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Journal articles on the topic 'Extracellular fluid volume'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Sánchez, M., M. Jiménez-Lendínez, M. Cidoncha, M. J. Asensio, E. Herrero, A. Collado, and M. Santacruz. "Comparison of Fluid Compartments and Fluid Responsiveness in Septic and Non-Septic Patients." Anaesthesia and Intensive Care 39, no. 6 (November 2011): 1022–29. http://dx.doi.org/10.1177/0310057x1103900607.

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Our objective was to study the response to a fluid load in patients with and without septic shock, the relationship between the response and baseline fluid distributions and the ratios of the various compartments. A total of 18 patients with septic shock and 14 control patients without pathologies that increase capillary permeability were evaluated prospectively. We used transpulmonary thermodilution to measure the extravascular lung water index, intrathoracic blood volume index and pulmonary blood volume. For the measurement of the initial distribution volume of glucose, plasma volume and extracellular water, we used dilutions of glucose, indocyanine green and sinistrin respectively. Transpulmonary thermodilution and dilutions of glucose were repeated 75 minutes after the beginning of the fluid load.The patients in the septic group had higher volumes of extracellular water (median 295 vs 234 ml/kg, P <0.001), lower intrathoracic blood volume index (median 894 vs 1157 ml/m2, P <0.003), higher pulmonary permeability ratios (extravascular lung water/pulmonary blood volume) (P <0.003) and higher systemic permeability ratios (interstitial/plasma volume) (P <0.04). The intrathoracic blood volume index increase after fluid loading was lower in the septic group (10 vs 145 ml/m2). The pulmonary permeability ratios did not correlate with the systemic permeability ratios, and in the septic group, the percentage volume retained in the intrathoracic blood volumes after fluid loading did not correlate with the systemic permeability ratios. Septic shock can cause a redistribution of fluids. Fluid administration in these patients produced a minimal increase in intrathoracic blood volume, and the percentage of volume retained in this space was not correlated with the interstitial/plasma volume ratio.

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2

Blaustein, M. P. "Sodium chloride, extracellular fluid volume, and hypertension." Hypertension 7, no. 5 (September 1985): 834–35. http://dx.doi.org/10.1161/01.hyp.7.5.834.

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3

Snelling, Hayley L. R., Myron B. Ciapryna, Philippe F. Bowles, Daphne M. Glass, Maria T. Burniston, and A. Michael Peters. "Extracellular fluid volume in patients with cancer." Nuclear Medicine Communications 31, no. 5 (May 2010): 359–65. http://dx.doi.org/10.1097/mnm.0b013e3283359073.

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4

Peters, A. Michael, Daphne M. Glass, and Nicholas J. Bird. "Extracellular fluid volume and glomerular filtration rate." Nuclear Medicine Communications 32, no. 7 (July 2011): 649–53. http://dx.doi.org/10.1097/mnm.0b013e3283457466.

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5

Simpson, John, and Terence Stephenson. "Regulation of extracellular fluid volume in neonates." Early Human Development 34, no. 3 (October 1993): 179–90. http://dx.doi.org/10.1016/0378-3782(93)90175-t.

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6

Peters, A. Michael. "Estimation of extracellular fluid volume in children." Pediatric Nephrology 27, no. 7 (March 16, 2012): 1149–55. http://dx.doi.org/10.1007/s00467-012-2117-9.

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7

Wong, William W. "Influence of ovariectomy on extracellular fluid volume in rats: Assessment of extracellular fluid volume by means of bromide." Journal of Laboratory and Clinical Medicine 135, no. 4 (April 2000): 298–99. http://dx.doi.org/10.1067/mlc.2000.105291.

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8

Bolscher, Marieke Dijkgraaf-ten, Rob Barto, Daphne A. Voorn, Dirk Compas, J. Coen Netelenbos, and Wim J. F. van der Vijgh. "Influence of ovariectomy on extracellular fluid volume in rats: Assessment of extracellular fluid volume by means of bromide." Journal of Laboratory and Clinical Medicine 135, no. 4 (April 2000): 303–8. http://dx.doi.org/10.1067/mlc.2000.105292.

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9

Hamlyn, J. M., and M. P. Blaustein. "Sodium chloride, extracellular fluid volume, and blood pressure regulation." American Journal of Physiology-Renal Physiology 251, no. 4 (October 1, 1986): F563—F575. http://dx.doi.org/10.1152/ajprenal.1986.251.4.f563.

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Data from humans and experimental animals indicate that hypertensive diseases triggered by extracellular fluid volume expansion are characterized, in their chronic phases, by relatively normal blood volume (BV) and heightened pressure-volume relationship may be viewed as corresponding to a condition of "virtual hypervolemia," where BV is inappropriately "high" relative to blood pressure. The limited data available on the phasic relationship between these variables indicate that the BV expansion appears to be a prerequisite to alterations in vascular ion metabolism, that both of these changes precede the rise in blood pressure, and that structures within the central nervous system may be a critical link between the body fluid volumes and vascular functional changes. In contrast, hypertensive diseases triggered by secretion of pressor agents or their precursors appear to be characterized in their chronic phases by low BV. These relationships and the associated alterations in plasma aldosterone and renin levels are summarized for a variety of clinical syndromes, including essential hypertension and pregnancy-induced hypertension. Direct or indirect evidence of a primary or secondary defect in renal function is apparent as an underlying event in many of these diseases.

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10

Manning, R. Davis. "Dynamics of extracellular fluid volume changes during hyperproteinemia." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 275, no. 6 (December 1, 1998): R1878—R1884. http://dx.doi.org/10.1152/ajpregu.1998.275.6.r1878.

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The dynamics of fluid volume distribution between the blood and interstitium during hyperproteinemia were studied in 12 anephric, conscious dogs during several states of hydration. After recovery from splenectomy and unilateral nephrectomy, plasma protein concentration was elevated to 8.4–8.7 g/dl by daily intravenous infusion of 330 ml of previously collected autologous plasma for 11 days. The remaining kidney was then removed, and the next day lactated Ringer solution equivalent to 10 or 20% of body weight was infused intravenously. By the end of the 25-h postinfusion period, Ringer infusion had increased circulating protein mass 20.9 ± 9.1% (mean ± SE) in the 10% group ( P< 0.05) and decreased it 10.5 ± 3.3% in the 20% group ( P < 0.05). The average increase in blood volume and arterial pressure during the postinfusion period was 27.4 ± 2.5 and 20.7 ± 3.7%, respectively, in the 10% group but only 17.8 ± 2.4 and 12 ± 1.6% in the 20% group (all changes significant compared with respective control). The relationship between blood volume and sodium space was similar to that found during normoproteinemia, such that elevations in sodium space of 40–50% increased blood volume but greater elevations in sodium space caused no further increases in blood volume. Overhydration during chronic hyperproteinemia causes hypervolemia and hypertension, but, in contrast to those in short-term studies, the increases in blood volume and arterial pressure are not greater than those achieved during normoproteinemia.

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11

Crabbé, J. "Aldosterone as a Factor Regulating Extracellular Fluid Volume." Acta Clinica Belgica 46, no. 1 (January 1991): 18–27. http://dx.doi.org/10.1080/17843286.1991.11718136.

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12

A. ESPEJO, MARIA GRACIA, JOSEF NEU, LYLE HAMILTON, BENJAMIN EITZMAN, PHYLLIS GIMOTTY, and RICHARD L. BUCCIARELLI. "Determination of extracellular fluid volume using impedance measurements." Critical Care Medicine 17, no. 4 (April 1989): 360–63. http://dx.doi.org/10.1097/00003246-198904000-00012.

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13

Jones, C. H., L. Martin, L. Ridley, and D. Richardson. "Extracellular fluid volume and EPO dose in haemodialysis." Nephrology Dialysis Transplantation 19, no. 4 (March 18, 2004): 1018–20. http://dx.doi.org/10.1093/ndt/gfh072.

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14

Rockson, Stanley G. "Assessing Extracellular Fluid Volume in Breast Cancer Lymphedema." Lymphatic Research and Biology 11, no. 2 (June 2013): 65. http://dx.doi.org/10.1089/lrb.2013.1122.

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15

Chung, Hsaio-Min, Rudiger Kluge, Robert W. Schrier, and Robert J. Anderson. "Clinical assessment of extracellular fluid volume in hyponatremia." American Journal of Medicine 83, no. 5 (November 1987): 905–8. http://dx.doi.org/10.1016/0002-9343(87)90649-8.

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16

Spital, Aaron. "Clinical assessment of extracellular fluid volume in hyponatremia." American Journal of Medicine 84, no. 3 (March 1988): 562. http://dx.doi.org/10.1016/0002-9343(88)90288-4.

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17

Palmer, Biff F. "Extracellular Fluid Volume in the Hypoalbuminemic Diabetic Patient." Heart Failure Clinics 4, no. 4 (October 2008): 439–48. http://dx.doi.org/10.1016/j.hfc.2008.03.003.

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18

Jeffrey Weidner, W., Leslie A. Selna, Diane E. McClure, and David O. DeFouw. "Effect of extracellular fluid volume expansion on avian lung fluid balance." Respiration Physiology 91, no. 1 (January 1993): 125–36. http://dx.doi.org/10.1016/0034-5687(93)90094-q.

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19

Lindinger, Michael I., Gloria McKeen, and Gayle L. Ecker. "Time course and magnitude of changes in total body water, extracellular fluid volume, intracellular fluid volume and plasma volume during submaximal exercise and recovery in horses." Equine and Comparative Exercise Physiology 1, no. 2 (May 2004): 131–39. http://dx.doi.org/10.1079/ecep200414.

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AbstractThe purpose of the present study was to determine the time course and magnitude of changes in extracellular and intracellular fluid volumes in relation to changes in total body water during prolonged submaximal exercise and recovery in horses. Seven horses were physically conditioned over a 2-month period and trained to trot on a treadmill. Total body water (TBW), extracellular fluid volume (ECFV) and plasma volume (PV) were measured at rest using indicator dilution techniques (D2O, thiocyanate and Evans Blue, respectively). Changes in TBW were assessed from measures of body mass, and changes in PV and ECFV were calculated from changes in plasma protein concentration. Horses exercised by trotting on a treadmill for 75–120 min incurred a 4.2% decrease in TBW. During exercise, the entire decrease in TBW (mean±standard error: 12.8±2.0 l at end of exercise) could be attributed to the decrease in ECFV (12.0±2.4 l at end of exercise), such that there was no change in intracellular fluid volume (ICFV; 0.9±2.4 l at end of exercise). PV decreased from 22.0±0.5 l at rest to 19.8±0.3 l at end of exercise and remained depressed (18–19 l) during the first 2 h of recovery. Recovery of fluid volumes after exercise was slow, and characterized by a further transient loss of ECFV (first 30 min of recovery) and a sustained increase in ICFV (between 0.5 and 3.5 h of recovery). Recovery of fluid volumes was complete by 13 h post exercise. It is concluded that prolonged submaximal exercise in horses favours net loss of fluid from the extracellular fluid compartment.

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20

Aukland, K., and R. K. Reed. "Interstitial-lymphatic mechanisms in the control of extracellular fluid volume." Physiological Reviews 73, no. 1 (January 1, 1993): 1–78. http://dx.doi.org/10.1152/physrev.1993.73.1.1.

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While the study of the physiochemical composition and structure of the interstitium on a molecular level is a large and important field in itself, the present review centered mainly on the functional consequences for the control of extracellular fluid volume. As pointed out in section I, a biological monitoring system for the total extracellular volume seems very unlikely because a major part of that volume is made up of multiple, separate, and functionally heterogeneous interstitial compartments. Even less likely is a selective volume control of each of these compartments by the nervous system. Instead, as shown by many studies cited in this review, a local autoregulation of interstitial volume is provided by automatic adjustment of the transcapillary Starling forces and lymph flow. Local vascular control of capillary pressure and surface area, of special importance in orthostasis, has been discussed in several recent reviews and was mentioned only briefly in this article. The gel-like consistency of the interstitium is attributed to glycosaminoglycans, in soft connective tissues mainly hyaluronan. However, the concept of a gel phase and a free fluid phase now seems to be replaced by the quantitatively more well-defined distribution spaces for glycosaminoglycans and plasma protein, apparently in osmotic equilibrium with each other. The protein-excluded space, determined mainly by the content of glycosaminoglycans and collagen, has been measured in vivo in many tissues, and the effect of exclusion on the oncotic buffering has been clarified. The effect of protein charge on its excluded volume and on interstitial hydraulic conductivity has been studied only in lungs and is only partly clarified. Of unknown functional importance is also the recent finding of a free interstitial hyaluronan pool with relatively rapid removal by lymph. The postulated preferential channels from capillaries to lymphatics have received little direct support. Thus the variation of plasma-to-lymph passage times for proteins may probably be ascribed to heterogeneity with respect to path length, linear velocity, and distribution volumes. Techniques for measuring interstitial fluid pressure have been refined and reevaluated, approaching some concensus on slightly negative control pressures in soft connective tissues (0 to -4 mmHg), zero, or slightly positive pressure in other tissues. Interstitial pressure-volume curves have been recorded in several tissues, and progress has been made in clarifying the dependency of interstitial compliance on glycosaminoglycan-osmotic pressure, collagen, and microfibrils.(ABSTRACT TRUNCATED AT 400 WORDS)

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21

Brown, Mark A., Vivienne C. Zammit, and Sandra A. Lowe. "Capillary Permeability and Extracellular Fluid Volumes in Pregnancy-Induced Hypertension." Clinical Science 77, no. 6 (December 1, 1989): 599–604. http://dx.doi.org/10.1042/cs0770599.

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1. Capillary permeability was determined by the disappearance rate of Evans Blue dye from plasma in healthy non-pregnant women, normal third-trimester primigravidae and primigravidae with pregnancy-induced hypertension 2. Extracellular fluid volume was determined from the disappearance curves of injected mannitol in the same subjects and the plasma volume was measured by the Evans Blue dye dilution technique 3. In normal pregnancy capillary permeability was not altered from that of non-pregnant subjects. Although extracellular fluid volume and plasma volume were increased in normal pregnant compared with nonpregnant women, the distribution of fluid between plasma volume and interstitial fluid volume was unaltered 4. Women with established pregnancy-induced hypertension had a more rapid Evans Blue disappearance rate and a lower plasma volume than normal pregnant women, independent of the presence of proteinuria. Maternal plasma volume correlated positively and significantly with fetal birth weight in women with pregnancy-induced hypertension, emphasizing the important relationship between maternal plasma volume and fetal outcome 5. The increased capillary permeability in women with pregnancy-induced hypertension was associated with a reduction in the plasma volume/interstitial fluid volume ratio but a normal extracellular fluid volume, suggesting that the reduced plasma volume did not result from sodium loss but rather from a redistribution of the total extracellular fluid volume. These changes did not differ significantly in subgroups with and without oedema.

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22

Valenzuela-Rendon, J., and R. D. Manning. "Chronic transvascular fluid flux and lymph flow during volume-loading hypertension." American Journal of Physiology-Heart and Circulatory Physiology 258, no. 5 (May 1, 1990): H1524—H1533. http://dx.doi.org/10.1152/ajpheart.1990.258.5.h1524.

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The chronic roles of the transcapillary fluid flux and lymph flow in the distribution of extracellular fluid volume during volume-loading hypertension were investigated in five conscious dogs. Similarly, the distribution of plasma proteins across the microvasculature was evaluated. During the early phases of volume-loading hypertension the fluid balance was positive, which caused the extracellular fluid volume and the plasma volume to increase 25 and 15%, respectively. The thoracic duct lymph flow more than doubled, but the increase in transcapillary fluid flux was even greater. Therefore the interstitial fluid volume increased 30%. This fluid shift from the vasculature into the interstitium probably prevented an even greater rise in arterial pressure. In addition, the transcapillary protein flux more than doubled, but the accompanying increase in lymph protein transport prevented any change in plasma protein mass. During the latter part of the saline-infusion period, the lymph flow declined toward its control, which caused a net transfer of fluid into the interstitium. In conclusion, the transcapillary fluid flux and lymph flow play significant roles in extracellular fluid volume distribution.

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23

Sasser, D. C., W. A. Gerth, and Y. C. Wu. "Monitoring of segmental intra- and extracellular volume changes using electrical impedance spectroscopy." Journal of Applied Physiology 74, no. 5 (May 1, 1993): 2180–87. http://dx.doi.org/10.1152/jappl.1993.74.5.2180.

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Osmotically induced cellular volume changes in the perfused rat hindlimb were used to validate the use of bioelectrical impedance spectroscopy as a method for observing fluid shifts between the intracellular and extracellular spaces. Electrical impedance spectra were measured as cell volumes were manipulated by perfusion with Krebs-Henseleit solutions having different concentrations of NaCl. A simple equivalent circuit model of current conduction through the monitored tissue was fit to each measured spectrum to obtain segmental values of the equivalent intracellular resistance, membrane capacitance, and extracellular resistance. These parameters are theoretically governed by variations in the average cell volume fraction and ionic concentrations in the intra- and extracellular fluid spaces. In accord with this theoretical dependence, the parameters changed systematically and reversibly in conformance with both the magnitudes and directions of the perfusate concentration changes and the resultant cell volume changes. Results indicate that bioelectrical impedance spectroscopy, coupled with computer-aided equivalent circuit analysis, can be used to monitor segmental intercompartmental fluid shifts at minute-by-minute resolution.

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24

Peters, A. M., I. Gordon, and R. Sixt. "128. Expressing GFR in relation to extracellular fluid volume." Nuclear Medicine Communications 14, no. 1 (April 1993): 291. http://dx.doi.org/10.1097/00006231-199304000-00130.

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25

Pavlin, D. J., M. L. Nessly, R. Haschke, and F. W. Cheney. "Extracellular fluid volume during pneumothorax and hypoxemia in rabbits." Journal of Applied Physiology 60, no. 1 (January 1, 1986): 204–8. http://dx.doi.org/10.1152/jappl.1986.60.1.204.

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This study was designed to test the hypothesis that persistent pneumothorax of greater than or equal to 6 days duration causes a decrease of extracellular fluid volume (ECF). Such changes are of interest as they may be causally related to persistent hypotension that has occurred in humans following pneumothorax evacuation. Experiments were done in rabbits to determine the effect on ECF of persistent pneumothorax with or without systemic hypoxemia. Animals were divided into four treatment groups: 1) pneumothorax with hypoxemia [fractional concentration of O2 in inspired gas (FIO2) = 0.21, n = 30], 2) pneumothorax without hypoxemia (FIO2 = 0.40, n = 25), 3) hypoxemia alone (FIO2 = 0.14, n = 11), and 4) normal controls (FIO2 = 0.21, n = 15). Measurements of ECF were made in the base-line control state and after 6 days of treatment using the dilution volume of thiocyanate sodium as an estimate of ECF volume. We found a reduction of ECF in 53% of animals with pneumothorax plus hypoxemia (range -47% to +13%) and in 54% of animals with hypoxemia alone (range -26% to +25%). ECF declined in only 7% of normal controls and 20% of animals with pneumothorax without hypoxemia. Arterial O2 tensions after 6 days of treatment were 58 +/- 12.6, 141 +/- 28, 60 +/- 5.1, and 97 +/- 9.3 Torr (mean +/- SD) in groups 1–4, respectively. The results suggest that pneumothorax with hypoxemia or hypoxemia alone may contribute to depletion of ECF, but this response is variable and unpredictable in individual animals.

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26

Mitchell, J. B., M. D. Phillips, S. P. Mercer, H. L. Baylies, and F. X. Pizza. "Postexercise rehydration: effect of Na+ and volume on restoration of fluid spaces and cardiovascular function." Journal of Applied Physiology 89, no. 4 (October 1, 2000): 1302–9. http://dx.doi.org/10.1152/jappl.2000.89.4.1302.

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Our purpose was to study the interaction between Na+ content and fluid volume on rehydration (RH) and restoration of fluid spaces and cardiovascular (CV) function. Ten men completed four trials in which they exercised in a 35°C environment until dehydrated by 2.9% body mass, were rehydrated for 180 min, and exercised for an additional 20 min. Four RH regimens were tested: low volume (100% fluid replacement)-low (25 mM) Na+ (LL), low volume-high (50 mM) Na+ (LH), high volume (150% fluid replacement)-low Na+ (HL), and high volume-high Na+ (HH). Blood and urine samples were collected and body mass was measured before and after exercise and every hour during RH. Before and after the dehydration exercise and during the 20 min of exercise after RH, cardiac output was measured. Fluid compartment (intracellular and extracellular) restoration and percent change in plasma volume were calculated using the Cl− and hematocrit/Hb methods, respectively. RH was greater ( P < 0.05) in HL and HH (102.0 ± 15.2 and 103.7 ± 14.7%, respectively) than in LL and LH (70.7 ± 10.5 and 75.9 ± 6.3%, respectively). Intracellular RH was greater in HL (1.12 ± 0.4 liters) than in all other conditions (0.83 ± 0.3, 0.69 ± 0.2, and 0.73 ± 0.3 liter for LL, LH, and HH, respectively), whereas extracellular RH (including plasma volume) was greater in HL and HH (1.35 ± 0.8 and 1.63 ± 0.4 liters, respectively) than in LL and LH (0.83 ± 0.3 and 1.05 ± 0.4 liters, respectively). CV function (based on stroke volume, heart rate, and cardiac output) was restored equally in all conditions. These data indicate that greater RH can be achieved through larger volumes of fluid and is not affected by Na+content within the range tested. Higher Na+ content favors extracellular fluid filling, whereas intracellular fluid benefits from higher volumes of fluid with lower Na+. Alterations in Na+ and/or volume within the range tested do not affect the degree of restoration of CV function.

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27

Hughes, Maryanne R. "Extracellular fluid volume and the initiation of salt gland secretion in ducks and gulls." Canadian Journal of Zoology 67, no. 1 (January 1, 1989): 194–97. http://dx.doi.org/10.1139/z89-026.

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The effect of intraperitoneal NaCl loading on extracellular fluid volume, plasma concentration, and initiation of salt gland secretion was measured in freshwater- and sea water-acclimated Glaucous-winged Gulls, Larus glaucescens, and Mallards, Anas platyrhynchos. In both species salt loading was associated with a significant increase in plasma [Na] and [Cl]. In freshwater- and sea water-acclimated gulls the extracellular fluid volume increased and salt gland secretion occurred; in freshwater- and seawater-acclimated ducks the extracellular fluid volume decreased and salt gland secretion did not occur.

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28

Smits, A. W. "Accessory lymph sacs and body fluid partitioning in the lizard, Sauromalus hispidus." Journal of Experimental Biology 121, no. 1 (March 1, 1986): 165–77. http://dx.doi.org/10.1242/jeb.121.1.165.

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Chuckwalla lizards (genus Sauromalus) may accumulate substantial quantities of body fluid in extracoelomic, lateral abdominal spaces called accessory lymph sacs. The lymph sac fluid (LSF) of S. hispidus is similar to that of serum in Na+, K+ and Cl- concentrations, but the total protein content (3.58 +/− 0.20 g dl-1) is only half that measured in serum (7.05 +/− 0.26 g dl-1). These analyses confirm that LSF is an extravascular form of extracellular fluid, similar in composition to true lymph. Measurements of body fluid partitioning by dilution analysis indicate that Sauromalus hispidus Stejnejer possesses a comparatively large (38.9% body mass) and labile extracellular fluid volume (ECFV), and that the volume of LSF is dependent on the ECFV. Expansion of the ECFV (and subsequent accumulation of LSF) is observed following large, intercompartmental fluid shifts from intracellular to extracellular locations when lizards are kept inactive in simulated hibernation, are injected with KCl in amounts similar to those found in their field diet, and are hydrated with NaCl that is isotonic to their body fluids. These data collectively suggest that the lymph sacs of chuckwallas facilitate expansion of the ECFV, and may be adaptive not only as a means to store body water, but to accommodate transient shifts in body fluid from intracellular to extracellular locations.

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29

Hamilton, M. T., D. S. Ward, and P. D. Watson. "Effect of plasma osmolality on steady-state fluid shifts in perfused cat skeletal muscle." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 265, no. 6 (December 1, 1993): R1318—R1323. http://dx.doi.org/10.1152/ajpregu.1993.265.6.r1318.

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Fluid redistribution in isolated perfused cat calf muscle caused by rapid increases in plasma osmolality was studied using NaCl or sucrose. Extracellular tracers (51Cr-labeled EDTA or [3H]mannitol) were added to the perfusate 90 min before solutes were added, and samples were taken from plasma immediately before osmolality was increased and 17, 40, and 65 min later. Interstitial fluid volume (IFV) was calculated as extracellular volume (ECV) minus plasma volume (Evans blue dye). Total tissue water changes (delta TTW) were measured by continuous recording of tissue weight. Change in intracellular volume (delta ICV) was obtained from delta TTW--delta IFV. TTW, IFV, ICV, and plasma osmolality were in steady state after 17 min. Changes in hydrostatic and colloid osmotic pressure were insignificant in comparison with small-molecule osmotic pressure changes. The apparent volume of TTW participating in the fluid shift averaged 65 +/- 1 ml/100 g (SE) over a wide range of osmolality increases. In contrast to the large changes in TTW, IFV was not altered by osmolality. Thus decreases in TTW were similar to cell dehydration. Hence, increases in plasma volume induced by hypertonic fluids may come entirely at the expense of cell volume, not interstitial volume.

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30

Robillard, Jean E., Jeffrey L. Segar, Francine G. Smith, and Pedro A. Jose. "Regulation of Sodium Metabolism and Extracellular Fluid Volume During Development." Clinics in Perinatology 19, no. 1 (March 1992): 15–31. http://dx.doi.org/10.1016/s0095-5108(18)30473-1.

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31

Finch, N. C., R. Heiene, J. Elliott, H. M. Syme, and A. M. Peters. "Determination of Extracellular Fluid Volume in Healthy and Azotemic Cats." Journal of Veterinary Internal Medicine 29, no. 1 (November 19, 2014): 35–42. http://dx.doi.org/10.1111/jvim.12506.

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32

Kamel, Kamel S., Peter O. C. Magner, Jean H. Ethier, and Mitchell L. Halperin. "Urine Electrolytes in the Assessment of Extracellular Fluid Volume Contraction." American Journal of Nephrology 9, no. 4 (1989): 344–47. http://dx.doi.org/10.1159/000167991.

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33

Hadchouel, Juliette, Cara Büsst, Giuseppe Procino, Giovanna Valenti, Régine Chambrey, and Dominique Eladari. "Regulation of Extracellular Fluid Volume and Blood Pressure by Pendrin." Cellular Physiology and Biochemistry 28, no. 3 (2011): 505–12. http://dx.doi.org/10.1159/000335116.

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34

Peters, A. M. "Expressing glomerular filtration rate in terms of extracellular fluid volume." Nephrology Dialysis Transplantation 7, no. 3 (1992): 205–10. http://dx.doi.org/10.1093/oxfordjournals.ndt.a092106.

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35

Gunasekera, R. D., and A. M. Peters. "Measuring GFR as the fractional turnover of extracellular fluid volume." Nuclear Medicine Communications 16, no. 11 (November 1995): 973. http://dx.doi.org/10.1097/00006231-199511000-00030.

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36

Jaffrin, M. Y., M. Maasrani, B. Boudailliez, and A. Le Gourrier. "EXTRACELLULAR AND INTRACELLULAR FLUID VOLUME DURING DIALYSIS BY MULTIFREQUENCY IMPEDANCEMETRY." ASAIO Journal 42, no. 2 (March 1996): 75. http://dx.doi.org/10.1097/00002480-199603000-00279.

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37

Jaffrin, M. Y., M. Maasrnai, and A. Le Gourrier. "EXTRACELLULAR AND INTRACELLULAR FLUID VOLUME DURING DIALYSIS BY MULTIFREQUENCY IMPEDANCEMETRY." ASAIO Journal 42, no. 2 (April 1996): 75. http://dx.doi.org/10.1097/00002480-199604000-00280.

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38

Wieling, W., J. J. van Lieshout, and R. Hainsworth. "Extracellular fluid volume expansion in patients with posturally related syncope." Clinical Autonomic Research 12, no. 4 (August 1, 2002): 242–49. http://dx.doi.org/10.1007/s10286-002-0024-z.

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39

Moore, L. C., and J. Mason. "Tubuloglomerular feedback control of distal fluid delivery: effect of extracellular volume." American Journal of Physiology-Renal Physiology 250, no. 6 (June 1, 1986): F1024—F1032. http://dx.doi.org/10.1152/ajprenal.1986.250.6.f1024.

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A closed-feedback loop micropuncture method was used to examine tubuloglomerular feedback (TGF) and the regulation of distal fluid delivery in hydropenic rats (CON), moderately hemorrhaged rats (HEM), and rats given desoxycorticosterone (DOC) and 0.6% saline to drink. Distal delivery and TGF response curves were measured with four samples per nephron: a spontaneous early distal collection, two distal collections during moderate (7.5 nl/min) and saturating (30 nl/min) perturbations in nephron fluid load, and a proximal collection to measure single-nephron glomerular filtration rate (SNGFR) during TGF inhibition. Arterial pressure, predistal volume reabsorption, SNGFR, and early distal flow were significantly higher in DOC than in HEM; the CON group exhibited intermediate values. Except for a greater maximum TGF response in HEM, the normalized TGF responses were similar in all three groups, as was the regulation of distal fluid delivery. However, the TGF onset threshold and the TGF operating point, defined by the spontaneous rates of early distal flow and SNGFR, were reset such that distal fluid delivery and SNGFR were higher in DOC than in HEM, as was renal sodium excretion. The results show that the level around which TGF stabilizes distal fluid delivery is reset when extracellular fluid volume is altered.

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40

Miki, K., G. Hajduczok, S. K. Hong, and J. A. Krasney. "Extracellular fluid and plasma volumes during water immersion in nephrectomized dogs." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 252, no. 5 (May 1, 1987): R972—R978. http://dx.doi.org/10.1152/ajpregu.1987.252.5.r972.

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Extracellular fluid volume (ECF, [125I]iothalamate space), blood volume (BV, 51Cr-labeled erythrocyte space), and hematocrit were measured continuously to study the kinetics of fluid movements between intracellular, interstitial, and plasma compartments during water immersion (WI) at 38 degrees C in seven splenectomized and acutely nephrectomized dogs. ECF and plasma volume (PV) increased linearly during WI by 10 +/- 2 ml/kg (4% of initial ECF volume, P less than 0.05) and 12 +/- 2 ml/kg (33% of initial PV, P less than 0.05), respectively, above the control level by 120 min of WI. We estimate that 83% of the fluid entering the intravascular compartment is derived from the intracellular space at 120 min of WI. The results of this study indicate that WI leads to a sustained fluid movement of intracellular fluid toward the intravascular compartment. The increase in interstitial hydrostatic pressure (wick method) by 28.5 mmHg from the control level at 5 min of WI in response to the external water pressure exceeds the increase in mean capillary pressure by 10-11 mmHg relative to the control level. We postulate that this negative hydrostatic pressure gradient across the capillary wall leads to an increase in PV during WI.

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41

Zhu, F., M. K. Kuhlmann, G. A. Kaysen, S. Sarkar, C. Kaitwatcharachai, R. Khilnani, L. Stevens, et al. "Segment-specific resistivity improves body fluid volume estimates from bioimpedance spectroscopy in hemodialysis patients." Journal of Applied Physiology 100, no. 2 (February 2006): 717–24. http://dx.doi.org/10.1152/japplphysiol.00669.2005.

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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.

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42

Smits, A. W., and M. M. Kozubowski. "Partitioning of body fluids and cardiovascular responses to circulatory hypovolaemia in the turtle, Pseudemys scripta elegans." Journal of Experimental Biology 116, no. 1 (May 1, 1985): 237–50. http://dx.doi.org/10.1242/jeb.116.1.237.

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Investigations were conducted (1) to measure the steady state compartmentation of body fluids and (2) to assess the efficacy of blood volume and pressure maintenance during haemorrhage-induced hypovolaemia in the pond turtle, Pseudemys scripta elegans. The pre-haemorrhage blood volume, as determined by tracer dilution of 51Cr-labelled erythrocytes, averaged 6.89 +/− 0.33% of the body mass, and was part of comparatively large extracellular (40.2 +/− 0.70%) and total body fluid volumes (75.25 +/− 1.48%). Turtles exhibited progressive reductions in systemic arterial pressure throughout a cumulative haemorrhage of −48% of their original blood volume, despite dramatic increases in heart rate and comparatively large magnitudes of transcapillary fluid transfer from interstitial to intravascular spaces. Arterial blood pressure returned to pre-haemorrhage values 2h after experimental haemorrhage ceased, concomitant with the restoration of the original blood volume. Our results support arguments made in previous studies that the resistance to fluid movement between vascular and extravascular locations in reptiles is comparatively low. Furthermore, the haemodynamic responses of turtles to experimental hypovolaemia suggest that barostasis through adjustments in vascular tone is less effective than that observed in other reptiles.

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43

Waki, M., J. G. Kral, M. Mazariegos, J. Wang, R. N. Pierson, and S. B. Heymsfield. "Relative expansion of extracellular fluid in obese vs. nonobese women." American Journal of Physiology-Endocrinology and Metabolism 261, no. 2 (August 1, 1991): E199—E203. http://dx.doi.org/10.1152/ajpendo.1991.261.2.e199.

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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.

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44

Kitzman, Joseph V., John F. Martin, Janis H. Holley, and William G. Huber. "Determinations of Plasma Volume, Extracellular Fluid Volume, and Total Body Water in Channel Catfish." Progressive Fish-Culturist 52, no. 4 (October 1990): 261–65. http://dx.doi.org/10.1577/1548-8640(1990)052<0261:dopvef>2.3.co;2.

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45

Jandhyala, Bhagavan S. "Is Expansion of Extracellular Fluid Volume Essential for the Development of “Volume Expanded” Hypertension?" Clinical and Experimental Hypertension. Part A: Theory and Practice 8, no. 3 (January 1986): 457–72. http://dx.doi.org/10.3109/10641968609039616.

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46

Hinghofer-Szalkay, H. "Volume and density changes of biological fluids with temperature." Journal of Applied Physiology 59, no. 6 (December 1, 1985): 1686–89. http://dx.doi.org/10.1152/jappl.1985.59.6.1686.

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High-precision (10(-5) g/ml) mass density measurements on human blood, plasma, plasma ultrafiltrate (using PM-10 membranes), and erythrocyte concentrate samples were performed with the mechanical oscillator technique. Measurement temperatures varied between 4 and 48 degrees C and were accurate to +/- 1 X 10(-2) K. The coefficient of thermal expansion (beta), defined as relative volume change with temperature, was calculated. It was shown that beta increases with temperature in these fluid samples over the entire temperature range investigated; the magnitude of this increase declines with increasing temperature; beta increases with density at temperatures below 40 degrees C but is independent of density above 40 degrees C; and the beta of the intracellular fluid has about twice the value of the beta for extracellular fluid at low (4–10 degrees C) temperatures but is equal for both fluids at greater than or equal to 40 degrees C. The mechanical oscillator technique provides data with an accuracy sufficient to perform precise (10(-5) K) calculations of beta of small volumes of biological fluids.

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47

Lyons, Owen D., Toru Inami, Elisa Perger, Azadeh Yadollahi, Christopher T. Chan, and T. Douglas Bradley. "The effect of fluid overload on sleep apnoea severity in haemodialysis patients." European Respiratory Journal 49, no. 4 (April 2017): 1601789. http://dx.doi.org/10.1183/13993003.01789-2016.

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As in heart failure, obstructive and central sleep apnoea (OSA and CSA, respectively) are common in end-stage renal disease. Fluid overload characterises end-stage renal disease and heart failure, and in heart failure plays a role in the pathogenesis of OSA and CSA. We postulated that in end-stage renal disease patients, those with sleep apnoea would have greater fluid volume overload than those without.End-stage renal disease patients on thrice-weekly haemodialysis underwent overnight polysomnography on a nondialysis day to determine their apnoea–hypopnoea index (AHI). Extracellular fluid volume of the total body, neck, thorax and right leg were measured using bioelectrical impedance.28 patients had an AHI ≥15 (sleep apnoea group; OSA:CSA 21:7) and 12 had an AHI <15 (no sleep apnoea group). Total body extracellular fluid volume was 2.6 L greater in the sleep apnoea group than in the no sleep apnoea group (p=0.006). Neck, thorax, and leg fluid volumes were also greater in the sleep apnoea than the no sleep apnoea group (p<0.05), despite no difference in body mass index (p=0.165).These findings support a role for fluid overload in the pathogenesis of both OSA and CSA in end-stage renal disease.

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48

Ritter, M., M. Steidl, and F. Lang. "Inhibition of ion conductances by osmotic shrinkage of Madin-Darby canine kidney cells." American Journal of Physiology-Cell Physiology 261, no. 4 (October 1, 1991): C602—C607. http://dx.doi.org/10.1152/ajpcell.1991.261.4.c602.

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Osmotic swelling of Madin-Darby canine kidney (MDCK) cells enhances the ion conductances of the cell membrane, which allows release of cellular ions and subsequent regulatory cell volume decrease. The present study has been performed to test whether cell shrinkage similarly affects the ion conductances of MDCK cell membranes. Increase of extracellular osmolarity by addition of 50 mM NaCl or 100 mM mannitol leads within 3 min to a hyperpolarization of the cell membrane, a marked increase of cell membrane resistance [by 223 +/- 38% (n = 8) and 228 +/- 21% (n = 5), respectively], as well as a moderate increase of the K+ selectivity of the cell membrane (by 37 +/- 13%, n = 9). Thus exposure to hypertonic extracellular fluid decreases the cell membrane conductances including the K+ conductance. Cell volume measurements reveal a regulatory cell volume increase, which is sensitive to both furosemide and dimethylamiloride. Extracellular ATP (10 microM), which activates calcium-sensitive K+ channels, hyperpolarizes the cell membrane close to the K+ equilibrium potential. The respective values are -69.9 +/- 3.1 mV (n = 9) in isotonic fluid, -79.4 +/- 1.8 mV (n = 9) within 3 min, and -76.4 +/- 1.8 mV (n = 7) within 16-h exposure to hypertonic extracellular fluid. This observation points to a sustained increase of intracellular K+ activity after exposure to hypertonic extracellular fluid.

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49

Iversen, Per Ole, Ellen Berggreen, Gunnar Nicolaysen, and Karin Heyeraas. "Regulation of extracellular volume and interstitial fluid pressure in rat bone marrow." American Journal of Physiology-Heart and Circulatory Physiology 280, no. 4 (April 1, 2001): H1807—H1813. http://dx.doi.org/10.1152/ajpheart.2001.280.4.h1807.

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The volume and fluid pressure characteristics of the intact bone marrow is incompletely understood. We used microspheres and lipoproteins for measurements of intravascular volume (IVV) and EDTA for interstitial fluid volume (IFV) within the rat bone marrow. Interstitial fluid pressure (IFP) was determined with micropipettes connected to a servo-controlled counter-pressure system. Both the microspheres and the lipoproteins yielded estimates of IVV of ∼1 ml/100 g. After a brief reactive hyperemia, IVV increased to 2.5 ml/100 g, whereas IFV decreased with ∼1.5 ml/100 g, so that total extracellular volume did not change. Baseline bone marrow IFP was 9.7 mmHg. The hyperemia led to a transient twofold increase in IFP, whereas a marked blood loss decreased IFP by almost one-half. These novel data suggest that extracellular volume and IFP within the bone marrow can be measured with tracer methods and the micropuncture technique. The responses of IVV, IFV, and IFP during changes in blood flow to the bone marrow suggest a tight regulation and are thus compatible with those for a low-compliant tissue.

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50

Bartter, Frederic C. "REGULATION OF THE VOLUME AND COMPOSITION OF EXTRACELLULAR AND INTRACELLULAR FLUID." Annals of the New York Academy of Sciences 110, no. 2 (December 15, 2006): 682–703. http://dx.doi.org/10.1111/j.1749-6632.1963.tb15791.x.

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