carbamazepine and possibly phenobarbital concentrations when drug binding to the plastic tubing is considered. Reliable estimation of unbound phenytoin is not possible at present.

Adult↗
PubMedDate not supplied

Renal regulation of extracellular fluid volume and osmolality.

In order for our body cells to function properly, they must be surrounded in extracellular fluid that is relatively constant with regard to osmolality. The kidneys, in concert with neural and endocrine input, regulate the volume and osmolality of the extracellular fluid by altering the amount of sodium and water excreted. This is accomplished primarily through alterations in sodium and water reabsorption, the mechanisms of which differ within each nephron segment.

Absorption↗
PubMed1980

Effect of flow rate and the extracellular fluid volume on proximal urate and water absorption.

The in vivo microperfusion technique was used to examine the effect of variations in tubular flow rate and the extracellular fluid volume onf [2-14C]-urate and water absorption in the proximal tubule of the rat. In nondiuretic animals, fractional urate absorption was highest at the lowest perfusion rate examined and decreased as the rate of perfusion was increased. Increasing the initial concentration of urate in the perfusion solution had no effect on the fractional absorption of urate. Fractional water absorption was also inversely related to the rate of perfusion. Expansion of the extracellular fluid volume with isotonic saline resulted in rates of urate absorption similar to control values at any given microperfusion rate. Fractional water absorption showed the same flow rate dependency pattern observed in control animals, but at a significantly lower rate of absorption. These studies indicate that fractional urate absorption is dependent upon some parameter of tubular flow rate and that the relationship between urate absorption and perfusion rate is not related to the delivered load of urate per se and is not affected by the state of hydration of the extracellular fluid.

Absorption↗
PubMed1969

Effect of expansion of extracellular fluid volume on renal phosphate handling.

To examine the specific effect of extracellular fluid (ECF) volume expansion on phosphate excretion studies were performed in thyroparathyroidectomized dogs receiving saline solution intravenously. The natriuresis resulting from ECF volume expansion was consistently accompanied by an increase in phosphate excretion. The possible role of increased filtered load of phosphate was eliminated in experiments in which the filtered load of phosphate was reduced by acute reduction in the glomerular filtration rate. Despite considerable reductions in filtered phosphate, ECF volume expansion resulted in a consistent increase in phosphate excretion. Furthermore, the possible contribution of alteration in blood composition was investigated in experiments in which saline was infused during thoracic inferior vena cava constriction. In these experiments saline infusion failed to increase sodium or phosphate excretion. Cessation of saline infusion and release of caval constriction resulted in a prompt natriuresis and increased phosphate excretion. It is concluded from these studies that extracellular fluid volume expansion results in an increased phosphate excretion in the parathyroidectomized dog. This effect is the specific consequence of ECF volume expansion and is not due to increase in the filtered load of phosphate or alterations in blood composition.

Animals↗
PubMed1995

Evidence for energy-dependent transport of aluminum out of brain extracellular fluid.

Aluminum (Al) can cause CNS toxicity. The mechanism of its blood-brain barrier (BBB) permeation is poorly understood. In this study, microdialysis was used to determine extracellular fluid (ECF) unbound aluminum distribution between frontal cortex (FC) and blood during steady-state aluminum concentrations. The brain/blood aluminum ratio was determined. Over a 16-fold range of aluminum concentrations (dosed as aluminum citrate), brain/blood aluminum ratios were 0.10-0.15, consistently and significantly < 1. Aluminum diffusion cannot account for these results, suggesting the presence of a carrier that moves aluminum out of brain extracellular fluid. These aluminum brain/blood ratios (BBRs) were not significantly different over the range of concentrations studied, suggesting an inability to saturate the carrier. Brain/blood aluminum ratios obtained with four aluminum-hydroxypyridinones were also significantly < 1 (0.1-0.3), and were generally significantly different among themselves and from the aluminum citrate BBR. Movement of a BBB permeability marker from blood into brain extracellular fluid suggested partial BBB opening. The aluminum BBRs obtained (all << 1), in the presence of a partially opened BBR, suggest an efficient carrier moving aluminum out of brain ECF. Addition of cyanide to the brain microdialysis probe solution significantly increased the Al (citrate) BBR to 1. These results suggest the presence of an efficient, energy-dependent carrier that removes aluminum from brain ECF, either into brain cells or blood.

Aluminum↗
PubMed2003

Effects of hypertonic saline (7.5%) on extracellular fluid volumes in healthy volunteers.

This study evaluated the effects of 7.5% saline on plasma and other extracellular fluid volumes. After baseline measurements, eight healthy postmenopausal female volunteers received 4 ml.kg-1 of hypertonic saline over 30 min. After the fluid infusion, the volunteers were studied for 60 min. Plasma volume was measured using a dilution of 125-iodine-labelled human albumin. Extracellular water and cardiac output were measured by whole body impedence cardiography. The infused volume was 4 ml.kg-1 (average 260 ml). Plasma volume increased rapidly during the infusion (mean +/- standard deviation, 442 +/- 167 ml). At the end of the 1-h follow-up period, plasma volume had increased by on average 465 ml (SD 83). The increase of extracellular water at the end of infusion and at the end of study was 650 ml (SD 93) and 637 ml (SD 192), respectively. The highest serum sodium recorded in the volunteers was 158 mmol.l-1. The effect of 7.5% saline on plasma volume was rapid and lasted for at least 1 h. Plasma volume remained elevated by more than the infused volume at the end of the study. The increase in plasma and extracellular fluid volumes was partly achieved by mobilizing intracellular water to extracellular compartment.

Aged↗
PubMed2002

Can a reduction in extracellular fluid volume result in increased serum albumin in peritoneal dialysis patients?

Serum albumin predicts survival in end-stage renal failure. The literature has emphasized the dependence of albumin on inflammation. We previously proposed an independent relationship with overhydration. To date, there is no proven therapy that increases serum albumin in dialysis patients. We investigated whether decreasing dry weight increases serum albumin in peritoneal dialysis patients. Twenty-one subjects (15 continuous ambulatory peritoneal dialysis patients and 6 continuous cycled peritoneal dialysis patients) were assessed at 0 and 4 weeks. Body weight, blood pressure, 4-site skin-fold thickness, subjective global assessment score, and use of antihypertensive medication were recorded. Fluid samples were collected for estimation of serum albumin, C-reactive protein, and 24-hour dialysate and urine volume. The extracellular fluid volume was estimated by multiple-frequency bioelectric impedance. Between the 0- and 4-week assessments, dialysis prescription was altered to increase the daily ultrafiltrate volume (1.00 +/- 0.71 L to 1.29 +/- 0.75 L; P = 0.04). Significant decreases were seen in body weight (70.7 +/- 12.1 kg to 69.9 +/- 12.2 kg; P = 0.0002), extracellular fluid volume (16.2 +/- 3.3 L to 15.5 +/- 3.2 L; P = 0.0006), systolic blood pressure (147.7 +/- 26.3 mm Hg to 124.2 +/- 20.9 mm Hg; P < 0.0001), diastolic blood pressure (84.2 +/- 14.5 mm Hg to 76.6 +/- 11.7 mm Hg; P = 0.01), and number of antihypertensive drugs (1.9 +/- 1.0 to 1.6 +/- 1.1; P = 0.02). Serum albumin increased (34.6 +/- 4.1 g/L to 35.9 +/- 3.6 g/L; P = 0.01). C-reactive protein did not change. Decreasing dry weight in peritoneal dialysis by an increase in ultrafiltration volume results in a decreased extracellular fluid volume, which is reflected by an improvement in blood pressure control. This improvement in blood pressure was associated with an increase in serum albumin. This finding strengthens the argument that overhydration is a cause of hypoalbuminemia in peritoneal dialysis and offers a therapeutic option in management of this patient group.

Cohort Studies↗
PubMed1996

Amperometric microsensors for monitoring choline in the extracellular fluid of brain.

Selective amperometric enzyme microsensors for monitoring low micromolar concentrations of choline in extracellular fluid of rat brain have been developed. Preparation of the choline microsensors involved the modification of carbon fiber microcylinder electrodes (10 microns diameter, 300-400 microns long) with a cross-linked redox-active gel containing horseradish peroxidase and choline oxidase. Rejection of the noise recorded from the choline microsensors implanted in living brain tissue improved the in vivo detection capabilities of the sensors. The microsensors and a differential detection scheme were used to estimate the basal concentration of choline in striatal tissue at 6.6 +/- 2.9 microM and to measure changes in choline concentrations of 6.1 +/- 2.7 microM in vivo. The microsensors were also used to monitor choline produced following the injections of acetylcholine in vivo. Coinjections of neostigmine and acetylcholine significantly lowered the choline response recorded with the microsensors, confirming that the response following the injections of acetylcholine alone was due to the activity of endogenous acetylcholinesterase. Comparison of the maximal rate of decrease in choline concentration following the injections of 1 mM choline and 1 mM acetylcholine was used to estimate the rate of acetylcholine clearance from extracellular fluid through cholinesterase activity at approx. 2.5 microM/min.

Acetylcholine↗
PubMed1998

Aluminum transport out of brain extracellular fluid is proton dependent and inhibited by mersalyl acid, suggesting mediation by the monocarboxylate transporter (MCT1).

Blood brain barrier transport of aluminum citrate was assessed in rats by microdialysis of the jugular vein as well as the right and left frontal cortices. Previous studies (Allen et al., 1995. Evidence for energy-dependent transport of aluminum out of brain extracellular fluid. Toxicology 92, 193-202; Ackley and Yokel, 1997. Aluminum citrate is transported from brain into blood via the monocarboxylic acid transporter located at the blood-brain barrier. Toxicology 120, 89-97), and the current study, demonstrated that the steady-state brain-to-blood ratio of the unbound extracellular aluminum immediately surrounding the microdialysis probe is less than 1, suggesting the presence of a process other than diffusion across the blood brain barrier. It was speculated that a monocarboxylate transporter at the blood brain barrier was maintaining this ratio at less than 1 (Ackley and Yokel, 1997). Monocarboxylate transporters are proton co-transporters. Decreasing extracellular pH (increasing proton availability) increases monocarboxylate transport. After alkalinizing the dialysate perfusing a brain microdialysis probe (to pH = 10.2), the steady-state aluminum brain-to-blood ratio increased from 0.35 to 0.80. The addition of the proton ionophore, p-(trifluoromethoxy)phenylhydrazone (FCCP) (1 mM), to brain dialysate increased this ratio from 0.21 to 0.61. These increased ratios suggest that a proton-dependent process is removing Al from brain extracellular fluid. The monocarboxylate transporter is the only known proton-dependent transporter at the blood-brain barrier. There are two known isoforms of this transporter in the rodent, MCT1 and MCT2. Organomercurial thiol reagents, such as mersalyl acid, inhibit MCT1 but not MCT2. Mersalyl acid (50 mM) addition to brain dialysate increased the steady-state aluminum brain-to-blood ratio from 0.19 to 0.87, suggesting that MCT1 is at least partially mediating the efflux of aluminum from brain extracellular fluid.

Aluminum↗
PubMed1985

Diffusion coefficients of neurotransmitters and their metabolites in brain extracellular fluid space.

Diffusion coefficients of catecholamine neurotransmitters, their metabolites and related species was measured in brain extracellular fluid using in vivo voltammetric techniques. Nanoliter volumes of the species were pressure-ejected into the rat caudate nucleus and their concentration profiles were determined at nearby voltammetric detector electrodes. Thorough testing was carried out to show that the present methodology gave results which agreed with brain diffusion coefficients measured previously by ion-selective microelectrode techniques. All of the species which are anionic at pH 7.4 have brain diffusion coefficients about one-third of their solution counterparts in accord with earlier studies of diffusion in tortuous media. However, the brain diffusion coefficients of all the cation species are about three-times slower than those of the anions. This phenomenon is believed to be caused by ion binding with the polyanionic glycosaminoglycans and related species in brain tissue. In vitro model experiments lend support to this interpretation. This new information on biogenic amines and their metabolites provides meaningful predictions of the spatio-temporal concentration distribution of these species in the extracellular fluid.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1996

Renal regulation of extracellular fluid volume and osmolality.

In order for our body cells to function properly, they must be surrounded in extracellular fluid that is relatively constant with regard to osmolality. The kidneys, in concert with neural and endocrine input, regulate the volume and osmolality of the extracellular fluid by altering the amount of sodium and water excreted. This is accomplished primarily though alterations in sodium and water reabsorption, the mechanisms of which differ within each nephron segment.

Chlorides↗