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At least 955 records · Page 53Linked to original sources
PubMed1982

A computerized model to analyze transcellular fluid shift during hemofiltration.

Using urea and inulin as markers, we have developed a simple method to calculate intracellular and extracellular fluid volume in patients before and after hemofiltration therapy. During conventional hemofiltration using substitution fluid with a Na+ concentration of 140 mEq/L, a decrease in extracellular fluid volume was noted whereas the intracellular fluid volume was unaltered. Furthermore, we have developed a computerized mathematical model to analyze transcellular fluid shifts during hemofiltration. This model also indicates a decrease in extracellular fluid volume only, the intracellular fluid volume remaining unchanged. High-Na+ hemofiltration using substitution fluid with an Na+ concentration of 160 mEq/L has enabled us to remove fluid from both intracellular and extracellular compartments. Thus, high-Na+ hemofiltration is expected to normalize the intracellular hydration in uremic patients, and to reduce the decrease in extracellular fluid volume during hemofiltration therapy. Our data therefore suggest that high-Na+ hemofiltration could prevent hypotension due to large decreases in extracellular fluid volume by inducing a transcellular fluid shift out of body cells. Our computerized model can be a useful tool in the prescription of the optimal Na+ concentration in substitution fluid for individualized hemofiltration therapy.

Adult↗
PubMed1987

Brain involvement in the regulation of renal sodium excretion.

The aim of the present work was to study some aspects of the brain involvement in renal sodium excretion from the point of view of renal regulation of the extracellular fluid volume and composition. It was found on the basis of experiments on conscious sheep that sodium concentration in the cerebrospinal fluid may be of importance for the mechanism of the extracellular fluid volume regulation. Higher concentrations potentiate a homeostatically effective natriuresis during extracellular fluid volume expansion and lower concentrations impair natriuresis. It was also found in sheep with lesions of the anterior third cerebral ventricle that this brain region is of crucial importance for the mechanism of natriuresis evoked by an i.v. hypertonic saline load but the regulation of the extracellular fluid volume is undisturbed provided the sheep is kept in water balance. Finally it was demonstrated in anesthetized dogs that the heart atrial natriuretic system may be under control of both the extracellular fluid volume and plasma osmolality (and/or plasma sodium concentration) and a circumstantial evidence was provided that it may also be under the control of a cerebral function.

Animals↗
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↗
PubMed2003

The extracellular fluid-to-intracellular fluid volume ratio is associated with large-artery structure and function in hemodialysis patients.

BACKGROUND: Large-artery derangement is a major risk factor for cardiovascular and all-cause mortality in patients with end-stage renal disease (ESRD). It is not clear how body fluid distribution affects large-artery structure and function in patients with ESRD. METHODS: One hundred fifty-seven hemodialysis (HD) patients (mean age, 55.9 +/- 15.1 years; 76 men, 81 women) were enrolled. Influence of the extracellular fluid (ECF)-to-intracellular fluid (ICF) ratio derived from bioimpedance spectroscopy on the structure and function of the common carotid artery (CCA) and aorta was analyzed. One hundred forty-four healthy subjects were examined to obtain normal reference values for body fluid compartments. Based on ECF-ICF ratio, 2 groups were identified: ECF-ICF ratio in the 95th percentile or less and ECF-ICF ratio greater than the 95th percentile of age- and sex-stratified normal reference values. RESULTS: ECF-ICF ratio was significantly related to CCA diameter (r2 = 0.26; P < 0.001), CCA incremental modulus (E(inc); r2 = 0.15; P < 0.001), carotid augmentation index (AGI; r2 = 0.10; P < 0.001), and aortic pulse wave velocity (aPWV; r2 = 0.21; P < 0.001). ECF-ICF ratio remained a significant independent determinant for CCA diameter (model r2 = 0.47; P < 0.001), E(inc) (r2 = 0.29; P < 0.001), aPWV (r2 = 0.51; P < 0.001), and AGI (r2 = 0.40; P < 0.001) when age, sex, mean blood pressure, anthropometrical parameters, HD duration, and status of diabetes mellitus were accounted for. HD patients with an ECF-ICF ratio greater than the 95th percentile had a greater CCA diameter, E(inc), aPWV, and AGI than their counterparts. CONCLUSION: ECF-ICF ratio is associated with large-artery structure and function in HD patients. Patients with ESRD with a high ECF-ICF ratio are characterized by significant large-artery derangement.

Adult↗
PubMed2003

Levels of nicotinamide adenine dinucleotide in extracellular body fluids of pigs may be growth-limiting for Actinobacillus pleuropneumoniae and Haemophilus parasuis.

During infection, nutrient deprivation can alter bacterial phenotype. This, in turn, may have implications for pathogenesis and prophylaxis. Actinobacillus pleuropneumoniae (biotype 1) and Haemophilus parasuis, respiratory tract pathogens of swine, are both V-factor-dependent. The concentrations of V factor in the extracellular fluids of pigs are unknown and may limit the growth of these bacteria in vivo. The aim of this study was to determine the concentrations of nicotinamide adenine dinucleotide (NAD) in select porcine body fluids and to compare the availability of NAD in vivo with the affinities of the organisms for this compound. Levels in plasma, tissue fluids (peritoneal, pleural, synovial, and cerebrospinal), and laryngeal, tracheal, and lung washings were determined with an enzymatic cycling assay. We concluded that, although the NAD supply in the respiratory tract is probably not growth-limiting, it may become limiting if the organisms are disseminated.

Actinobacillus Infections↗
PubMed1987

Electrical properties of Ehrlich ascites tumor cells.

The cell membrane potential (PD) of Ehrlich ascites tumor cells was measured continuously at 37 degrees C with conventional microelectrodes during rapid alterations of extracellular fluid composition. At extracellular electrolyte composition mimicking the in vivo situation PD is -56.7 +/- 0.7 mV and the apparent membrane resistance is 62.2 +/- 2.2 M omega. Increasing extracellular potassium concentration from 5.4 to 20.0 mmol/l depolarizes the cell membrane by +18.4 +/- 0.5 mV. Thus, the transference number for potassium (tk, apparent slope potassium conductance over slope membrane conductance) is 0.53 +/- 0.01. A significant correlation is observed between tk and PD: tk = -(0.014 +/- 0.001) [1/mV] X PD [mV] -(0.243 +/- 0.051). 0.7 mmol/l barium depolarizes the cell membrane by +28.2 +/- 0.7 mV, increases the apparent membrane resistance by a factor of 2.6 +/- 0.1 and abolishes the apparent potassium conductance. Reduction of extracellular sodium concentration from 141 to 21 mmol/l depolarizes the cell membrane by +3.1 +/- 1.3 mV. Similarly, 0.1 mmol/l amiloride depolarizes the cell membrane by +3.3 +/- 0.7 mV. Reduction of extracellular chloride concentration from 128 to 67 mmol/l hyperpolarizes the cell membrane by -2.5 +/- 0.2 mV. 1 mmol/l anthracene-9-COOH does not significantly alter PD. Temporary omission of glucose from the extracellular fluid has no appreciable effect on PD. In conclusion, PD of Ehrlich ascites tumor cells is in the range of other mammalian epithelial cells and is generated mainly by potassium diffusion, while the conductances to sodium and chloride appear to be small.

Animals↗
PubMed1978

Total effective compliance, cardiac output and fluid volumes in essential hypertension.

Total effective compliance, hemodynamic parameters, extracellular fluid volume, cardiopulmonary (CPBV) and total blood (TBV) volumes were determined in 32 men, including 14 normotensive controls and 18 sustained essential hypertensive patients. The effective compliance was calculated from the changes in central venous pressure recorded simultaneously with the changes in blood volume obtained after a rapid Dextran infusion. In normotensive controls, compliance was 2.08 +/- 0.09 ml/mm Hg/kg and was positively correlated with plasma (r = 0.79) and extracellular fluid (r = 0.84) volumes. In hypertensives, compliance was significantly reduced (1.49 +/- 0.06 ml/mm Hg/kg; P is less than 0.001) and was correlated negatively with the CPBV/TBV ratio (r = -0.75) and positively with the plasma volume/interstitial fluid volume ratio (r = 0.84). These results suggest that in normotensives, there is a regulatory mechanism between volume and compliance and that this contributes to maintaining filling pressure and cardiac output within normal ranges. In hypertensives, the reduced compliance could participate in the maintenance of normal values of cardiac output and extracellular fluid volume by influencing the partition of intravascular and extracellular fluid volumes.

Cardiac Output↗
PubMed1997

Selective chronic sodium or chloride depletion specifically modulates subfornical organ atrial natriuretic peptide receptor number in young rats.

1. We studied the effects of selective chronic sodium depletion of chloride depletion on atrial natriuretic peptide receptor number in the subfornical organ and paraventricular nucleus of young rats. 2. Sodium or chloride depletion decreased plasma levels of atrial natriuretic peptide, increased plasma renin activity, and induced extracellular fluid volume contraction. Chloride depletion induced more significant changes in extracellular fluid volume contraction than sodium depletion. 3. In the subfornical organ, atrial natriuretic peptide receptor number significantly decreased (30%) after sodium depletion, while chloride depletion induced a smaller, not statistically significant decrease. Conversely, atrial natriuretic peptide receptors located in the paraventricular nucleus of young rats were not significantly affected by sodium or chloride depletion. 4. Water deprivation reversed the decrease in atrial natriuretic peptide receptors produced by sodium depletion. Water-deprived sodium-depleted rats actually had higher numbers of atrial natriuretic peptide receptors in the subfornical organ than control rats. These changes were associated with severe extracellular fluid volume contraction and up regulation of brain vasopressin mRNA steady-state levels. Thus, the direction of change in the number of subfornical organ atrial natriuretic peptide receptors was dependent on the degree of extracellular fluid volume contraction. 5. Our results suggest that atrial natriuretic peptide receptors located in the subfornical organ, and not in the paraventricular nucleus, are selectively regulated by sodium depletion and extracellular fluid volume contraction.

Age Factors↗
PubMed1981

Plasma and interstitial fluid volume in extensive skin disease.

Plasma volume and extracellular fluid volume were determined simultaneously in 17 patients with extensive skin disease and 18 matched normal subjects after an intravenous bolus injection of 131I-labeled human serum albumin and inulin. The patients had a decrease in plasma volume (-6%), which, however, was statistically significant only when related tao body weight or surface area. There was a concomitant increase in extracellular fluid volume (+7%) and interstitial fluid volume (+12%). These deviations from control data were statistically significant neither in absolute values nor when related to body size. Interstitial fluid volume was calculated as the difference between extracellular fluid volume and plasma volume. The mean plasma volume: interstitial fluid volume ratio was significantly lower in the patients (0.35 +/- 0.05 SD) than in the control group (0.42 +/0 0.05 SD) (p < 0.001). These results show that a shift of fluid from the intra- to the extracellular spaces is present in patients with extensive skin disease. Elevated microvascular water filtration in the skin is suggested as a major mechanism of this abnormal fluid distribution.

Body Water↗
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↗
PubMed1987

Intracellular ion content of skeletal muscle measured by instrumental neutron activation analysis.

The intracellular contents of sodium (Na+), potassium (K+), calcium (Ca2+), magnesium (Mg2+), and chloride (Cl-) in rat hindlimb muscles (soleus, plantaris, white and red gastrocnemii) were measured by instrumental neutron activation analysis (INAA) and atomic absorption spectrophotometry (AAS). Muscle extracellular fluid volume (ECFV) was determined using [3H]mannitol, [14C]mannitol, [3H]polyethylene glycol (PEG, mol wt 900, PEG-900) or the chloride (Cl) method and intracellular fluid volume (ICFV) calculated. Rats were anesthetized with pentobarbital sodium. The muscles were biopsied, frozen in liquid nitrogen, freeze-dried, weighed, and transferred to vials for analysis. For a given muscle, ion contents measured by the two methods showed a consistent small difference which could not be explained. The PEG-900 space and the Cl method yielded a larger ECFV than did mannitol; it is concluded that PEG-900 and Cl overestimate ECFV. There were significant differences in total tissue water (TTW), ECFV, ICFV, and intracellular ion contents between the different muscle types. The fast glycolytic muscles (white gastrocnemius, plantaris) had lower TTW (758 ml/kg wet wt) and ECFV (6.5-8.5% TTW) but the highest ICFV; the soleus (slow oxidative fibers) had the highest TTW (766 ml/kg wet wt) and ECFV (10-15% TTW) but the lowest ICFV. The fast-twitch white gastrocnemius and plantaris muscles have a higher intracellular content of K+ and lower Na+ and Cl- than the slow-twitch soleus muscle. The technique of INAA provides a rapid and accurate means of determining intramuscular ion content in small samples of tissue.

Animals↗
PubMed1977

Failure of sodium restriction to abolish exaggerated natriuresis in poststreptococcal glomerulonephritis.

Exaggerated natriuresis in response to hypertonic saline infusion occurs with great regularity in patients with documented previous attacks of poststreptococcal glomerulonephritis. Five patients were studied before and after 1 week of dietary sodium restriction in order to examine the possibility that increased extracellular fluid volume might play a role in the response to acute saline infusion. Plasma renin activity (PRA) and PRA responsiveness to sodium depletion were normal, suggesting that extracellular fluid volume was not increased. In all patients, extracellular fluid volume decreased during sodium restriction, as judged by weight loss, cumulative negative sodium balance, small decreases in measured plasma volume, and appropriate increases of PRA and plasma aldosterone concentration. Hypertonic saline infusion provoked exaggerated natriuresis in all patients equally as well after dietary sodium restriction as before. Exaggerated natriuresis in poststreptococcal glomerulonephritis occurs without evidence of chronic expansion of extracellular fluid volume and is not affected by reduction of extracellular fluid volume.

Adolescent↗
PubMed1995

Neurotransmitter release evoked by nerve impulses without Ca2+ entry through Ca2+ channels in frog motor nerve endings.

1. The requirement for extracellular Ca2+ in the process of evoked acetylcholine (ACh) release by nerve impulses was tested at endplates in frog skeletal muscle. Ca(2+)-containing lipid vesicles (Ca2+ liposomes) were used to elevate cytoplasmic Ca2+ concentrations under conditions in which Ca2+ entry from the extracellular fluid was prevented. 2. In an extracellular solution containing no added Ca2+ and 1 mM Mg2+ ('Ca(2+)-free' solution), Ca2+ liposomes promoted the synchronous release of ACh quanta, reflected electrophysiologically as endplate potentials (EPPs), in response to temporally isolated nerve impulses. 3. Motor nerve stimulation generated EPPs during superfusion with Ca2+ liposomes in Ca(2+)-free solutions containing the Ca2+ channel blocker Co2+ (1 mM), and the Ca2+ chelator EGTA (2 mM). As a physiological control for Ca2+ leakage from the liposomes to the extracellular fluid, the effect of Ca2+ liposomes on asynchronous evoked ACh release mediated by Ba2+ was examined. In contrast to the effects of 0.2-0.3 mM extracellular Ca2+, which generated EPPs but antagonized Ba(2+)-mediated asynchronous ACh release, Ca2+ liposomes generated EPPs but did not reduce asynchronous release mediated by Ba2+. The effects of Ca2+ liposomes were thus not due to leakage of Ca2+ from the liposome to the extracellular fluid. 4. Morphological studies using fluorescently labelled liposomes in conjunction with a confocal microscope demonstrate that lipid is transferred from the liposomes to nerve endings and liposomal contents are delivered to the nerve terminal cytoplasm. 5. The results suggest that when intracellular Ca2+ is elevated using liposomes as a vehicle, evoked ACh release can occur in the absence of Ca2+ entry via Ca2+ channels.

Acetylcholine↗
PubMed1984

[Changes in body fluid spaces in hypertension patients treated with different diuretics].

Body fluid spaces: total body fluid volume, extracellular fluid volume, circulating plasma volume, intracellular and interstitial fluid volumes were studied in 60 patients with essential hypertension, stage IIB. The studies were performed prior and following a two-week treatment with diuretics ( furosemid , oxodolin , hydrochlorothiazide, brinaldix ). The patients were divided into 3 groups. I--patients whose total body fluid volume was considerably increased due to intracellular fluid. They had the highest blood pressure level. Treatment with diuretics was the most effective in this group and was accompanied by intracellular fluid reduction and slight circulating plasma volume decrease. II--patients whose fluid spaces did not differ from those of normal subjects. Treatment with diuretics was effective and accompanied by simultaneous reduction in intracellular and interstitial fluid volumes. III--patients with reduced interstitial fluid volume and raised circulating plasma/interstitial fluid ratio. Treatment with diuretics was ineffective and accompanied by intracellular fluid level reduction and fluid passage from the vascular bed into the interstitial space. Furosemid and oxodolin were most effective decreasing intracellular fluid volume, hydrochlorothizide --reducing interstitial fluid volume and brinaldix was equally effective decreasing both fluid volumes.

Adult↗
PubMed1989

Insulin-like growth factor-I (IGF-I) infusion into hypophysectomized or protein-deprived rats induces specific IGF-binding proteins in serum.

The insulin-like growth factors (IGFs) are small peptides that are present in serum and extracellular fluids and stimulate the growth of many cell types. In extracellular fluids the IGFs are bound to carrier proteins that are believed to modify the biological actions of the IGFs. At least three structurally distinct IGF-binding proteins (IGF-BPs) have been identified, and the serum concentrations of one of these has been shown to be regulated by pituitary GH. We report here that this GH responsive protein [39,000-45,000 mol wt (Mr)] can be induced (7-fold) by infusion of IGF-I in hypophysectomized rats or (3.5-fold) in protein-deprived rats, whereas two other forms of IGF-BP (e.g. 31,000-34,000 and 24,000 Mr) showed no change in the hypophysectomized animals and minimal increases in the protein-deprived animals. Likewise, GH injections in hypophysectomized animals resulted in a 7-fold increase in the 39,000-45,000 Mr form and no change in the 31,000-34,000 and 24,000 Mr forms. The protein-deprived animals showed a 3.2-fold increase in the 39,000-45,000 Mr and 2.4- to 1.8-fold increases in the 31,000-34,000 and 24,000 Mr forms, respectively. Changes in the larger Mr IGF-BP in these experimental models are paralleled by changes in serum IGF-I, suggesting that the GH dependence of the former protein is mediated at least partially via IGF-I. Our findings also suggest that the secretion of IGF-I and at least one IGF-BP may be linked, providing a mechanism by which their extracellular fluid concentrations are coordinated. Because IGF-BPs are present in extracellular fluids and can modulate IGF-I-receptor interaction, induction of this protein may be an important mediator of IGF action.

Animals↗
PubMed1994

Apical cochlear nerve exposed to perilymph in the gerbil and rat.

There is considerable controversy regarding the origin and composition of perilymph in the scala vestibuli and scala tympani and the barriers and transport mechanisms between them. To elucidate the anatomical separation between perilymph and the extracellular fluid which surrounds the cochlear nerve in Mongolian gerbils (Meriones unguiculatus) and Sprague Dawley rats (Rattus rattus) we examined the modiolus, osseous spiral lamina and the bone of the perilymphatic scalae using light and electron microscopy. Although the cochlear nerve, spiral ganglion and their extracellular fluid are separated from perilymph by the bone of the modiolus in the middle and basal turns, no bone separates these neural structures from perilymph in the apical turn in the two species examined. Instead, the spiral ganglion and axonal elements of the apical turn were covered by a continuation of the bone lining cell layer of the scala tympani. Gaps between lining cells appeared to provide direct communication between the perilymphatic fluid and the extracellular fluid investing the cochlear nerve. Various authors have described openings in modiolar bone in both the scala vestibuli and the scala tympani. While the bone and cellular covering of the modiolus in the basal middle turns of the cochlea is not presumed to be a complete barrier to fluid exchange between the two scalae and the modiolar canal it can be expected to impose some limitation on the rate of passive diffusion. Therefore our data indicates that in the apical turn of the Mongolian gerbil and Sprague-Dawley rat there may be a more significant communication between perilymph and the extracellular fluid and neural elements of the apical modiolar canal than previously reported.

Animals↗
PubMed1975

Tumor extracellular triglycerides in mice during growth of Ehrlich ascites carcinoma.

Our earlier work with Swiss-Webster mice has shown that most of the lipid in Ehrlich ascites tumor extracellular fluid is in the form of free fatty acids. This finding is in direct contradiction to earlier and subsequent reports from another laboratory that has found free fatty acids to be a very minor component and triglycerides to be the major lipid of Ehrlich ascites tumor extracellular fluid. In light of these contradictory reports, we have carried out a study patterned after that of other workers, but using our Swiss-Webster mice. As predicted from our earlier study, we have found very little triglyceride in Ehrlich ascites tumor extracellular fluid. Although we could demonstrate a significant, transient hypertriglyceridemia during tumor growth, maximum plasma triglyceride concentrations were an order of magnitude lower than those reported by other workers. In addition, and again in contrast to other reports, we found that plasma triglyceride and tumor extracellular fluid triglyceride levels in tumorous mice fell significantly with fasting. Thus, interesting differences in triglyceride metabolism between mouse and/or tumor strains seem to exist. Our present findings suggest, but do not prove, that triglycerides in the tumor extracellular fluid probably are not a major source of the rapidly turning over, tumor extracellular fluid free fatty acid in our mice.

Animals↗