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.

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.

Atrial Natriuretic Peptide as a Regulator of Transvascular Fluid Balance

Physiology ◽  
1996 ◽  
Vol 11 (3) ◽  
pp. 138-143 ◽  
Author(s):  
EM Renkin ◽  
VL Tucker
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Plasma Volume ◽  
Fluid Balance ◽  
Interstitial Fluid ◽  
Fluid Volume ◽  
Interstitial Fluid Volume ◽  
Atrial Natriuretic

Unlike other natriuretics, which act via the kidneys to reduce interstitial fluid volume with little change in plasma volume, atrial natriuretic peptide has important extrarenal actions that enable it to reduce plasma volume preferentially.

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.

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.

scholarly journals Interstitial Fluid Pressure in Normal and Inflamed Pulp

1999 ◽  
Vol 10 (3) ◽  
pp. 328-336 ◽  
Author(s):  
K.J. Heyeraas ◽  
E. Berggreen
Keyword(s):  
Blood Volume ◽  
Dental Pulp ◽  
Interstitial Fluid ◽  
Fluid Pressure ◽  
Lymph Flow ◽  
Fluid Volume ◽  
Tissue Pressure ◽  
Interstitial Fluid Volume ◽  
Harmful Substances ◽  
Transport Fluid

Tissue pressure is the hydrostatic pressure in the interstitial fluid which surrounds the pulpal cells. This pressure outside the vessels is normally considerably lower than the blood pressure inside the vessels. The dental pulp has a relatively low interstitial compliance due to its enclosure between rigid dentin walls. Accordingly, even a modest increase in pulpal fluid volume will raise the tissue pressure, which may compress blood vessels, leading to ischemia and necrosis. Inflammation may lead to an increase in both interstitial fluid volume and blood volume in the low-compliant pulp and thereby increase the tissue pressure. However, the increased tissue pressure may, in turn, initiate increased lymph flow and absorption of fluid into capillaries in nearby non-inflamed tissue. Both of these latter factors will transport fluid out of the affected area and subsequently out of the tooth and consequently lower the tissue pressure. Increased tissue pressure, whether caused by increased blood volume or increased capillary filtration, will promote outward flow of fluid through exposed dentin tubules and thereby help to protect the pulp against entry of harmful substances. It seems physiologically beneficial, therefore, for the pulp to have a high tissue pressure, which promptly increases when blood flow increases due to its low compliance.

Regulation of microvascular filtration in the myocardium by interstitial fluid pressure

1996 ◽  
Vol 271 (6) ◽  
pp. R1465-R1469 ◽  
Author(s):  
R. H. Stewart ◽  
D. A. Rohn ◽  
U. Mehlhorn ◽  
K. L. Davis ◽  
S. J. Allen ◽  
...  
Keyword(s):  
Protein Concentration ◽  
Filtration Rate ◽  
Interstitial Fluid ◽  
Superior Vena ◽  
Fluid Pressure ◽  
Lymph Flow ◽  
Fluid Volume ◽  
Superior Vena Caval ◽  
Plasma Protein Concentration ◽  
Interstitial Fluid Volume

We hypothesized that myocardial microvascular filtration rate (Jv) could be manipulated by varying end-diastolic myocardial interstitial hydrostatic (P(int)) pressure. Dogs under general anesthesia were instrumented with intramyocardial capsules to measure P(int) and with prenodal myocardial lymphatic trunk cannulas and superior vena caval balloon-tipped catheters to manipulate myocardial lymph flow. Because, for a given surface area, the lymph-to-plasma protein concentration ration (CL/CP) varies inversely with JV, CL/CP was utilized as an index of changes in JV. When lymphatic outflow pressure (P0) was elevated to abolish lymph flow and force myocardial interstitial fluid volume to expand, P(int) rose significantly from 15.0 +/- 0.8 to 27.6 +/- 1.0 mmHg and CL/CP increased significantly from 0.75 +/- 0.04 to 0.85 +/- 0.04, indicating a decrease in JV. When P0 was lowered and lymph flow resumed, P(int) and CL/CP decreased significantly to 15.3 +/- 0.9 mmHg and 0.75 +/- 0.04, respectively, indicating an increase in JV. We conclude that myocardial microvascular filtration rate may be modulated by changes in P(int) resulting from alterations in myocardial interstitial fluid volume secondary to variations in lymph flow from the heart.

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 Evaluation of renal and cardiovascular protection mechanisms of SGLT2 inhibitors: model-based analysis of clinical data

2018 ◽  
Vol 315 (5) ◽  
pp. F1295-F1306 ◽  
Author(s):  
K. Melissa Hallow ◽  
Peter J. Greasley ◽  
Gabriel Helmlinger ◽  
Lulu Chu ◽  
Hiddo J. Heerspink ◽  
...  
Keyword(s):  
Renal Impairment ◽  
Clinical Data ◽  
Healthy Subjects ◽  
Interstitial Fluid ◽  
Sglt2 Inhibitors ◽  
Fluid Volume ◽  
Diabetic Patients ◽  
Pressure Reduction ◽  
Physiological Variables ◽  
Interstitial Fluid Volume

The mechanisms of cardiovascular and renal protection observed in clinical trials of sodium-glucose cotransporter 2 (SGLT2) inhibitors (SGLT2i) are incompletely understood and likely multifactorial, including natriuretic, diuretic, and antihypertensive effects, glomerular pressure reduction, and lowering of plasma and interstitial fluid volume. To quantitatively evaluate the contribution of proposed SGLT2i mechanisms of action on changes in renal hemodynamics and volume status, we coupled a mathematical model of renal function and volume homeostasis with clinical data in healthy subjects administered 10 mg of dapagliflozin once daily. The minimum set of mechanisms necessary to reproduce observed clinical responses (urinary sodium and water excretion, serum creatinine and sodium) was determined, and important unobserved physiological variables (glomerular pressure, blood and interstitial fluid volume) were then simulated. We further simulated the response to SGLT2i in diabetic virtual patients with and without renal impairment. Multiple mechanisms were required to explain the observed response: 1) direct inhibition of sodium and glucose reabsorption through SGLT2, 2) SGLT2-driven inhibition of Na+/H+ exchanger 3 sodium reabsorption, and 3) osmotic diuresis coupled with peripheral sodium storage. The model also showed that the consequences of these mechanisms include lowering of glomerular pressure, reduction of blood and interstitial fluid volume, and mild blood pressure reduction, in agreement with clinical observations. The simulations suggest that these effects are more significant in diabetic patients than healthy subjects and that while glucose excretion may diminish with renal impairment, improvements in glomerular pressure and blood volume are not diminished at lower glomerular filtration rate, suggesting that cardiorenal benefits of SGLT2i may be sustained in renally impaired patients.

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