A simplified method for estimation of the extracellular fluid space.
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The contribution to the extracellular fluid volume (ECV) from plasma volume (PV) and the total interstitial volumes contained in skin ( IFVS ) and skeletal muscle ( IFVM ) has been studied in rats over a wide range of overhydration and dehydration. ECV was measured as the two-hour distribution space for 51Cr-EDTA after nephrectomy while PV was measured with radiolabelled albumin or erythrocytes. Total interstitial volumes in skin and skeletal muscle were calculated from measurement of local interstitial volumes and the amount of skin and skeletal muscle in the rat. In control conditions ECV was on average 24.12 ml/100 g body weight. PV was 11.0% of ECV in control while IFVS and IFVM was 28.1% and 19.0% respectively. In dehydration the change in PV was 13.3% of the change in ECV, while the change in IFVS and IFVM was 30.0% and 21.0% of the change in ECV respectively. In overhydration (ECV on average 33.76 ml/100 g rat) the changes in PV, IFVS and IFVM were 7.5%, 22.1% and 17.2% of the change in ECV respectively. The regression coefficients describing the change between ECV and IFVS and IFVM were not significantly different in overhydration and dehydration while the regression coefficient between ECV and PV in overhydration was significantly less than the regression coefficient in dehydration. Thus, the fraction of ECV contained in skin and skeletal muscle is similar over the range of hydration studied. The fraction of ECV located in plasma is similar in control and dehydration, while in overhydration less of ECV is localized in plasma.(ABSTRACT TRUNCATED AT 250 WORDS)
The extracellular fluid space in dog bone has been examined using a series of isotopically labelled compounds. Sodium-77 bromide and indium-113m ethylenediaminetetracetic acid were used as extracellular fluid space markers, radioactive water as a total fluid space marker, and potassium-43 chloride to examine the existence of a bone membrane. The clearance of each tracer from bone was monitored for a period of 2h post-injection. Graphical analysis of the clearance curves shows that the number of exponential functions vary depending on the type of tracer used. The fact that a sum of three exponential terms can completely describe each curve indicates that a simple model consisting of three compartments is sufficient to approximate the clearance of these tracers from bone and its associated fluid space. It is concluded that bone consists of an extracellular fluid space, and that this space may well play an important part in the transference of solutes and the mechanisms involved in their localization on the hydroxyapatite crystals of bone.
1. The effects of pentobarbitone sodium (Nembutal) anaesthesia in dogs on extracellular fluid and plasma volumes, plasma protein concentration, haematocrit and extracellular fluid electrolyte composition were measured.2. Induction of pentobarbitone anaesthesia caused a rapid rise in extracellular fluid volume, accompanied by decreases in the haematocrit, in extracellular fluid potassium concentration, and in plasma calcium, magnesium, and protein concentrations. There were no significant changes in plasma osmolality and extracellular fluid concentrations of sodium and chloride.3. Extracellular fluid volume did not alter significantly during six hours of anaesthesia, but the haematocrit and extracellular fluid potassium concentration showed an increase towards control values.4. The relevance of these findings to the interpretation of experiments carried out under pentobarbitone anaesthesia is noted.
Twenty-three patients undergoing transurethral resection of the prostate (TURP) under spinal anesthesia were studied. The irrigating fluid widely used in Japan is a hypo-osmolar solution with 3% sorbitol (Uromatic S, 170 mOsm.kgH2O-1, Baxter). The blood loss and the distribution of the irrigating fluid absorbed were computed from serum osmolality, blood urea nitrogen, and hematocrit using the equation we had formulated. The blood loss, the total fluid absorbed (ABS), and the volumes distributed to intracellular space (delta ICF) and extracellular space (delta ECF) were 419 +/- 677 ml, 1,582 +/- 1,446 ml, 384 +/- 348 ml and 778 +/- 1,279 ml (mean+/-SD), respectively. The correlation coefficient of delta OSM (difference between pre- and post-surgical serum osmolality) vs ABS and that of delta OSM vs delta ICF were high (0.98, 0.98) but that of delta Na (difference between pre- and postsurgical serum sodium) vs ABS was low (0.56). The linear regression equations of ABS vs delta OSM and delta ICF vs delta OSM were ABS (L) = 0.362 x delta OSM and delta ICF (L) = 0.088 x delta OSM, respectively. These equations means that one mOsm.kgH2O-1 reduction of the serum osmolality is the result of 362 ml of irrigating fluid absorbed, 88 ml of which shifting into the intracellular space.
Extracellular fluid levels of the neurotoxin quinolinic acid in the corpus striatum of rats, measured by in vivo microdialysis, were increased in a dose-dependent manner following the intraperitoneal administration of tryptophan. The lowest dose of tryptophan (12.5 mg/kg), equivalent to about 5% of the normal daily intake, increased peak quinolinic acid levels nearly 3-fold. At higher doses of tryptophan (up to 250 mg/kg), concentrations of quinolinic acid increased over 200-fold and exceeded potentially neurotoxic levels (10 microM). In contrast, the increase in extracellular serotonin following even the highest tryptophan dose was small (less than 2-fold). These data indicate that quinolinic acid is present in the extracellular fluid where it may function as a neuromodulator and that it is very responsive to physiological changes in precursor availability.
The viscosity of plasma and extracellular fluid has been shown to be a regulator of lipoprotein production both in cultured hepatocytes and in vivo. The possibility that this extracellular effect on cell function involves modulation of cell surface membrane components was examined. In the present work, we studied the effect of medium viscosity on liver cell gangliosides known to be involved in various membrane functions and to be located predominantly at the cell surface membrane. Cultivation of isolated hepatocytes as primary cultures markedly reduced the ganglioside content, but this reduction process was attenuated by increasing the viscosity of the culture medium. Elevation of extracellular fluid viscosity inhibited the degradation of the cell gangliosides and secretion of lysosomal enzymes involved in ganglioside degradation. The cellular activity of these enzymes as well as the activity of enzymes involved in ganglioside synthesis, CMP-NANA:GM1 sialyltransferase, CMP-NANAP:GM3 sialyltransferase and UDP-galactose:GD2 galactosyltransferase, were not affected by modulation of the extracellular medium viscosity. It is proposed that the modulation of cell ganglioside content by extracellular fluid viscosity is due to an effect on enzymes involved in ganglioside catabolism.
Organic acids in unstimulated saliva and extracellular fluids of dental plaques from 12 middle school students were measured by ion-chromatography. The acids in the plaques were analyzed before and 5-10, 30-35, 60-65 minutes after rinsing with 10% sucrose solution. The differences of the acids between the extracellular fluids of resting plaques and unstimulated saliva were significant. In the extracellular fluids of plaques, the concentration of high pK acids, i.e. acetic and propionic acids was higher than that of low pK acids i.e., lactic and formic acids before and after sucrose rinse. The relations of time-dependent changes between the ratio of low pK to high pK acids and pH were observed in the extracellular fluids of plaques after sucrose rinse. No significant difference of lactic acid concentrations was found between the caries-active and caries-free subjects 30-35 minutes after sugar rinse. The concentration of acetic acid was much higher in the extracellular fluids of dental plaque at any time. It is suggested that there may be some relationship between acetic acid and caries process.
Plasma renin activity and extracellular fluid volume were determined in 34 normotensive and in 35 sustained essential hypertensive patients with normal renal function, balanced sodium intake and urinary output. In normotensives, plasma renin activity was negatively correlated to extracellular fluid volume (r = 0.54; p = 0.001). The 95% confidence limits of the normotensive curve was used as nomogram to classify the hypertensive patients into two groups: those (23 cases) that fell within the limits of the normal curve (group I) and those (12 cases) that were below these limits (group II). In comparison with group I, group II was characterized by: (i) similar values for age, blood pressure, inulin clearance and extracellular fluid volume and (ii) significantly but lower values (p less than 0.001) for plasma renin activity with maintenance of the relationship between extracellular fluid volume and renin. The study strongly suggests that (i) the hypertensives of group I had no abnormal regulation of the renin-angiotensin system in comparison with the control subjects and (ii) the hypertensives of group II had an extracellular fluid volume-renin relationship set for lower values of renin.
Changes in extracellular fluid volume and cell membrane transport during hemorrhagic shock and the effects of dexamethasone treatment on these changes were measured. It is well known that prolonged hemorrhagic shock leads to irreversible changes and a progressive decrease in blood pressure despite reinfusion for lost blood. Pharmacologic doses of glucocorticoids provide some protection against these changes. Therefore, one purpose in the present study was to identify possible sites of glucocorticoid action whicy may prevent the irreversible changes from occurring. The extracellular fluid volume in normal control, nontreated dogs in shock, and dexamethasone-treated dogs in shock were measured by a dilution technique, using [35S] sodium sulfate. Cell membrane cation transport capabilities were measured in liver slices, diaphragm slices, and red blood cells taken from normal control, nontreated rats in shock, and dexamethasone-treated rats in shock. The accumulation of radioactivity by the tissues incubated with 22Na served as an indicator of cell membrane ion transport capabilities. The results indicate that in animals subjected to prolonged hemorrhagic shock, there is a fluid shift from the extracellular space into intracellular spaces, reducing blood volume. Cell membranes are damaged and transport mechanisms are altered; therefore, the cells are unable to extrude ions along with water. Dexamethasone treatment was shown to prevent extracellular fluid volumes from decreasing below that amount due to the plasma lost during hemorrhage. Also, it prevented some cell membrane damage and maintained membrane transport mechanisms near normal. In addition, at the onset of dexamethasone injection, blood pressure increased, and urine output was restored.
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