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.

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

Cytochalasin D induces edema formation and lowering of interstitial fluid pressure in rat dermis

2001 ◽  
Vol 281 (1) ◽  
pp. H7-H13 ◽  
Author(s):  
Ansgar Berg ◽  
Kristofer Rubin ◽  
Rolf K. Reed
Keyword(s):  
Extracellular Matrix ◽  
Interstitial Fluid ◽  
Acute Inflammation ◽  
Cultured Cells ◽  
Circulatory Arrest ◽  
Fluid Pressure ◽  
Cytochalasin D ◽  
Interstitial Fluid Pressure ◽  
Edema Formation ◽  
Fluid Filtration

The increased capillary fluid filtration required to create a rapid edema formation in acute inflammation can be generated by lowering the interstitial fluid pressure (PIF). The lowering of PIF appears to involve dynamic β1-integrin-mediated interactions between dermal cells and extracellular matrix fibers. The present study specifically investigates the role of the cell cytoskeleton, i.e., the contractile apparatus of cells, in controlling PIF in rat skin as the integrins are linked to both the cytoskeleton and the extracellular matrix. PIF was measured using a micropuncture technique in the dorsal skin of the hind paw at a depth of 0.2–0.5 mm and following the induction of circulatory arrest with the intravenous injection of KCl in pentobarbital anesthesia. This procedure prevented the transcapillary flux of fluid and protein leading to edema formation in acute inflammation, which in turn can increase the PIF and therefore potentially mask a decrease of PIF. Control PIF ( n = 42) averaged −0.8 ± 0.5 (means ± SD) mmHg. In the first group of experiments, subdermal injection of 2 μl cytochalasin D, a microfilament-disrupting drug, lowered PIF to an average of −2.8 ± 0.7 mmHg within 40 min postinjection ( P< 0.05 compared with control). Subdermal injection of vehicle (10% DMSO in PBS or PBS alone) did not change the PIF( P > 0.05). Lowering of the PIF was not observed after the injection of colchicine or nocodazole, which specifically disrupts microtubuli in cultured cells. In the second group of experiments, 2 μl of cytochalasin D injected subdermally into rats with intact circulation increased the total tissue water (TTW) and albumin extravasation rate ( E ALB) by 0.7 ± 0.2 and 0.4 ± 0.3 ml/g dry wt, respectively ( P < 0.05 compared with vehicle). Nocodazole and colchicine did not significantly alter the TTW or E ALB compared with the vehicle ( P > 0.05). Taken together, these findings strongly suggest that the connective tissue cells can participate in control of PIF via the actin filament system. In addition, the observation that subdermal injection of cytochalasin D lowered PIF indicates that a dynamic assembly and disassembly of actin filaments also occurs in the cells of dermal tissues in vivo.

Micropuncture measurements of interstitial fluid pressure in rat nasal mucosa during early inflammatory reactions

1998 ◽  
Vol 85 (2) ◽  
pp. 465-470 ◽  
Author(s):  
Ansgar Berg ◽  
Arne Kirkebø ◽  
Karin J. Heyeraas
Keyword(s):  
Nasal Mucosa ◽  
Interstitial Fluid ◽  
Circulatory Arrest ◽  
Fluid Pressure ◽  
Nasal Bone ◽  
Interstitial Fluid Pressure ◽  
Edema Formation ◽  
Inflammatory Reactions ◽  
Inflammatory Stimuli ◽  
Transvascular Fluid Shifts

Interstitial fluid pressure (Pif) has been studied in rat nasal mucosa during early inflammatory reactions induced by dextran anaphylaxis and local application of histamine. Pif was measured by using sharpened micropipettes connected to a servo-controlled counterpressure system. Access to the nasal mucosa was obtained from the facial side of the head through a small cavity drilled in the nasal bone. During dextran anaphylaxis, Pif increased significantly from control values of 2.2 ± 0.4 to 3.8 ± 0.21 mmHg ( P < 0.05) within 1 h. Corresponding Pif values for histamine were 1.6 ± 0.9 and 2.9 ± 0.9 mmHg ( P < 0.05), respectively. These measurements support the hypothesis that a major driving force for the rapid exudation across inflamed respiratory mucosa is a hydrostatic pressure gradient created by increased mucosa Pif. When the transvascular fluid shifts accompanying the inflammatory reactions are prevented by circulatory arrest, Pif decreased significantly to subatmospheric values, −0.8 ± 0.8 and −3.3 ± 1.2 mmHg in the dextran and histamine group, respectively ( P < 0.05). The decrease in Pif in the nasal mucosa after inflammatory stimuli, during circulatory arrest, provides further evidence for “active” modulation of Pif through changes in mechanical properties of the interstitial matrix. The decrease in Pif seen under these circumstances reveals a possible mechanism participating in the rapid and initial edema formation after inflammatory provocations.

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

Increased negativity of interstitial fluid pressure in rat trachea in dextran anaphylaxis

1992 ◽  
Vol 72 (1) ◽  
pp. 53-57 ◽  
Author(s):  
M. E. Koller ◽  
R. K. Reed
Keyword(s):  
Interstitial Fluid ◽  
Circulatory Arrest ◽  
Fluid Pressure ◽  
Fluid Volume ◽  
Interstitial Fluid Pressure ◽  
Tracheal Mucosa ◽  
Interstitial Fluid Volume ◽  
Dextran 70 ◽  
Mean Pressure ◽  
Rat Trachea

This study shows that, in rat trachea, dextran anaphylaxis is associated with increased negativity of interstitial fluid pressure (Pif) as measured with sharpened glass capillaries (tip diameter 3–7 microns) connected to a servo-controlled counterpressure system. Experiments were carried out in pentobarbital-anesthetized Wistar-Moller rats. Pif in the control situation was -2.5 +/- 0.38 (SD) mmHg. The mean pressure in animals killed 2 min after initiation of the anaphylactic reaction by injection of 1 ml of 10% Dextran 70 in 0.9% NaCl was -10.3 +/- 2.6 mmHg. In another experimental series, interstitial fluid volume was measured after dextran administration but without inducing circulatory arrest. Interstitial fluid volume increased from 0.94 +/- 0.16 to 1.56 +/- 0.42 ml/g dry wt after 10 min to 1.57 +/- 0.30 and 1.10 +/- 0.27 ml/g dry wt after 30 and 60 min, respectively. The increased negativity in Pif in tracheal mucosa in the early phase of dextran anaphylaxis will markedly increase the transcapillary net filtration pressure in the initial phase of edema development.

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
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