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At least 235 records · Page 13Linked to original sources
PubMed2005

Measuring the size of the extracellular fluid space using bromide, iohexol, and sodium dilution.

There is a need to find methods to assess the size of the extracellular fluid (ECF) volume without involving radioactive tracers. For this purpose, we applied 3 methods for measuring the ECF volume in 10 male volunteers (mean age, 34 yr). Steady-state plasma bromide concentration (control) was compared to the results of kinetic analysis of plasma iohexol and to kinetic analysis of the dilution of serum sodium after IV infusion of 1 L of isotonic mannitol. The volume of distribution of these tracers was used to indicate the ECF volume. The results disclosed statistically significant correlations between the results of all 3 methods, although the average sodium dilution showed 0.7 L lower values than iohexol and 1.4 L lower than bromide. All three methods correlated significantly with body weight. The percentage of the body weight indicated by the methods was 18.3% (3.1%) for sodium, 19.6% (1.0%) for iohexol, and 20.5% (1.1%) for bromide. We conclude that sodium dilution may be performed at bedside but iohexol and bromide showed less intersubject variability. Iohexol simultaneously measures the glomerular filtration rate and should be a viable clinical option if the hospital performs routine assessments of kidney function using this tracer.

Adult↗
PubMed1975

Simultaneous determination of extracellular fluid and total body water. I.

A method for the simultaneous determination of extracellular fluid volume by radiosulfate-35 and total body water by tritiated water is described. Protein was precipitated from plasma with 10 per cent trichloroacetic acid. Radiosulfate-35 and tritiated water were counted in a dual-channel liquid scintillation spectrometer, using an automatic external standard to correct for quench. The sulfate space was calculated by the isotope dilution principle. Crossover counts contributed by radiosulfate-35 into the tritium channel were subtracted from the total counts in that channel. The tritiated water space was then calculated by the isotope dilution principle. Studies were performed in vitro and in 8 bilaterally nephrectomized rats. In vitro extracellular space by radiosulfate-35 and total body water by tritiated water demonstrated less than 3 per cent variation from the predicted volumes. In the rat, total body water determined with tritiated water demonstrated 4 per cent variation from that determined by desiccation. The method is simple, accurate, reproducible, and readily applicable for use in man and animals.

Animals↗
PubMed1983

Effects of respiratory and (isocapnic) metabolic arterial acid-base disturbances on medullary extracellular fluid pH and ventilation in cats.

Ventilation is influenced by the brain extracellular fluid (ecf) pH which is sensed by the central chemoreceptors. In the present experiments we have investigated to what extent ventilatory effects of brain ecf pH changes depend on the origin of these pH changes. With this aim we have compared the effects of 'respiratory' (via changes in PaCO2) and 'metabolic' (via isocapnic pHa changes) ecf pH changes on steady state ventilatory activity. Experiments were performed in anaesthetized (both artificially ventilated and spontaneously breathing) cats with cut sinus nerves; medullary surface ecf pH was measured with a glass electrode with a flat pH-sensitive surface. We found that ecf pH changes caused by changes in PaCO2 give rise to greater ventilatory responses than the same ecf pH changes caused by (isocapnic) changes in pHa. Moreover, within the pH ranges measured, isocapnic pHecf-ventilatory response lines at higher PaCO2 are shifted upwards compared with those at lower PaCO2 levels. It was concluded that with the present technique it is impossible to show a unique relation between ecf pH and ventilation.

Acid-Base Imbalance↗
PubMed1985

Extracellular fluid deficit following operation and its correction with Ringer's lactate. A reassessment.

The changes in extracellular fluid volume (ECV) in two groups of surgical patients, one receiving Ringer's lactate solution intraoperatively and the other receiving only dextrose and water, were assessed. A deficit in the ECV, as measured by radioactive sulfate, of 1.9 +/- 0.8 l (p less than 0.003) compared to the preoperative volume was found in the dextrose group. This was accompanied by a decrease in the mean creatinine clearance (-13% p less than 0.01), the mean urinary sodium excretion (-57% p less than 0.05), and the mean rate of clearance of the sulfate tracer (-18% p less than 0.01). The use of intraoperative Ringer's lactate (1660 cc +/- 96 cc) resulted in no change in the ECV, an increase in the mean creatinine clearance (+10% p less than 0.05), and no change in sodium excretion or tracer clearance. As a result of these findings, it appears that postoperative sodium retention is a physiologic response to a decreased ECV, which can be prevented by the administration of Ringer's lactate.

Adult↗
PubMed2005

Extracellular fluid S100B in the injured brain: a future surrogate marker of acute brain injury?

The authors describe the measurement of S100B protein in brain extracellular fluid (ECF) of patients with acute brain injury (traumatic brain injury and subarachnoid haemorrhage) using the technique of microdialysis. To our knowledge, this is the first report of S100B measurement in the human brain. Acute Brain Injury (ABI) is a leading cause of death and disability and the need for a practical and sensitive biochemical marker for monitoring these patients is urgent. The calcium binding astrocyte protein, S100B, may be a candidate for this role. Previous serum studies have shown S100B to be a sensitive predictor of mortality and rise in intracranial pressure in ABI, but it has never before been measured directly within the brain. The ECF reflects the local biochemistry of the brain parenchyma, and the use of intracerebral microdialysis opens up the possibility of studying many novel surrogate markers of injury in the laboratory, in addition to the conventional markers it measures at the bedside (lactate, pyruvate, glucose, and glycerol). In this preliminary report of two cases, the authors demonstrate the quantification of S100B in ECF microdialysate, and investigate whether changes in hourly S100B profile can be related to secondary brain injury. It is shown that extracellular concentrations of S100B change markedly in response to secondary brain injury. Further investigation is required to determine whether extracellular S100B measurement in ABI could assist in patient management.

Adult↗
PubMed2007

Oral L-glutamine increases GABA levels in striatal tissue and extracellular fluid.

We explored the possibility that circulating glutamine affects gamma-aminobutyric acid (GABA) levels in rat striatal tissue and GABA concentrations in striatal extracellular fluid (ECF). Striatal microdialysates, each collected over a 20 min interval, were obtained after no treatment, oral L-glutamine (0.5 g/kg), or glutamine followed by NMDA (administered via the microdialysis probe). GABA concentrations were measured by HPLC using a stable OPA/sulfite precolumn derivatization and an electrochemical detection method. L-Glutamine administration significantly increased ECF GABA concentrations by 30%, and enhanced the response evoked by NMDA alone (70%) to 120% over baseline (all P<0.05). Striatal GABA levels increased significantly 2.5 h after oral L-glutamine (e.g., from 1.76 +/- 0.04 micromol/g in vehicle-treated rats to 2.00 +/- 0.15 micromol/g in those receiving 2.0 g/kg of glutamine). Striatal glutamine levels also increased significantly, but not those of glutamate. These data suggest that GABA synthesis in, and release from, rat striatum may be regulated in part by circulating glutamine. Hence, glutamine administration may provide a useful adjunct for treating disorders (e.g., anxiety, seizures) when enhanced GABAergic transmission is desired. Moreover, the elevation in plasma and brain glutamine associated with hepatic failure may, by increasing brain GABA release, produce some of the manifestations of hepatic encephalopathy.

Administration, Oral↗