Platelet activating factor (PAF) increases plasma protein extravasation and induces lowering of interstitial fluid pressure (Pif) in rat skin

2005 ◽  
Vol 185 (1) ◽  
pp. 5-12 ◽  
Author(s):  
V. V. Iversen ◽  
T. Nedrebo ◽  
B. A. Borge ◽  
G. S. Salvesen ◽  
R. K. Reed
Keyword(s):  
Plasma Protein ◽  
Interstitial Fluid ◽  
Fluid Pressure ◽  
Platelet Activating Factor ◽  
Interstitial Fluid Pressure ◽  
Rat Skin ◽  
Protein Extravasation ◽  
Plasma Protein Extravasation

Lowering of interstitial fluid pressure after neurogenic inflammation is inhibited by mystixin-7 peptide

2000 ◽  
Vol 279 (3) ◽  
pp. H1377-H1382 ◽  
Author(s):  
Eli-Anne B. Gjerde ◽  
Kathrine Woie ◽  
Edward T. Wei ◽  
Rolf K. Reed
Keyword(s):  
Interstitial Fluid ◽  
Structural Integrity ◽  
Tissue Injury ◽  
Fluid Pressure ◽  
Soft Tissue Injury ◽  
Structural Similarity ◽  
Interstitial Fluid Pressure ◽  
Protein Extravasation ◽  
Plasma Protein Extravasation ◽  
Intravenous Saline

Soft tissue injury is accompanied by lowering of interstitial fluid pressure (Pif), plasma protein extravasation, and edema. Inflammation was produced by electrical stimulation (ES) of the vagus and the effects of the synthetic peptide mystixin-7 ( p-anisoyl-Arg-Lys-Leu-Leu-d-Thi-Ile-d-Leu-NH2) on Pif were examined. Micropuncture measurement of Pif in submucosa, without opening the trachea, was conducted on rats anesthetized with pentobarbital sodium (50 mg/kg) and euthanized with intravenous KCl. Pif in control (intravenous saline) was −1.2 ± 0.7 mmHg before ES and decreased to −4.7 ± 1.0 mmHg ( P < 0.01, n= 8) after ES. Mystixin-7 (10 and 20 μg/kg iv) blocked the fall in Pif after ES (−1.1 ± 0.3 and −0.8 ± 0.2 mmHg, P < 0.01, n = 8 and n= 4). The 1 μg/kg dose was without effect. When trachea from animals pretreated with mystixin-7 (20 μg/kg iv) were soaked in phosphate-buffered saline (0.15 M, pH 7.4), the rate of fluid accumulation was significantly reduced. This study suggests that mystixin peptides, which have structural similarity to a fragment from laminin-α1 chain, may be useful tools for studying cell adhesion and factors that maintain the structural integrity of connective tissue after injury.

Simultaneous Measurement of Interstitial Fluid Pressure and Load in Rat Skin After Strain Application In Vitro

2003 ◽  
Vol 31 (10) ◽  
pp. 1246-1254 ◽  
Author(s):  
David M. Wright ◽  
Helge Wiig ◽  
C. Peter Winlove ◽  
Joel L. Bert ◽  
Rolf K. Reed
Keyword(s):  
Simultaneous Measurement ◽  
Interstitial Fluid ◽  
Fluid Pressure ◽  
Interstitial Fluid Pressure ◽  
Rat Skin

Increased negativity of interstitial fluid pressure during the onset stage of inflammatory edema in rat skin

1991 ◽  
Vol 260 (6) ◽  
pp. H1985-H1991 ◽  
Author(s):  
R. K. Reed ◽  
S. A. Rodt
Keyword(s):  
Interstitial Fluid ◽  
Circulatory Arrest ◽  
Fluid Pressure ◽  
Interstitial Fluid Pressure ◽  
System Control ◽  
Rat Skin ◽  
Glass Capillaries ◽  
Inflammatory Edema ◽  
Rat Paw ◽  
Observation Period

Interstitial fluid pressure (Pif) was measured in skin of pentobarbital-anesthetized rats during anaphylaxis toward dextran and after subdermal injection of histamine by using sharpened glass capillaries (tip diam 5–7 microns) connected to a servo-controlled counterpressure system. Control Pif averaged -1.5 mmHg (SD = 1.0). After intravenous dextran Pif in the rat paw fell transiently to -3 mmHg up to 20 min and thereafter increased to +1-2 mmHg when edema had developed. To study the full magnitude of the increased negativity of Pif, circulatory arrest was induced 1 min after dextran injection. This procedure prevents accumulation of edema that will cause underestimation of Pif. In this group Pif fell to about -10 mmHg in 20 min and remained at this level throughout the observation period of 90 min. Subdermal injection of 1–10 micrograms histamine in 10 microliters saline reduced Pif to about -6 mmHg within 5 min after injection. Injection of 10 microliters saline increased Pif by +2 mmHg. Indomethacin or cyproheptadine did not alter the response in the above situations. The increased negativity in Pif of about 6–8 mmHg will add directly to normal transcapillary net filtration pressure of 0.5 mmHg and increase the latter pressure 10–20 times.

α-Trinositol prevents increased negativity of interstitial fluid pressure in rat skin and trachea induced by dextran anaphylaxis

1997 ◽  
Vol 331 (2-3) ◽  
pp. 259-266 ◽  
Author(s):  
Mai-Elin Koller ◽  
Ansgar Berg ◽  
Svein Åge Rodt ◽  
Eva Westerberg ◽  
Rolf K Reed
Keyword(s):  
Interstitial Fluid ◽  
Fluid Pressure ◽  
Interstitial Fluid Pressure ◽  
Rat Skin

The neurotensin fragment AcNT(8–13) inhibits lowering of interstitial fluid pressure in rat trachea

2002 ◽  
Vol 283 (3) ◽  
pp. H933-H940 ◽  
Author(s):  
Eli-Anne B. Gjerde ◽  
Edward T. Wei ◽  
Rolf K. Reed
Keyword(s):  
Interstitial Fluid ◽  
Structural Integrity ◽  
Fluid Pressure ◽  
Interstitial Fluid Pressure ◽  
Related Factors ◽  
Protein Extravasation ◽  
Female Wistar Rats ◽  
Intravenous Saline ◽  
Excised Tissues ◽  
Rat Trachea

Injury to soft tissue results in the lowering of interstitial fluid pressure (Pif), plasma protein extravasation, and increased total tissue volume. In this study, the effects of N-acetyl neurotensin(8–13) [AcNT(8–13)] on Pif in rat trachea were examined after electrical stimulation (ES) of the vagus nerve. Pif was measured with glass capillaries connected to a servocontrolled counterpressure system. In pentobarbital-anesthetized female Wistar rats, the Pif after intravenous saline was −1.8 ± 0.3 mmHg (means ± SD) and decreased to −5.0 ± 0.6 mmHg ( P < 0.01, n = 9) after ES. AcNT(8–13) (10 μg/kg) blocked the fall in Pif after ES (−2.5 ± 2.3 mmHg, P < 0.01, n = 8). In tracheal tissue from animals pretreated with AcNT(8–13) at the same dose and immersed in phosphate-buffered saline (0.15 M, pH 7.4), the rate of fluid accumulation in excised tissues was significantly reduced after 2 h. The ability of AcNT(8–13) to modulate the fluid mechanics of tracheal interstitium after inflammation suggests that it may be a useful tool for studying cell adhesion and related factors that maintain structural integrity of connective tissue after injury.

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

2001 ◽  
Vol 21 (3) ◽  
pp. 222-230 ◽  
Author(s):  
Rolf K. Reed ◽  
Ansgar Berg ◽  
Eli-Anne B. Gjerde ◽  
Kristofer Rubin
Keyword(s):  
Interstitial Fluid ◽  
Fluid Pressure ◽  
Interstitial Fluid Pressure

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

2015 ◽  
Vol 137 (9) ◽  
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.

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