Intercompartmental fluid shifts after dextran infusion in rabbits

Intercompartmental fluid shifts were studied in New Zealand White rabbits after infusion of hyperoncotic dextran solution with a mean molecular weight of 64,200 and osmolality of 220 mosmol/kg H2O. In comparison with the control period, it was found that 1) plasma volume increased by a net volume of 83 +/- 12 ml; 2) systemic blood pressure increased slightly but significantly and central venous pressure increased markedly (this was accompanied by a reduction of interstitial fluid pressure from a control of -1 to -8 cmH2O after dextran); 3) plasma volume expansion was not accompanied by plasma sodium and chloride dilution when they were expressed in meq/kg of plasma water; and 4) plasma osmolality did not change after dextran infusions. The increase in plasma volume unaccompanied by any change in plasma sodium, chloride, or osmolality may be explained by a transcapillary fluid shift from the interstitial space to the bloodstream caused by an increase in plasma oncotic pressure. Because the more negative interstitial fluid pressure did not seem to attract any appreciable amount of fluid from the cells, we concluded that the interstitial space did not hydrodynamically couple the intravascular space to the cellular compartment.

Download Full-text

Tissue pressure and plasma oncotic pressure during exercise

Journal of Applied Physiology ◽

10.1152/jappl.1984.56.1.102 ◽

1984 ◽

Vol 56 (1) ◽

pp. 102-108 ◽

Cited By ~ 13

Author(s):

V. Mohsenin ◽

R. R. Gonzalez

Keyword(s):

Osmotic Pressure ◽

Plasma Volume ◽

Interstitial Fluid ◽

Vastus Lateralis ◽

Fluid Pressure ◽

Colloid Osmotic Pressure ◽

Interstitial Fluid Pressure ◽

Plasma Sodium ◽

Vastus Lateralis Muscle ◽

Base Line

Six healthy male subjects exercised on a cycle ergometer for 3 min for assessment of forces involved in transvascular fluid shift during intense exercise. The work load was at 105% of peak O2 uptake of the subjects. This caused a 17.2 +/- 1.2% reduction in plasma volume. The plasma volume loss was associated with an increase in plasma sodium, from 142.6 +/- 0.5 to 148.1 +/- 1.0 meq X 1(-1) (P less than 0.005); chloride, from 101.8 +/- 0.6 to 104.6 +/- 0.9 meq X 1(-1) (P less than 0.005); lactate, from 1.4 +/- 0.2 to 14.0 +/- 1.5 meq X 1(-1) (P less than 0.005); and osmolality, from 283 +/- 2 to 299 +/- 3 mosmol X kg-1 H2O (P less than 0.005) within 2 min after cessation of exercise. Plasma protein increased from 7.0 +/- 0.2 to 8.1 +/- 0.3 g X dl-1 (P less than 0.005), and plasma colloid osmotic pressure from 25.1 +/- 0.6 to 30.6 +/- 1.4 mmHg (P less than 0.005) after exercise. Interstitial fluid pressure in the exercising vastus lateralis muscle increased from a base-line value (SE) of -1.0 +/- 0.9 to + 1.5 +/- 1.1 cmH2O, 14 min after the end of exercise (P less than 0.05). Interstitial fluid pressure of the triceps brachii (inactive) did not change significantly after exercise. Our data suggest that increased transvascular colloid osmotic pressure and elevation of interstitial fluid pressure become increasingly important in preventing loss of plasma volume during maximal exercise.

Download Full-text

Intercompartmental fluid shifts due to glucose release during hemorrhage in rabbits

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1983.245.1.h143 ◽

1983 ◽

Vol 245 (1) ◽

pp. H143-H149

Author(s):

V. Mohsenin ◽

A. B. DuBois

Keyword(s):

New Zealand ◽

Plasma Volume ◽

Plasma Glucose ◽

Interstitial Space ◽

Volume Replacement ◽

Plasma Sodium ◽

Fluid Shift ◽

New Zealand White Rabbits ◽

Fluid Shifts ◽

Chloride Concentrations

Intercompartmental fluid shifts were studied in 18 anesthetized New Zealand White rabbits after hemorrhage. During graded hemorrhage the plasma volume spontaneously replaced was proportional both in time and amount to the hyperosmolar response. This, in turn, was mainly due to hyperglycemia. In 5 fed rabbits and 5 rabbits unfed for 40 h, all subjected to 16 ml/kg of hemorrhage, plasma volume replacement was closely correlated with the hyperglycemic response. Plasma glucose concentration gradually increased in fed animals throughout a 2-h posthemorrhagic period, whereas the hyperglycemic response ceased 15 min after hemorrhage in unfed animals, and further fluid shift also stopped. During the first 30 min after hemorrhage most of the fluid that shifted into the bloodstream came from the interstitial space, as judged by a lack of change in plasma sodium and chloride concentrations. However, during the second hour of the posthemorrhagic period of well-fed rabbits, plasma sodium and chloride concentrations decreased, suggesting that dilute fluid had shifted from the cells to the interstitial space and bloodstream. We concluded that the hyperglycemic response during and after hemorrhage played a significant role in plasma volume replacement, but this was less after a period of food deprivation.

Download Full-text

Pressure-volume behavior of perivascular interstitium measured in isolated dog lung

Journal of Applied Physiology ◽

10.1152/jappl.1980.48.6.939 ◽

1980 ◽

Vol 48 (6) ◽

pp. 939-946 ◽

Cited By ~ 32

Author(s):

S. J. Lai-Fook ◽

B. Toporoff

Keyword(s):

Interstitial Fluid ◽

Venous Pressure ◽

Fluid Pressure ◽

Transpulmonary Pressure ◽

Interstitial Fluid Pressure ◽

Alveolar Pressure ◽

Lung Weight ◽

Lung Volumes ◽

Water Accumulation ◽

Alveolar Surface

Pulmonary perivascular interstitial fluid pressure (Px) was measured as a function of extravascular water accumulation (W). Px was measured directly by wick catheters and open-ended needles inserted in the interstitium near the hilus of isolated perfused dog lobes. Lobes were studied at constant transpulmonary pressure (Ptp) and vascular pressure (Pv, arterial equal to venous pressure). Px-W behavior had two distinct phases: an initial low compliance phase interpreted as perivascular filling, followed sometimes by an abrupt transition to a high compliance phase interpreted as alveolar flooding. W at transition was between 20 and 50% of the initial lung weight. Perivascular compliance during filling at a Ptp of 6 cmH2O was 0.1 g.g wet lobe wt-1.cmH2O-1, which was one-sixth that during alveolar flooding and 2.5 times that at a Ptp of 25 cmH2O. At the start of alveolar flooding, estimated alveolar interstitial fluid pressure was slightly (2 cmH2O) below alveolar pressure (PAlv) at a Ptp of 6 cmH2O but considerably belov PAlv at high lung volumes. These findings support the concept that alveolar surface tension reduces the interstitial fluid pressure below PAlv.

Download Full-text

Intestinal capillary filtration in acute and chronic portal hypertension

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1988.254.3.g339 ◽

1988 ◽

Vol 254 (3) ◽

pp. G339-G345 ◽

Cited By ~ 3

Author(s):

R. J. Korthuis ◽

D. A. Kinden ◽

G. E. Brimer ◽

K. A. Slattery ◽

P. Stogsdill ◽

...

Keyword(s):

Blood Flow ◽

Portal Hypertension ◽

Capillary Pressure ◽

Vascular Resistance ◽

Interstitial Fluid ◽

Venous Pressure ◽

Fluid Pressure ◽

Lymph Flow ◽

Interstitial Fluid Pressure ◽

Capillary Filtration

The impact of acute and chronic portal hypertension on the dynamics of intestinal microvascular fluid exchange was examined in anesthetized, fasted, sham-operated control rats with normal portal pressures (CON), during acute elevations in portal pressure (APH) in control rats, and in rats in which chronic portal hypertension (CPH) was produced by calibrated stenosis of the portal vein 10 days prior to the experiments. Although intestinal blood flow and vascular resistance were not altered by APH in control rats, CPH was associated with an increased intestinal blood flow and reduced intestinal vascular resistance when compared with CON and APH. Intestinal capillary pressure and lymph flow were elevated in APH and CPH relative to control values. However, the increase in both variables was greater in CPH. The capillary filtration coefficient was elevated only in CPH. The transcapillary oncotic pressure gradient was not altered by APH or CPH. Interstitial fluid pressure was increased from -1.1 mmHg in CON to 3.9 mmHg during APH and to 5.0 mmHg in CPH. The results of this study indicate that chronic elevations in portal venous pressure produce larger increments in intestinal capillary pressure and filtration rate than do acute elevations in portal venous pressure of the same magnitude. However, the potential edemagenic effects of elevated capillary pressure in both acute and chronic portal hypertension are opposed by increases in lymph flow and interstitial fluid pressure.

Download Full-text

Hemodynamics and interstitial fluid pressure in the rat tail

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1984.247.1.h80 ◽

1984 ◽

Vol 247 (1) ◽

pp. H80-H87 ◽

Cited By ~ 9

Author(s):

K. Aukland ◽

H. Wiig

Keyword(s):

Blood Flow ◽

Plasma Volume ◽

Volume Expansion ◽

Interstitial Fluid ◽

Cuff Pressure ◽

Subcutaneous Tissue ◽

Fluid Pressure ◽

Interstitial Fluid Pressure ◽

Venous Stasis ◽

Plasma Volume Expansion

Blood flow in the rat was measured during pentobarbital anesthesia by plethysmographic and thermometric techniques. Tail arterial and venous pressures (Pa and Pv) were measured by glass micropipettes and interstitial fluid pressure (PIF) by wick-in-needle technique. Large pressure gradients were measured along the tail, Pa decreasing and Pv increasing toward the tip. In the vasoconstricted tail, distal arterial and venous pressures (Pad and Pvd, respectively, 10 cm from the tail root) were 55 and 11% of aortic pressure (PA), while PIF was 0-2 mmHg. Plasma volume expansion increased blood flow by a factor of 10 to 35. Pad rose to 74% and Pvd to 20% of PA. PIF increased to 15 mmHg, in parallel with Pv. Venous stasis (cuff pressure 14.7 mmHg) increased PIF and Pv by 3.5 and 9 mmHg, respectively, while tail volume increased by 0.4 to 1.2%. In conclusion, the large flow increase induced by plasma volume expansion depends strongly on dilation of the tail artery, with two- to threefold increase in internal radius. Simultaneously the tail veins relax and expand. Subcutaneous tissue is compressed between the expanding vessels and the tight skin, and PIF increases almost sufficiently to prevent a rise in net capillary filtration pressure. This immediate edema-preventing mechanism is less efficient during venous stasis, which presumably does not induce "active" dilation of the tail vessels. Similar mechanisms probably exist in other "encapsulated" tissues.

Download Full-text

Interstitial Fluid Pressure: II. Pressure-Volume Curves of Interstitial Space

Circulation Research ◽

10.1161/01.res.16.5.452 ◽

1965 ◽

Vol 16 (5) ◽

pp. 452-460 ◽

Cited By ~ 207

Author(s):

ARTHUR C. GUYTON

Keyword(s):

Interstitial Fluid ◽

Fluid Pressure ◽

Interstitial Space ◽

Interstitial Fluid Pressure

Download Full-text

Control of interstitial fluid pressure: Role of [beta ]-integrins

Seminars in Nephrology ◽

10.1053/snep.2001.21646 ◽

2001 ◽

Vol 21 (3) ◽

pp. 222-230 ◽

Cited By ~ 42

Author(s):

Rolf K. Reed ◽

Ansgar Berg ◽

Eli-Anne B. Gjerde ◽

Kristofer Rubin

Keyword(s):

Interstitial Fluid ◽

Fluid Pressure ◽

Interstitial Fluid Pressure

Download Full-text

Dynamics of Interstitial Fluid Pressure in Extracellular Matrix Hydrogels in Microfluidic Devices

Journal of Biomechanical Engineering ◽

10.1115/1.4031020 ◽

2015 ◽

Vol 137 (9) ◽

Cited By ~ 5

Author(s):

Joe Tien ◽

Le Li ◽

Ozgur Ozsun ◽

Kamil L. Ekinci

Keyword(s):

Extracellular Matrix ◽

Pressure Distribution ◽

Interstitial Fluid ◽

Scaling Laws ◽

Fluid Pressure ◽

Interstitial Fluid Pressure ◽

External Loading ◽

Interstitial Pressure ◽

Time Resolved ◽

Long Time

In order to understand how interstitial fluid pressure and flow affect cell behavior, many studies use microfluidic approaches to apply externally controlled pressures to the boundary of a cell-containing gel. It is generally assumed that the resulting interstitial pressure distribution quickly reaches a steady-state, but this assumption has not been rigorously tested. Here, we demonstrate experimentally and computationally that the interstitial fluid pressure within an extracellular matrix gel in a microfluidic device can, in some cases, react with a long time delay to external loading. Remarkably, the source of this delay is the slight (∼100 nm in the cases examined here) distension of the walls of the device under pressure. Finite-element models show that the dynamics of interstitial pressure can be described as an instantaneous jump, followed by axial and transverse diffusion, until the steady pressure distribution is reached. The dynamics follow scaling laws that enable estimation of a gel's poroelastic constants from time-resolved measurements of interstitial fluid pressure.

Download Full-text