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Results for “EXTRACELLULAR FLUID”

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PubMed1990

Regulation of expression of a baculovirus ecdysteroid UDPglucosyltransferase gene.

The Autographa californica nuclear polyhedrosis virus egt gene encodes an ecdysteroid UDPglucosyltransferase which catalyzes the transfer of glucose from UDPglucose to ecdysteroid insect molting hormones. Expression of this gene allows the virus to block molting and pupation of infected insect larvae. In this study, we present the nucleotide sequence of the A. californica nuclear polyhedrosis virus egt gene and characterize egt gene expression at the transcriptional and translational levels. egt was transcribed as two 5'-coterminal mRNAs early in infection. Transferase activity was detected in infected cells and in the extracellular fluid by 3 h after infection. The majority of the activity accumulated in the extracellular fluid. We show that the egt gene product is a 60-kilodalton protein which is secreted from the infected cell. The egt gene is located in a region of the A. californica nuclear polyhedrosis virus genome which exhibited hypervariability in serially passaged virus stocks. Nucleotide sequence analysis revealed that the most common deletion occurring in these serially passaged virus isolates is located in the egt gene.

Amino Acid Sequence↗

PubMed1997

Turning off the signal: mechanisms that attenuate signaling by G protein-coupled receptors.

Cellular responses to agonists of G protein-coupled receptors are rapidly attenuated. Mechanisms of signal attenuation include ligand removal from the extracellular fluid and receptor desensitization, endocytosis, and downregulation. Cell surface peptidases degrade neuropeptides in the extracellular fluid and thereby terminate their biological actions. G protein receptor kinases and second messenger kinases phosphorylate receptors, permit interaction with arrestins, and thus uncouple receptors from G proteins to mediate desensitization. Agonist-induced receptor endocytosis contributes to desensitization by depleting the cell surface of high-affinity receptors, while recycling of internalized receptors mediates resensitization of cellular responses. Receptor downregulation is a form of desensitization that occurs during continuous, long-term exposure of cells to receptor agonists. Downregulation is characterized by the depletion of the cellular receptor content due to alterations in the rate of receptor degradation and synthesis. These regulatory mechanisms are important, for they govern the ability of cells to respond to agonists.

Animals↗

PubMed2005

Essentials in the diagnosis of acid-base disorders and their high altitude application.

This report describes the historical development in the clinical application of chemical variables for the interpretation of acid-base disturbances. The pH concept was already introduced in 1909. Following World War II, disagreements concerning the definition of acids and bases occurred, and since then two strategies have been competing. Danish scientists in 1923 defined an acid as a substance able to give off a proton at a given pH, and a base as a substance that could bind a proton, whereas the North American Singer-Hasting school in 1948 defined acids as strong non-buffer anions and bases as non-buffer cations. As a consequence of this last definition, electrolyte disturbances were mixed up with real acid-base disorders and the variable, strong ion difference (SID), was introduced as a measure of non-respiratory acid-base disturbances. However, the SID concept is only an empirical approximation. In contrast, the Astrup/Siggaard-Andersen school of scientists, using computer strategies and the Acid-base Chart, has made diagnosis of acid-base disorders possible at a glance on the Chart, when the data are considered in context with the clinical development. Siggaard-Andersen introduced Base Excess (BE) or Standard Base Excess (SBE) in the extracellular fluid volume (ECF), extended to include the red cell volume (eECF), as a measure of metabolic acid-base disturbances and recently replaced it by the term Concentration of Titratable Hydrogen Ion (ctH). These two concepts (SBE and ctH) represent the same concentration difference, but with opposite signs. Three charts modified from the Siggaard-Andersen Acid-Base Chart are presented for use at low, medium and high altitudes of 2500 m, 3500 m, and 4000 m, respectively. In this context, the authors suggest the use of Titratable Hydrogen Ion concentration Difference (THID) in the extended extracellular fluid volume, finding it efficient and better than any other determination of the metabolic component in acid-base disturbances. The essential variable is the hydrogen ion.

Acclimatization↗

PubMed2004

Regulation of epithelial ion transport by aldosterone through changes in gene expression.

The year 2003 marks the 50th year since the unfolding of the chemical structures of both aldosterone and DNA. Since the recognition in the early 1960's that aldosterone and its cousin cortisol act through DNA binding proteins that alter gene transcription, research on these corticosteroid hormones and their receptors has attracted fervent attention, both for their importance in endocrine physiology, and as model systems for understanding gene regulation. Recently, aldosterone has emerged as arguably the single most important physiological regulator of extracellular fluid volume and blood pressure in mammals, and has been implicated in a variety of disease states in humans. Moreover, its principal receptor, the mineralocorticoid receptor is increasingly recognized as an important therapeutic target for the treatment of hypertension and congestive heart failure, as well as an important model system for understanding aspects of gene regulation. This increased insight into the functional and pathophysiologic importance of aldosterone has been accompanied by increased insight into its cellular and molecular mechanisms of action. Aldosterone acts in a variety of epithelial and non-epithelial tissues to influence extracellular fluid volume, blood pressure, salt appetite, and can under the appropriate conditions cause cardiac fibrosis. This review will address the current view of aldosterone's molecular mechanism of action in epithelia focusing primarily on the classical MR and on a particular MR target gene, SGK1.

Aldosterone↗

PubMed1999

KA-672 inhibits rat brain acetylcholinesterase in vitro but not in vivo.

KA-672, a lipophilic benzopyranone derivative which is currently under development as a cognitive enhancer and antidementia drug, has previously been shown to have facilitatory effects on learning and memory in rats at doses of 0.1-1 mg/kg. We now report that KA-672 inhibited the activity of acetylcholinesterase (AChE), measured in vitro in rat brain cortical homogenate, with an IC50 value of 0.36 microM indicating that KA-672 may improve cognitive functions as a consequence of AChE inhibition. However, when we employed the microdialysis procedure to monitor acetylcholine (ACh) release from rat hippocampus, no effect of KA-672 (0.1-10 mg/kg) was found, indicating a lack of inhibition of brain AChE under in vivo-conditions. [14C]-labelled KA-672 was found to easily penetrate the blood-brain barrier, and an apparent concentration of 0.22 nmol/g brain (equivalent to 0.39 microM tissue concentration) was calculated following an i.p. injection of 1 mg/kg KA-672. However, no labelled substance could be detected in hippocampal microdialysates or in cerebrospinal fluid (CSF) taken from the cisterna magna, indicating that the concentration of KA-672 in brain extracellular fluid must have been below 0.01 microM. We conclude that KA-672 is a potent AChE inhibitor, an activity which, however, does not contribute to its behavioural effects in vivo because the lipophilic drug does not reach sufficient concentrations in the extracellular fluid, apparently due to cellular sequestration.

Acetylcholine↗

PubMed1994

Bone lining cells of the mammalian cochlea.

It is generally believed that all bone surfaces are covered by a nearly continuous layer of cells known as bone lining cells (BLC) which separate the general extracellular fluid (GECF) from bone and its fluid compartment. Within the cochlea of some mammals regions of bone matrix are exposed to extracellular fluid. Within the scalae of the cochlea, perilymph is in contact with bone matrix; there is no evidence of a lining endothelium. Within the modiolus and subjacent to the spiral ligament, bone matrix is in contact with GECF. These findings may have importance in understanding calcium homeostasis within the scalae and may relate to the pathophysiology of labyrinthitis ossificans. Additionally, since BLCs probably represent a specific phenotype, the presence of a pure population of BLCs within the scalae may provide a source for the development of a pure culture of this cell.

Animals↗

PubMed1992

Multi-frequency bioelectrical impedance augments the diagnosis and management of lymphoedema in post-mastectomy patients.

The value of multiple frequency bioelectric impedence analysis (MFBIA) in the monitoring and management of post-mastectomy lymphoedema of the arm was evaluated in 15 patients and controls. The technique was found to produce quantitative agreement with a clinical diagnosis of lymphoedema and with the currently-used measure (limb volume calculated from circumferential measurements) of limb size. The significance of this finding lies in MFBIA being diagnostically informative: it indicates when an observed change in limb volume is directly, albeit theoretically, attributable to accumulation of extracellular fluid. MFBIA potentially offers the means for earlier definitive diagnosis and more-accurate monitoring of extracellular fluid changes during and after treatment.

Adult↗

PubMed1990

[Studies on intracellular kinetics of ara-C triphosphate in HL-60, human leukemia cells in relation to reasonable administration of ara-C].

To study the pharmacokinetics of 1-beta-D-arabinofuranosylcytosine (ara-C), which is one of the main drugs used in chemotherapy for acute leukemia, its intracellular metabolism was investigated using HL-60 cells derived from human acute non-lymphocytic leukemia. The concentration of the drug and its metabolites in the cells were serially determined and the following results were obtained. 1) The uptake of ara-C into HL-60 cell (1 X 10(7)/ml) was very rapid when they were incubated with 2 microM ara-C. The total intracellular ara-C content per 10(9) cells exceeded the ara-C concentration in the extracellular fluid at about 7 minutes after the start of incubation. It reached about 4 times higher than the extracellular concentration after 60 minutes. 2) Conversion of ara-C to the active form, ara-CTP, was also rapid. The intracellular concentration of ara-CTP was about 3 times higher than the ara-C concentration in the extracellular fluid after incubation for 60 minutes. 3) Total accumulation of ara-C in the cells was dependent on the extracellular ara-C concentration up to a concentration of 100 microM. The production of ara-CTP occurred in such a way that, when the extracellular ara-C concentration was lower than 10 microM, more than 90% of the uptake of ara-C was converted to ara-CTP, while at concentrations above 10 microM the efficiency at production (the ratio of total ara-C to ara-CTP production) was decreased. The maximum intracellular ara-CTP concentration was estimated to reach to 45 microM.(ABSTRACT TRUNCATED AT 250 WORDS)

Arabinofuranosylcytosine Triphosphate↗

PubMed2001

A microdialysis study of the novel antiepileptic drug levetiracetam: extracellular pharmacokinetics and effect on taurine in rat brain.

Using a rat model which allows serial blood sampling and concurrent brain microdialysis sampling, we have investigated the temporal kinetic inter-relationship of levetiracetam in serum and brain extracellular fluid (frontal cortex and hippocampus) following systemic administration of levetiracetam, a new antiepileptic drug. Concurrent extracellular amino acid concentrations were also determined. After administration (40 or 80 mg kg(-1)), levetiracetam rapidly appeared in both serum (T(max), 0.4 - 0.7 h) and extracellular fluid (T(max), 2.0 - 2.5 h) and concentrations rose linearly and dose-dependently, suggesting that transport across the blood-brain barrier is rapid and not rate-limiting. The serum free fraction (free/total serum concentration ratio; mean+/-s.e.mean range 0.93 - 1.05) was independent of concentration and confirms that levetiracetam is not bound to blood proteins. The kinetic profiles for the hippocampus and frontal cortex were indistinguishable suggesting that levetiracetam distribution in the brain is not brain region specific. However, t(1/2) values were significantly larger than those for serum (mean range, 3.0 - 3.3 h vs 2.1 - 2.3 h) and concentrations did not attain equilibrium with respect to serum. Levetiracetam (80 mg kg(-1)) was associated with a significant reduction in taurine in the hippocampus and frontal cortex. Other amino acids were unaffected by levetiracetam. Levetiracetam readily and rapidly enters the brain without regional specificity. Its prolonged efflux from and slow equilibration within the brain may explain, in part, its long duration of action. The concurrent changes in taurine may contribute to its mechanism of action.

Amino Acids↗

PubMed2006

Effect of various diuretic treatments on rosiglitazone-induced fluid retention.

The efficacy of diuretics in the management of rosiglitazone (RSG)-induced fluid retention was evaluated in a multicenter, randomized, open-label, parallel-group, proof-of-concept study. Of 381 patients who had type 2 diabetes and were on treatment with sulfonylurea or sulfonylurea plus metformin, 260 (63% male, 37% female) showed evidence of volume expansion as defined by an absolute reduction in hematocrit (Hct) of > or =0.5% after 12 wk of rosiglitazone 4 mg twice daily. They were randomly assigned to five treatments for 7 d: (1) Continuation of RSG (RSG-C), (2) RSG + furosemide (RSG+FRUS), (3) RSG + hydrochlorothiazide (RSG+HCTZ), (4) RSG + spironolactone (RSG+SPIRO), and (5) discontinuation of RSG. The primary end point was change in Hct at day 7 of diuretic treatment phase, powered to compare each diuretic group and the RSG discontinuation with the control group of RSG-C, with adjustments for multiple testing. After 12 wk on RSG, Hct fell by mean of 2.92% (95% confidence interval [CI] -3.10 to -2.63%; P < 0.001) and extracellular fluid volume increased by 0.62 L/1.73 m(2) (95% CI 0.26 to 0.90 L/1.73 m(2); P < 0.001). After treatment, the RSG+SPIRO group only showed a mean increase in Hct of 0.24%. The estimated mean difference in Hct reduction was significant: 1.14% (95% CI 0.29 to 1.98%) for RSG+SPIRO (P = 0.004) and 0.87% (95% CI 0.03 to 1.71%) for RSG+HCTZ (P = 0.041) only. In additional analyses of between-diuretic treatment effects SPIRO induced a greater Hct rescue at 0.88% (95% CI -0.12 to 1.87%; P = 0.095) and extracellular fluid volume reduction of -0.75 L/1.73 m(2) (95% CI -1.52 to 0.03 L/1.73 m(2); P = 0.06) compared with FRUS, suggesting superiority in the management of RSG-associated fluid retention. There were no significant differences between SPIRO and HCTZ. These findings are consistent with peroxisome proliferator-activated receptor-gamma agonist activation of the epithelial sodium channel in the distal collecting duct, a site of action of SPIRO and a potential target for thiazide diuretics.

Adult↗

PubMed1983

Fluid therapy for alimentary disease: origins and objectives.

Fluid therapy took nearly a century to gain acceptance in human medicine, despite excellent early work demonstrating its rationale and its effectiveness. Progress in veterinary fluid therapy lagged behind, partly because of skepticism and partly because of real practical difficulties. From the earliest to the most recent developments, human cholera has provided the impetus for much of the progress in fluid therapy. The challenge of treating such a severe diarrhoea in primitive surroundings with severe limits on cost and supervision has led to the emergence of oral fluid therapy as the prime technique. It is not simply an alternative to parenteral treatment but, in most cases, a superior approach relating more directly to the underlying problem--electrolyte malabsorption. Similar principles can be applied to other forms of diarrhoea and in various species. The example is clear for those concerned with veterinary fluid therapy. Repair of extracellular fluid volume is the key objective in all forms of fluid therapy; oral hydration offers not only a practicable way of achieving this in farm animals but one with the potential for outstanding clinical and economic success.

Animals↗

PubMed2006

Role of striatal L-DOPA in the production of dyskinesia in 6-hydroxydopamine lesioned rats.

We explored possible differences in the peripheral and central pharmacokinetics of L-DOPA as a basis for individual variation in the liability to dyskinesia. Unilaterally, 6-hydroxydopamine (6-OHDA) lesioned rats were treated chronically with L-DOPA for an induction and monitoring of abnormal involuntary movements (AIMs). Comparisons between dyskinetic and non-dyskinetic cases were then carried out with regard to plasma and striatal L-DOPA concentrations, tissue levels of dopamine (DA), DA metabolites, and serotonin. After a single intraperitoneal injection of L-DOPA, plasma L-DOPA concentrations did not differ between dyskinetic and non-dyskinetic animals, whereas peak levels of L-DOPA in the striatal extracellular fluid were about fivefold larger in the former compared with the latter group. Interestingly, the time course of the AIMs paralleled the surge in striatal L-DOPA levels. Intrastriatal infusion of L-DOPA by reverse dialysis concentration dependently induced AIMs in all 6-OHDA lesioned rats, regardless of a previous priming for dyskinesia. Steady-state levels of DA and its metabolites in striatal and cortical tissue did not differ between dyskinetic and non-dyskinetic animals, indicating that the observed difference in motor response to L-DOPA did not depend on the extent of lesion-induced DA depletion. These results show that an elevation of L-DOPA levels in the striatal extracellular fluid is necessary and sufficient for the occurrence of dyskinesia. Individual differences in the central bioavailability of L-DOPA may provide a clue to the varying susceptibility to dyskinesia in Parkinson's disease.

Animals↗

PubMed1993

Gadolinium-DTPA enhanced MRI demonstrates uterine vascular changes associated with artificially induced decidualization and ovoimplantation in rats.

Gadolinium-DTPA enhanced magnetic resonance (MR) imaging has been used to demonstrate uterine vascular changes during ovoimplantation and artificially induced decidualization in rats. Evans blue dye and Gd-DTPA were injected i.v. into rats 10 h after unilateral decidualization was induced by injection of sesame oil into the lumen of one uterine horn. Animals were killed various times later and uteri were removed, T1-weighted proton imaging was performed, and mean image intensities for stimulated and control uterine horns were calculated by computer-assisted image analysis. Macroscopic bluing confined to stimulated horns was apparent 5 min after tracer injection and increased in intensity until the experiment was terminated at 320 min. Analysis of MR images showed that mean image intensity of control horns did not change significantly at any time after injection of the Gd-DTPA and Evans blue whereas mean image intensity of stimulated horns increased significantly by 5 min after injection, peaked at 20 min, and returned to values not different from controls by 320 min. T1-weighted images of day 6 pregnant rats injected with Gd-DTPA and Evans blue revealed patterns of image enhancement that matched those of macroscopic bluing. Uterine concentrations of radioactivity after injection of 153Gd-DTPA indicated that increased extracellular fluid volume (ECFV) produces the image enhancement of stimulated horns since the tracer permeates the extracellular fluid of both horns. Gd-DTPA-enhanced MR imaging of uteri after deciduogenic stimulation revealed significant image enhancement for stimulated horns at both 9 and 27 h after stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1988

Tyrosine: effects on catecholamine release.

Tyrosine administration elevates striatal levels of dopamine metabolites in animals given treatments that accelerate nigrostriatal firing, but not in untreated rats. We examined the possibility that the amino acid might actually enhance dopamine release in untreated animals, but that the technique of measuring striatal dopamine metabolism was too insensitive to demonstrate such an effect. Dopamine release was assessed directly, using brain microdialysis of striatal extracellular fluid. Tyrosine administration (50-200 mg/kg IP) did indeed cause a dose related increase in extracellular fluid dopamine levels with minor elevations in levels of DOPAC and HVA, its major metabolites, which were not dose-related. The rise in dopamine was short-lived, suggesting that receptor-mediated feedback mechanisms responded to the increased dopamine release by diminishing neuronal firing or sensitivity to tyrosine. These observations indicate that measurement of changes in striatal DOPAC and HVA, if negative, need not rule out increases in nigrostriatal dopamine release.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1999

Renal function in the AT1A receptor knockout mouse during normal and volume-expanded conditions.

BACKGROUND: Genetically altered mice lacking the AT1A angiotensin II (Ang II) receptor were used to examine the role of AT1A receptors in regulating renal hemodynamics, sodium excretion, glomerulotubular balance, and Ang II levels in plasma and kidney during normal and volume-expanded conditions. METHODS: AT1A receptor-deficient mice and their wild-type controls were anesthetized with inactin and ketamine, and were prepared to allow intravenous infusions of solutions and measurements of aortic pressure and urine collections. Inulin and para-aminohippurate (PAH) solutions were infused intravenously for clearance determinations under conditions of euvolemia (2.5 microliter/min infusion of isotonic saline) or volume-expansion conditions (12.5 microliter/min). After three 30-minute urine collections, blood samples were collected, and kidneys were harvested. Plasma and kidney Ang II measurements were made by radioimmunoassay. RESULTS: In the euvolemic state, mean arterial pressures (MAPs) were significantly lower in the AT1A receptor-deficient mice (68 +/- 4 mm Hg) compared with wild-type controls (89 +/- 3 mm Hg). Despite the lower MAP, the glomerular filtration rate (GFR), renal plasma flow (RPF), absolute sodium excretion, and fractional sodium excretion were not significantly different between wild-type and AT1A-/- mice. Volume expansion did not alter MAP in wild-type mice, but significantly increased MAP in the AT1A-/- mice (68 +/- 4 to 83 +/- 5 mm Hg). Similar increases in GFR, RPF, absolute sodium excretion, and fractional sodium excretion in AT1A+/+ and AT1A-/- mice were observed. Glomerulotubular balance was not disrupted by the absence of AT1A receptors. During euvolemia, plasma Ang II concentrations were significantly higher in the AT1A-/- mice compared with wild-type mice (536 +/- 172 vs. 198 +/- 36 fmol/ml). Although volume expansion had no effect on plasma Ang II levels in the AT1A+/+ group, plasma Ang II concentrations were markedly suppressed in the AT1A-/- mice to levels that were not different from those in wild-type mice. In contrast, kidney tissue Ang II contents were reduced in the AT1A-/- mice and were not significantly altered during volume expansion in either the AT1A-/- or the AT1A+/+ mice. CONCLUSIONS: The absence of AT1A receptors does not impair chronic regulation of renal blood flow, GFR, or glomerulotubular balance. The prompt restoration of MAP following volume expansion suggests that low blood pressure in the AT1A receptor-deficient mice is primarily due to reduced effective plasma and extracellular fluid volume. Normalization of plasma Ang II levels with volume expansion demonstrates a dominant effect of extracellular fluid volume and blood pressure over AT1A receptor-mediated short-loop feedback in the regulation of plasma Ang II levels.

Angiotensin II↗

PubMedDate not supplied

The influence of dialysate sodium and variable ultrafiltration on fluid balance during hemodialysis.

An important factor in the development of hypotension during hemodialysis (HD) is a decrease in blood volume, due to ultrafiltration (UF) and an insufficient refill of the intravascular compartment. This insufficient refill might be caused by a transcellular fluid shift from the extracellular to the intracellular compartment. We studied the influence of dialysate sodium concentration and UF rate on the refill rate, blood volume, intracellular (ICV) and extracellular fluid volume (ECV). Three different HD strategies were studied in 15 patients: (A) conventional HD (dialysate sodium 140 mmol/L); (B) HD with a sodium profile (140-148 mmol/L); and (C) HD with a sodium profile and a variable UF rate (high-low UF rate). ICV and ECV were measured by non-invasive conductivity measurements, blood volume was calculated from erythrocyte counts before and after treatment. Blood volume decrease was most pronounced during conventional HD, due to insufficient refilling without a detectable transcellular fluid shift. The sum of the decrease in ICV and EVC was less than during (B) and (C). The insufficient refill led to a higher prevalence of hypotension and cramps. The strategies (B) and (C) led to an significant and comparable transcellular fluid shift to the extracellular compartment. Thus, the use of a sodium profile led to a better intravascular refill and clinical tolerance of HD. Addition of a UF profile did not improve this any further.

Blood Volume↗

PubMed1995

Increased dopamine and norepinephrine release in medial prefrontal cortex induced by acute and chronic stress: effects of diazepam.

We have examined the effects of diazepam on the stress-induced increase in extracellular dopamine and norepinephrine in the medial prefrontal cortex using in vivo microdialysis. In naive rats, acute tail pressure (30 min) elicited an increase in the concentrations of dopamine and norepinephrine in extracellular fluid of medial prefrontal cortex (+54 and +50%, respectively). Diazepam (2.5 mg/kg, i.p.) decreased the basal concentration of extracellular dopamine and norepinephrine. Diazepam also attenuated the stress-evoked increase in the absolute concentrations of extracellular dopamine (+17%), but did not alter the stress-induced increase in norepinephrine (+41%). However, when the drug-induced decrease in basal dopamine and norepinephrine concentration was taken into account, the stress-induced net increase in dopamine above the new baseline was equivalent to that obtained in vehicle pretreated rats, whereas the net increase in norepinephrine was almost twice that obtained in control subjects. In rats previously exposed to chronic cold (three to four weeks at 5 degrees C), tail pressure again produced an increase in the concentrations of dopamine and norepinephrine in the medial prefrontal cortex (+42% and +92%, respectively). However, in these chronically stressed rats, diazepam no longer decreased basal dopamine or norepinephrine in extracellular fluid, nor did it affect the stress-induced increase in the concentrations of these catecholamines. These data indicate that diazepam has complex effects on the extracellular concentrations of dopamine and norepinephrine which vary depending upon whether the rat is undisturbed or stressed during the period of drug exposure as well as the rat's prior history of exposure to stress. Moreover, these data raise questions regarding the role of catecholamines in the mechanism by which diazepam exerts its anxiolytic properties.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1985

[Behavior of renal filtration performance in the massive intraoperative administration of crystalloid solutions].

Renal function of 12 adult patients was studied pre- and postoperatively using tracer techniques in a black-box model. Chrom 51 EDTA was employed to determine extracellular fluid volume and glomerular filtration rate, Iodine 125-albumin to measure plasma volume. These patients who received during two 4-h periods pre- and postoperatively 3 ml/kg/h of a salt-sugar solution had a significantly increased extracellular fluid volume postoperatively. Glomerular filtration rate was also increased, plasma volume was significantly reduced and colloidosmotic pressure in spite of attempts to supplement albumin solution intraoperatively was found to be postoperatively reduced. Hemodynamic parameters were virtually unchanged postoperatively with the exception of a small but significant increase of cardiac index. It is concluded, that these patients who received 12 ml/kg/h of crystalloid solutions apart from colloid replacement of measured bloodloss intraoperatively through natural regulation were about to excrete this extra amount of fluid, which had been relocated in the extracellular space. This regime, however, might help to decrease the rate of oliguric perioperative renal function failure, which has a high mortality.

Adult↗