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.

scholarly journals Balance point characterization of interstitial fluid volume regulation

2009 ◽  
Vol 297 (1) ◽  
pp. R6-R16 ◽  
Author(s):  
R. M. Dongaonkar ◽  
G. A. Laine ◽  
R. H. Stewart ◽  
C. M. Quick
Keyword(s):  
Fluid Balance ◽  
Interstitial Fluid ◽  
Fluid Pressure ◽  
Fluid Volume ◽  
Interstitial Fluid Pressure ◽  
Lymphatic Function ◽  
Balance Point ◽  
Interstitial Fluid Volume ◽  
Algebraic Solutions

The individual processes involved in interstitial fluid volume and protein regulation (microvascular filtration, lymphatic return, and interstitial storage) are relatively simple, yet their interaction is exceedingly complex. There is a notable lack of a first-order, algebraic formula that relates interstitial fluid pressure and protein to critical parameters commonly used to characterize the movement of interstitial fluid and protein. Therefore, the purpose of the present study is to develop a simple, transparent, and general algebraic approach that predicts interstitial fluid pressure ( P i) and protein concentrations ( C i) that takes into consideration all three processes. Eight standard equations characterizing fluid and protein flux were solved simultaneously to yield algebraic equations for P i and C i as functions of parameters characterizing microvascular, interstitial, and lymphatic function. Equilibrium values of P i and C i arise as balance points from the graphical intersection of transmicrovascular and lymph flows (analogous to Guyton's classical cardiac output-venous return curves). This approach goes beyond describing interstitial fluid balance in terms of conservation of mass by introducing the concept of inflow and outflow resistances. Algebraic solutions demonstrate that P i and C i result from a ratio of the microvascular filtration coefficient (1/inflow resistance) and effective lymphatic resistance (outflow resistance), and P i is unaffected by interstitial compliance. These simple algebraic solutions predict P i and C i that are consistent with reported measurements. The present work therefore presents a simple, transparent, and general balance point characterization of interstitial fluid balance resulting from the interaction of microvascular, interstitial, and lymphatic function.

Relationship between interstitial fluid volume and pressure (compliance) in hypothyroid rats

2001 ◽  
Vol 281 (3) ◽  
pp. H1085-H1092 ◽  
Author(s):  
Helge Wiig ◽  
Tjøstolv Lund
Keyword(s):  
Skeletal Muscle ◽  
Peritoneal Dialysis ◽  
Thyroid Hormones ◽  
Interstitial Fluid ◽  
Experimental Situation ◽  
Fluid Pressure ◽  
Extracellular Fluid ◽  
Fluid Volume ◽  
The Body ◽  
Interstitial Fluid Volume

There is clinical and experimental evidence that lack of thyroid hormones may affect the composition and structure of the interstitium. This can influence the relationship between volume and pressure during changes in hydration. Hypothyrosis was induced in rats by thyroidectomy 8 wk before the experiments. Overhydration was induced by infusion of acetated Ringer, 5, 10, and 20% of the body weight, while fluid was withdrawn by peritoneal dialysis with hypertonic glucose. Interstitial fluid pressure (Pi) in euvolemia (euvolemic control situation) and experimental situation was measured with micropipettes connected to a servocontrolled counterpressure system. The corresponding interstitial fluid volume (Vi) was found as the difference between extracellular fluid volume measured as the distribution volume of 51Cr-labeled EDTA and plasma volume measured using125I-labeled human serum albumin. In euvolemia, Vi was similar or lower in the skin and higher in skeletal muscle of hypothyroid than in euthyroid control rats, whereas the corresponding Pi was higher in all tissues. During overhydration, Pi rose to the same absolute level in both types of rats, whereas during peritoneal dialysis there was a linear relationship between volume and pressure in all tissues and types of rats. Interstitial compliance (Ci), calculated as the inverse value of the slope of the curve relating changes in volume and pressure in dehydration, did not differ significantly in the hindlimb skin of hypothyroid and euthyroid rats. However, in skeletal muscle, Ci was 1.3 and 2.0 ml · 100 g−1 · mmHg−1 in hypothyroid and euthyroid rats ( P < 0.01), with corresponding numbers for the back skin of 2.7 and 5.0 ml · 100 g−1 · mmHg−1 ( P < 0.01). These experiments suggest that lack of thyroid hormones in rats changes the interstitial matrix, again leading to reduced Ci and reduced ability to mobilize fluid from the interstitium.

scholarly journals Edemagenic gain and interstitial fluid volume regulation

2008 ◽  
Vol 294 (2) ◽  
pp. R651-R659 ◽  
Author(s):  
R. M. Dongaonkar ◽  
C. M. Quick ◽  
R. H. Stewart ◽  
R. E. Drake ◽  
C. S. Cox ◽  
...  
Keyword(s):  
Fluid Balance ◽  
Interstitial Fluid ◽  
Fluid Pressure ◽  
Venous Hypertension ◽  
Fluid Volume ◽  
Balance Equations ◽  
Factors Affecting ◽  
Venous Circulation ◽  
Interstitial Fluid Volume ◽  
Simplifying Assumptions

Under physiological conditions, interstitial fluid volume is tightly regulated by balancing microvascular filtration and lymphatic return to the central venous circulation. Even though microvascular filtration and lymphatic return are governed by conservation of mass, their interaction can result in exceedingly complex behavior. Without making simplifying assumptions, investigators must solve the fluid balance equations numerically, which limits the generality of the results. We thus made critical simplifying assumptions to develop a simple solution to the standard fluid balance equations that is expressed as an algebraic formula. Using a classical approach to describe systems with negative feedback, we formulated our solution as a “gain” relating the change in interstitial fluid volume to a change in effective microvascular driving pressure. The resulting “edemagenic gain” is a function of microvascular filtration coefficient ( K f), effective lymphatic resistance ( R L), and interstitial compliance ( C). This formulation suggests two types of gain: “multivariate” dependent on C, R L, and K f, and “compliance-dominated” approximately equal to C. The latter forms a basis of a novel method to estimate C without measuring interstitial fluid pressure. Data from ovine experiments illustrate how edemagenic gain is altered with pulmonary edema induced by venous hypertension, histamine, and endotoxin. Reformulation of the classical equations governing fluid balance in terms of edemagenic gain thus yields new insight into the factors affecting an organ's susceptibility to edema.

Edema in Oral Mucosa after LPS or Cytokine Exposure

2006 ◽  
Vol 85 (5) ◽  
pp. 442-446 ◽  
Author(s):  
A. Bletsa ◽  
T. Nedrebø ◽  
K.J. Heyeraas ◽  
E. Berggreen
Keyword(s):  
Oral Mucosa ◽  
Interstitial Fluid ◽  
Fluid Pressure ◽  
Fluid Volume ◽  
Volume Distribution ◽  
Connective Tissues ◽  
Edema Formation ◽  
Necrosis Factor Alpha ◽  
Interstitial Fluid Volume ◽  
Tnf Α

Lowering of interstitial fluid pressure (Pif) is an important factor that explains the rapid edema formation in acute inflammation in loose connective tissues. Lipopolysaccharide (LPS) and the pro-inflammatory cytokines interleukin-1beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) are pathogenetic in gingivitis. To test if these substances induce lowering of Pif in rat oral mucosa, we measured Pif with a micropuncture technique. IL-1β and TNF-α caused lowering of Pif, whereas LPS induced an immediate increase in Pif, followed by lowering after 40 min. Measurements of fluid volume distribution showed a significant change in interstitial fluid volume (Vi) 1.5 hr after LPS exposure as Vi changed from 0.41 ± 0.02 to 0.51 ± 0.03 mL/g wet weight ( p < 0.05), confirming edema. These findings show that LPS, IL-1β, and TNF-α induce lowering of Pif in the rat oral mucosa and contribute to edema formation in LPS-induced gingivitis.

Interstitial fluid pressure, composition of interstitium, and interstitial exclusion of albumin in hypothyroid rats

2000 ◽  
Vol 278 (5) ◽  
pp. H1627-H1639 ◽  
Author(s):  
Helge Wiig ◽  
Rolf K. Reed ◽  
Olav Tenstad
Keyword(s):  
Thyroid Hormones ◽  
Interstitial Fluid ◽  
Fluid Pressure ◽  
Interstitial Fluid Pressure ◽  
Albumin Concentration ◽  
Rat Serum ◽  
Interstitial Fluid Volume ◽  
Hindlimb Muscle ◽  
The Difference ◽  
And Control

Lack of thyroid hormones may affect the composition and structure of the interstitium. Hypothyrosis was induced in rats by thyroidectomy 4–12 wk before the experiments. In hypothyroid rats ( n = 16), interstitial fluid pressure measured with micropipettes in hindlimb skin and muscle averaged +0.1 ± 0.2 and +0.5 ± 0.2 mmHg, respectively, with corresponding pressures in control rats ( n = 16) of −1.5 ± 0.1 ( P < 0.001) and −0.8 ± 0.1 mmHg ( P < 0.001). Interstitial fluid volume, measured as the difference between the distribution volumes of 51Cr-EDTA and125I-labeled BSA, was similar or lower in skin and higher in hypothyroid muscle. Total protein and albumin concentration in plasma and interstitial fluid (isolated from implanted wicks) was lower in hypothyroid compared with control rats. Hyaluronan content ( n = 9) in rat hindlimb skin was 2.05 ± 0.15 and 1.92 ± 0.09 mg/g dry wt ( P > 0.05) in hypothyroid and control rats, respectively, with corresponding content in hindlimb skeletal muscle of 0.35 ± 0.07 and 0.23 ± 0.01 mg/g dry wt ( P < 0.01). Interstitial exclusion of albumin in skin and muscle was measured after 125I-labeled rat serum albumin infusion for 120–168 h with an implanted osmotic pump. Relative excluded volume for albumin (Ve/Vi) was calculated as 1 − Va/Vi, and averaged 28 and 28% in hindlimb muscle ( P > 0.05), 44 and 45% in hindlimb skin ( P > 0.05), and 19 and 32% in back skin ( P < 0.05) in hypothyroid and control rats, respectively. Albumin mass was higher in back skin in spite of a lower interstitial fluid albumin concentration, a finding explained by a reduced Ve/Vi in back skin in hypothyroid rats. These experiments suggest that lack of thyroid hormones in rats changes the interstitial matrix again leading to reduced interstitial compliance and changes in the transcapillary fluid balance.

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.

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.

Increased negativity of interstitial fluid pressure in rat trachea after mast cell degranulation

1993 ◽  
Vol 74 (5) ◽  
pp. 2135-2139 ◽  
Author(s):  
M. E. Koller ◽  
K. Woie ◽  
R. K. Reed
Keyword(s):  
Mast Cell ◽  
Interstitial Fluid ◽  
Control Level ◽  
Fluid Pressure ◽  
Polymyxin B ◽  
Mast Cell Degranulation ◽  
Interstitial Fluid Pressure ◽  
Tissue Water ◽  
Edema Formation ◽  
Interstitial Fluid Volume

The present study was performed to investigate whether the increased negativity of interstitial fluid pressure (Pif) observed after intravenous injection of dextran could be mediated via mast cell degranulation induced by C48/80 and polymyxin B sulfate. Increased negativity of Pif, concomitant with edema formation and increased albumin extravasation, was seen with both substances. However, the two substances differed in that polymyxin B sulfate induced less negativity in Pif and a larger but transient increase in capillary albumin extravasation and interstitial fluid volume. Total tissue water (TTW) increased from 2.11 to 2.71 ml/g dry wt 10 min after polymyxin B and returned to control level at 30 and 60 min. Injection of C48/80 increased TTW to 2.68 ml/g dry wt at 30 min, and TTW was still elevated at 60 min. Albumin extravasation followed a similar pattern; polymyxin B sulfate increased albumin extravasation from < 0.08 to 1.18 ml/g dry wt during the first 5 min after administration. C48/80 was less potent, and maximal albumin leakage was seen after 10–25 min (0.25 ml/g dry wt). The observations demonstrate the importance of the interstitium and the loose connective tissues as "active" participants in the edema-generating process and suggest an interaction with the structural components of the interstitium, as well as an important role for the mast cells in the chain of events creating increased negativity of Pif.

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