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PubMed2005

Segment-specific resistivity improves body fluid volume estimates from bioimpedance spectroscopy in hemodialysis patients.

Discrepancies in body fluid estimates between segmental bioimpedance spectroscopy (SBIS) and gold-standard methods may be due to the use of a uniform value of tissue resistivity to compute extracellular fluid volume (ECV) and intracellular fluid volume (ICV). Discrepancies may also arise from the exclusion of fluid volumes of hands, feet, neck, and head from measurements due to electrode positions. The aim of this study was to define the specific resistivity of various body segments and to use those values for computation of ECV and ICV along with a correction for unmeasured fluid volumes. Twenty-nine maintenance hemodialysis patients (16 men) underwent body composition analysis including whole body MRI, whole body potassium (40K) content, deuterium, and sodium bromide dilution, and segmental and wrist-to-ankle bioimpedance spectroscopy, all performed on the same day before a hemodialysis. Segment-specific resistivity was determined from segmental fat-free mass (FFM; by MRI), hydration status of FFM (by deuterium and sodium bromide), tissue resistance (by SBIS), and segment length. Segmental FFM was higher and extracellular hydration of FFM was lower in men compared with women. Segment-specific resistivity values for arm, trunk, and leg all differed from the uniform resistivity used in traditional SBIS algorithms. Estimates for whole body ECV, ICV, and total body water from SBIS using segmental instead of uniform resistivity values and after adjustment for unmeasured fluid volumes of the body did not differ significantly from gold-standard measures. The uniform tissue resistivity values used in traditional SBIS algorithms result in underestimation of ECV, ICV, and total body water. Use of segmental resistivity values combined with adjustment for body volumes that are neglected by traditional SBIS technique significantly improves estimations of body fluid volume in hemodialysis patients.

Algorithms↗
PubMedDate not supplied

A new technique for the quantification of peripheral edema with application in both unilateral and bilateral cases.

Current noninvasive techniques for the routine and frequent quantification of peripheral lymphedema in patients are total limb volume measurement (by water immersion or by circumferential measurements) and bioelectrical impedance analysis (BIA). However both of these techniques require standardizing the measurement using a contralateral measurement from the unaffected limb. Hence these techniques are essentially restricted to unilateral lymphedema. This paper describes the results from a preliminary study to investigate an alternative approach to the analysis of the data from multiple frequency BIA to produce an index of lymphedema without the need for normalization to another body segment. Twenty patients receiving surgical treatment for breast cancer were monitored prior to surgery and again after diagnosis with unilateral lymphedema. The data recorded were total limb volume, by circumferential measurements; and BIA measurements of both limbs. From these measurements total limb volumes and extracellular fluid volumes were calculated and expressed as ratios of the affected limb to that of the unaffected limb. An index of the ratio of the extracellular fluid volume to the intracellular fluid volume was determined. This ECW/ICW index was calculated for both the affected and unaffected limbs at both measurement times. Results confirmed that the established techniques of total limb volume and extracellular fluid volume normalized to the unaffected contralateral limb were accurate in the detection of lymphedema (p < 10(-6)). Comparison of the ECW/ICW index from the affected limb after diagnosis with that from the pre-surgery measurement revealed a significant (p < 10(-6)) and considerable (75%) increase. The results of this pilot study suggest that by using multiple frequency bioelectrical impedance analysis, an index of the ECW/ICW ratio can be obtained and this index appears to have an equal, or better, sensitivity than the other techniques in detecting lymphedema. More importantly, this index does not require normalization to another body segment and can be used to detect all types of peripheral edema including both unilateral and bilateral lymphedema.

Adult↗
PubMed1996

[Distribution of irrigating fluid in intracellular and extracellular spaces during transurethral prostatectomy II--TUR syndrome and hyponatremia].

Thirty four patients undergoing transurethral resection of the prostate (TURP) under spinal anesthesia were assigned to a TUR syndrome (TURS) group (n = 7) or an asymptomatic (ASP) group (n = 27) depending on the clinical manifestations of the TUR syndrome. Blood loss and distribution of absorbed irrigating fluid (3% sorbitol-Uromatic S, 170 mOsm.kgH2O-1, Baxter) were computed together with serum osmolality, blood urea nitrogen and hematocrit. Postoperative serum sodium concentration and hematocrit were significantly lower in the TURS group than in the ASP group (124 +/- 8.7 vs. 133.9 +/- 5.9 mOsm.l-1 and 26. 8 +/- 4.2 vs. 35.0 +/- 4.6%, respectively). Postoperative serum osmotic pressure did not differ between the groups despite the difference in sodium concentration because 3% sorbitol could contribute to osmoles in the serum. The volume of irrigating fluid absorbed and its distribution into the intracellular space (delta ICF) did not differ between the groups. However, blood loss was significantly greater in the TURS group than in the ASP group (1457 +/- 434 ml vs. 173 +/- 450 ml, P < 0.01), and consequently extracellular fluid (ECF) volume was significantly reduced in the TURS group (-354 +/- 1201 ml vs. 802 +/- 1302 ml, P < 0.05). Thus, massive blood loss and reduced ECFs rather than dilutional hyponatremia, are thought to contribute to clinical manifestation of the TUR syndrome.

Aged↗
PubMed2005

Anti-hepatocarcinoma effects of 5-fluorouracil encapsulated by galactosylceramide liposomes in vivo and in vitro.

AIM: To study the anti-hepatocarcinoma effects of 5-fluorouracil (5-Fu) encapsulated by galactosylceramide liposomes (5-Fu-GCL) in vivo and in vitro. METHODS: Tumor-bearing animal model and HepA cell line were respectively adopted to evaluate the anti-tumor effects of 5-Fu-GCL in vivo and in vitro. Tumor cell growth inhibition effects of 5-Fu-GCL in vitro were assessed by cell viability assay and MTT assay. In vivo experiment, the inhibitory effects on tumor growth were evaluated by tumor inhibition rate and animal survival days. High performance liquid chromatography was used to detect the concentration-time course of 5-Fu-GCL in intracellular fluid in vitro and the distribution of 5-Fu-GCL in liver tumor tissues in vivo. Apoptosis and cell cycle of tumor cells were demonstrated by flow cytometry. RESULTS: In vitro experiment, 5-Fu-GCL (6.25-100 micromol/L) and free 5-Fu significantly inhibited HepA cell growth. Furthermore, IC50 of 5-Fu-GCL (34.5 micromol/L) was lower than that of free 5-Fu (51.2 micromol/L). In vivo experiment, 5-Fu-GCL (20, 40, 80 mg/kg) significantly suppressed the tumor growth in HepA bearing mice model. Compared with free 5-Fu, the area under curve of 5-Fu-GCL in intracellular fluid increased 2.6 times. Similarly, the distribution of 5-Fu-GCL in liver tumor tissues was significantly higher than that of free 5-Fu. After being treated with 5-Fu-GCL, the apoptotic rate and the proportion of HepA cells in the S phase increased, while the proportion in the G0/G1 and G2/M phases decreased. CONCLUSION: 5-Fu-GCL appears to have anti-hepato-carcinoma effects and its drug action is better than free 5-Fu. Its mechanism is partly related to increased drug concentrations in intracellular fluid and liver tumor tissues, enhanced tumor cell apoptotic rate and arrest of cell cycle in S phase.

Animals↗
PubMed1991

Relative expansion of extracellular fluid in obese vs. nonobese women.

There is a conflict in previous studies with regard to the relation between adipose tissue mass and total body fluid distribution. This study tested the hypothesis that obesity is accompanied by an increase in the extracellular-to-intracellular fluid ratio above that observed in nonobese subjects. Extracellular fluid was evaluated in obese (n = 39) and nonobese (n = 26) healthy women, using two different dilution volumes, 35SO4 [extracellular water (ECW)] and 24NaCl [exchangeable sodium (Nae)]. Intracellular water (ICW = 3H2O dilution volume-ECW) and total body potassium (TBK; 40K whole body counting) were assumed to represent intracellular fluid. Two independent markers of relative fluid distribution were formulated as ECW/ICW and Nae/TBK. Obese and nonobese women were of similar age and height but differed in body weight and TBW by 67.7 kg and 12.9 liters, respectively. The obese women had significantly larger absolute ECW, Nae, ICW, and TBK compared with the nonobese women (all P less than 0.001). The ratios ECW/ICW and Nae/TBK were significantly higher in obese vs. nonobese women and were highly correlated with each other (r = 0.54, P less than 0.001) in the pooled group of subjects. Fluid volumes are thus increased in obese women, and the expansion is relatively greater for the extracellular compartment. These results have implications in the study of human body composition and may also account in part for the fluid-overload states that often accompany severe obesity.

Adult↗
PubMedDate not supplied

The major electrolytes: sodium, potassium, and chloride.

Electrolytes are substances that dissociate in solution and have the ability to conduct an electrical current. These substances are located in the extracellular and intracellular fluid. Within the extracellular fluid, the major cation is sodium and the major anion is chloride. The major cation in the intracellular fluid is potassium. These electrolytes play an important role in maintaining homeostasis. In this article, the etiology, signs, symptoms, and treatments for imbalances of these three electrolytes are reviewed.

Chlorides↗
PubMed1993

Can insulin administration cause an acute metabolic acidosis in vivo? An experimental study in dogs.

Insulin is the cornerstone of therapy for diabetic ketoacidosis because it causes the rate of ketoacid production to fall; this action takes several hours to occur. Insulin also causes H+ to be transported from the intracellular fluid to the extracellular fluid in vitro. The purpose of this study was to determine if insulin led to the acute export of H+ from the intracellular fluid in vivo. If so, we wished to determine if this also occurred during chronic metabolic acidosis, to quantitate the magnitude of the H+ shift, and to evaluate the mechanisms involved. The administration of low- or high-dose insulin to normal dogs and high-dose insulin to dogs with chronic metabolic acidosis caused the concentration of bicarbonate in plasma to decline by close to 3 mmol/l. The PCO2 fell by close to 15% in all three groups of dogs, so one component of the fall was due to hyperventilation. As the pH of blood did not change, a primary metabolic acidosis also occurred. The fall in bicarbonataemia was not due to net accumulation of organic acids or to a loss of bicarbonate or organic anions in the urine. Taken together, insulin, when given at doses used to treat diabetic ketoacidosis, might induce a significantly greater degree of acidaemia in the extracellular fluid acutely after it is given.

Acidosis↗
PubMed2000

Pancreatitis-associated ascitic fluid increases intracellular Ca(2+) concentration on hepatocytes.

BACKGROUND: We have reported that pancreatitis-associated ascitic fluid (PAAF) contains a cytotoxic factor(s) inducing apoptosis on renal tubular cells and hepatocytes. It has been suggested that elevation of intracellular Ca(2+) concentration ([Ca(2+)](i)) is associated with the development of cell damage and apoptosis. METHODS: To clarify the mechanism of hepatocellular injury in acute pancreatitis, the effect of PAAF on hepatocyte [Ca(2+)](i) was investigated. Primary cultures of rat hepatocytes were loaded with Fura-2/acetoxymethyl, and the changes of [Ca(2+)](i) were measured using spectrofluorometer. RESULTS: The baseline of hepatocyte [Ca(2+)](i) was 172 +/- 17 nM. [Ca(2+)](i) increased from 1 min after the addition of PAAF in a dose-dependent manner. Fractionation of PAAF revealed only one fraction (molecular weight >/= 5 x 10(4)) possessed both [Ca(2+)](i) elevation activity and cytotoxic activity. Neither 8-(N,N-diethyl-amino) octyl-3,4,5-trimethoxybenzoate (TMB-8) nor thapsigargin inhibited the PAAF-evoked [Ca(2+)](i) elevation. Chelation of extracellular Ca(2+) by ethylene glycol bis-(beta-aminoethyl ether) N,N,N',N'-tetraacetic acid (EGTA) prevented the elevation of [Ca(2+)](i), but verapamil did not prevent it. Platelet-activating factor antagonist (TCV-309) blocked the PAAF-elicited [Ca(2+)](i) elevation. Pancreatitis-associated serum also increased hepatocyte [Ca(2+)](i). Moreover, PAAF increased [Ca(2+)](i) on Madin-Darby canine kidney cells in a dose-dependent manner. CONCLUSIONS: These results suggest that the dramatic elevation of hepatocyte [Ca(2+)](i) due to PAAF may be closely related to the hepatocellular injury in severe acute pancreatitis and that platelet-activating factor may play a pivotal role in increasing hepatocyte [Ca(2+)](i). Elevation of [Ca(2+)](i) in various cells may be involved in the mechanism of multiple organ failure in this disease.

Acute Disease↗
PubMed1980

Absence of transcellular fluid shift during haemofiltration.

Total body and extracellular fluid volume before and after haemofiltration were calculated using urea and inulin as markers. The change in plasma volume and interstitial fluid volume were also evaluated by haemoglobin concentration and hematocrit value. The extracellular fluid volume, especially interstitial fluid volume, was reduced, while intracellular fluid volume was not altered by haemofiltration.

Blood↗
PubMed1998

Prolactin in follicular fluid and intracellular store calcium in follicular cells are related to morphological signs of ovarian follicle atresia in cows: work in progress.

It is known that prolactin (PRL) is the third pituitary hormone serving gonadotropic function in mammals. However, its role in the regulation of ovarian folliculogenesis and, in particular, its relationship to follicular atresia as well as the mechanism of its influence on follicular cells are poorly understood. We investigated PRL levels in follicular fluids (FFs) and intracellular store calcium ([Ca2+]is) in cell walls of bovine ovarian follicles with diameters of 10 to 20 mm and their relationship to follicular atresia. Ovarian follicles were categorized on the basis of macroscopic criteria and of microscopic examination of granulosa cell (GC) smears. Prolactin concentrations in FFs were measured by RIA and levels of [Ca2+]is in follicular cells were determined by using the fluorophore chlortetracycline. Compared to atretic follicles, morphologically normal follicles were characterized by higher concentrations of PRL in FFs (P < 0.001) and lower contents of [Ca2+]is in follicular cells (P < 0.01). Furthermore, follicles containing no more than 20% of pycnotic GCs had higher levels of PRL in their fluids than those containing over 40% of pycnotic GCs (P < 0.05). Finally, the direct effect of PRL on [Ca2+]is content in follicular cells was studied in vitro. Compared to control, PRL decreased (P < 0.001) the levels of [Ca2+]is in the cells after 24 h culture of follicular walls from morphologically normal follicles in TCM 199 supplemented by 10% fetal calf serum. Our findings suggest that the decline of PRL concentrations in FFs and the rise of [Ca2+]is contents in follicular cells are related to atresia of large bovine follicles and that there appears to be a relationship between the two biochemical parameters.

Animals↗
PubMed2000

Body water content of extremely preterm infants at birth.

BACKGROUND: Preterm birth is often associated with impaired growth. Small for gestational age status confers additional risk. AIM: To determine the body water content of appropriately grown (AGA) and small for gestational age (SGA) preterm infants in order to provide a baseline for longitudinal studies of growth after preterm birth. METHODS: All infants born at the Hammersmith and Queen Charlotte's Hospitals between 25 and 30 weeks gestational age were eligible for entry into the study. Informed parental consent was obtained as soon after delivery as possible, after which the extracellular fluid content was determined by bromide dilution and total body water by H(2)(18)O dilution. RESULTS: Forty two preterm infants were studied. SGA infants had a significantly higher body water content than AGA infants (906 (833-954) and 844 (637-958) ml/kg respectively; median (range); p = 0.019). There were no differences in extracellular and intracellular fluid volumes, nor in the ratio of extracellular to intracellular fluid. Estimates of relative adiposity suggest a body fat content of about 7% in AGA infants, assuming negligible fat content in SGA infants and lean body tissue hydration to be equivalent in the two groups. CONCLUSIONS: Novel values for the body water composition of the SGA preterm infant at 25-30 weeks gestation are presented. The data do not support the view that SGA infants have extracellular dehydration, nor is their regulation of body water impaired.

Adipose Tissue↗
PubMed1984

Aspects of the regulation of cell volume.

It is generally thought that osmoregulation is aimed not at osmotic pressure, or extracellular Na concentration per se, but at the regulation of cell volume. Tacit assumptions often made in considering body fluid distribution include the following: cell membranes support no significant hydrostatic pressure gradient; cell membranes are much more permeable to water than to the major solutes; therefore intracellular and extracellular osmotic pressure are equal; cell solute content is stable and not related to cell volume or osmotic pressure; accordingly cell volume varies inversely with osmotic pressure. In fact, counter examples are known to each of these and the one generalisation that seems to hold is that there are no water pumps and that water rapidly attains thermodynamic equilibrium between interstitial and intracellular fluid. Three topics will be discussed that illustrate some of these points. Even in the simplest model cells are not expected to shrink in direct proportion to increasing osmotic pressure, since they contain 20 to 30% solids. However, after allowing for this, cells still shrink less than predicted. One way of interpreting this retention of water is in terms of an increasing negative intracellular fluid pressure that results from the gelled nature of cytoplasm (Hladky and Rink, 1978). Many cell types respond to osmotic swelling or shrinking by subsequent adjustment of their solute content to return the volume towards normal. Human lymphocytes can do this remarkably quickly, via large increases in permeability to K and Cl. The mechanisms that produce these changes have possible implications for the functioning of osmoreceptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1997

Extra- and intracellular volume monitoring by impedance during haemodialysis using Cole-Cole extrapolation.

A method is presented for monitoring the relative variation of extracellular and intracellular fluid volumes using a multifrequency impedance meter and the Cole-Cole extrapolation technique. It is found that this extrapolation is necessary to obtain reliable data for the resistance of the intracellular fluid. The extracellular and intracellular resistances can be approached using frequencies of, respectively, 5 kHz and 1000 kHz, but the use of 100 kHz leads to unacceptable errors. In the conventional treatment the overall relative variation of intracellular resistance is found to be relatively small.

Blood Volume↗
PubMed1984

Estimation of viscous dissipation inside an erythrocyte during aspirational entry into a micropipette.

Viscous dissipation inside the erythrocyte during its aspirational entry into a micropipette is analyzed. The motion of the intracellular fluid is approximated by a flow into the micropipette orifice from a half space (the portion of the erythrocyte outside the micropipette). The stream function and intracellular pressure (p) in the half space are obtained as a function of radial and axial positions near the orifice. Solution of the boundary value problem for a uniform stream entering a circular hole gives p = 2 eta HQ/pi R3p, where eta H is the intracellular viscosity, Q is the total discharge, and Rp is the pipette radius. The results indicate that the moving erythrocyte membrane helps to drive the intracellular fluid into the orifice. For normal erythrocytes, p is only approximately 0.5% of the total aspiration pressure (delta P). The contribution of p to delta P, however, may become significant when there is a large increase in eta H due to a markedly elevated intracellular hemoglobin concentration or an alteration of the physical state of hemoglobin.

Animals↗
PubMed2004

Heterogeneity in the effect of albumin and other resuscitation fluids on intracellular oxygen free radical production.

BACKGROUND: We hypothesized that by studying a suspension of a single cell type in various resuscitation fluids, we could compare their effects on parameters associated with cell death. METHODS: Jurkat cells were suspended in resuscitation fluids. Using flow cytometry, light scatter, phosphatidylserine translocation, propidium iodide uptake, and intracellular H2O2 production were measured. RESULTS: Buffer (pH, 7.4) and albumin added to Ringer's lactate inhibited the adverse changes, including intracellular oxygen free radical production. Oxygen free radical production was variable within the cell population and inhibited by albumin but not other colloids or crystalloids. This correlated well with the ability of albumin to enhance metabolic activity. A flavoprotein inhibitor blocked H2O2 production, suggesting that mitochondria are the source of the H2O2 and the variability. CONCLUSION: Oxygen free radical inhibition by albumin could explain both its beneficial and its harmful effects.

Albumins↗
PubMed1995

The effect of follicular fluid on intracellular free calcium levels in human spermatozoa.

In this study, we demonstrate the effect of follicular fluid (FF) on free cytosolic calcium ion ([Ca2+]i) in human spermatozoa, using a fluorescent indicator "fura 2," and we evaluate the factors that increase [Ca2+]i in FF. A significant and immediate [Ca2+]i increase (656.3 +/- 148.6 nM) was elicited by intact FF. The increase in [Ca2+]i elicited by lipid-stripped FF was only 50% (322 +/- 68.7 nM) of that elicited by intact FF. However, 82% of the [Ca2+]i increase elicited by intact FF was observed when lipid-stripped FF was supplemented with progesterone, but not when it was supplemented with estradiol. Also, progesterone at the concentrations of 1 ng/ml to 1 microgram/ml caused a significant increase in [Ca2+]i by itself, but estradiol produced a small effect, ranging from 3% to 9% of the effect produced by progesterone. These results indicate that progesterone plays a major role in the lipid fraction in FF to elicit the entry of calcium into human spermatozoa.

Calcium↗
PubMed1987

Intestinal absorption of choline in rats.

The intestinal absorption of choline, an endogenous quaternary ammonium, from the rat jejunum has been investigated with an in situ ligated loop method and an in vitro everted sac method. Choline was absorbed rapidly from the ligated jejunum and structural analogs inhibited choline absorption competitively. In in vitro experiments, choline was transported from the mucosal fluid to the intracellular fluid against a concentration gradient and the rate of tissue uptake was highly affected by incubation temperature, aerobic condition and the presence of a metabolic inhibitor, 2,4-dinitrophenol. The tissue accumulation of choline was saturable at concentrations below 100 microM and, above this concentration the uptake ratio of choline (medium to tissue) was almost constant. One mM hemicholinium-3, which is well known to inhibit choline uptake by neurons through the choline specific carrier, also significantly inhibited choline uptake, especially at concentrations of choline below 100 microM. The fact that the choline uptake is linear in the presence of hemicholinium-3 shows that choline is partially absorbed by passive diffusion. The difference between the total tissue accumulation and choline uptake by the passive diffusional pathway followed Michaelis-Menten kinetics and the apparent Kt of 47 microM and Vmax of 4.1 nmol/ml intracellular fluid/min were determined by an in vitro everted sac method. These findings suggested that, a lower concentrations, choline was absorbed from the rat intestine mainly by an active transport system.

Animals↗