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.

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.

Adaptation of the hepatic transudation barrier to sinusoidal hypertension

2020 ◽  
Vol 318 (4) ◽  
pp. R722-R729 ◽  
Author(s):  
Ranjeet M. Dongaonkar ◽  
Christopher M. Quick ◽  
Glen A. Laine ◽  
Karen Uray ◽  
Charles S. Cox ◽  
...  
Keyword(s):  
Reflection Coefficient ◽  
Protein Concentration ◽  
Interstitial Fluid ◽  
Fluid Pressure ◽  
Vena Cava ◽  
Barrier Properties ◽  
Venous Hypertension ◽  
Lymph Flow ◽  
Acute Changes

The role of the hepatic transudation barrier in determining ascites volume and protein content in chronic liver disease is poorly understood. Therefore, the purpose of the present study was to characterize how chronic sinusoidal hypertension impacts hepatic transudation barrier properties and the transudation rate. The suprahepatic inferior vena cava was surgically constricted, and animals were exposed to either short-term (SVH; 2–3 wk) or long-term venous hypertension (LVH; 5–6 wk). Compared with SVH, LVH resulted in lower peritoneal fluid pressure, ascites volume, and ascites protein concentration. The transudation barrier protein reflection coefficient was significantly higher, and the transudation barrier hydraulic conductivity, transudation rate, and transudate-to-lymph protein concentration ratio were significantly lower in LVH animals compared with SVH animals. The sensitivity of transudation rates to acute changes in interstitial fluid pressures was also significantly lower in LVH animals compared with SVH animals. In contrast, there was no detectable difference in hepatic lymph flow rate or sensitivity of lymph flow to acute changes in interstitial fluid pressures between SVH and LVH animals. Taken together, these data suggest that decreased hepatic transudation barrier permeability to fluid and protein and increased reflection coefficient led to a decrease in the hepatic contribution to ascites volume. The present work, to the best of our knowledge, is the first to quantify an anti-ascites adaptation of the hepatic transudation barrier in response to chronic hepatic sinusoidal hypertension.

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.

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.

Superior vena caval pressure elevation causes pleural effusion formation in sheep

1988 ◽  
Vol 255 (3) ◽  
pp. H492-H495 ◽  
Author(s):  
S. J. Allen ◽  
G. A. Laine ◽  
R. E. Drake ◽  
J. C. Gabel
Keyword(s):  
Cardiac Output ◽  
Pleural Effusion ◽  
Protein Concentration ◽  
Superior Vena ◽  
Recovery Period ◽  
Balloon Catheter ◽  
Vena Cava ◽  
Base Line ◽  
Superior Vena Caval ◽  
Plasma Protein Concentration

The effect of superior vena caval pressure (SVCP) elevation on the formation of pleural effusions (PE) was studied in sheep. Through a right thoracotomy, a Silastic cuff was placed around the superior vena cava. Catheters for monitoring SVCP and pulmonary artery pressure (PAP) were also placed. After a 1- to 3-wk recovery period, we measured the SVCP, PAP, cardiac output, and plasma protein concentration (Cp). We then elevated the SVCP to various levels from base line [5.3 +/- 2.6 (SD) mmHg] to 33 mmHg. The cardiac output, PAP, and Cp were remeasured 1–2 h and 24 h after SVCP elevation. At the end of the 24-h period, the animals were killed. The PE volume and pleural fluid protein concentration (Cpl) were measured, and the Cpl/Cp was calculated. PE generally did not occur until the SVCP was elevated above 15 mmHg. To study the effect of the thoracotomy on the subsequent pleural effusion, we studied six additional sheep in which we did not perform a thoracotomy. In these animals, the SVCP was elevated to between 5 and 28 mmHg for 24 h by use of a 16-Fr balloon catheter placed via a left external jugular vein and a right carotid-external jugular shunt. We found that the PE volume, for a given SVCP elevation, was similar to that present in sheep that received a thoracotomy. For all sheep the volume of PE was related to SVCP by the equation PE (ml) = 0.24e0.26SVCP, r = 0.85. In the sheep without a thoracotomy, Cpl/Cp rose with increasing volume of PE. Our data demonstrate that elevation of SVCP greater than 15 mmHg for 24 h results in the formation of PE. The rise in Cpl/Cp with PE volume suggests that filtration through the pleural vessels is not the major contributor to PE formation.

Differential liquid and protein clearance from the alveoli of anesthetized sheep

1982 ◽  
Vol 53 (1) ◽  
pp. 96-104 ◽  
Author(s):  
M. A. Matthay ◽  
C. C. Landolt ◽  
N. C. Staub
Keyword(s):  
Protein Concentration ◽  
Fluid Pressure ◽  
Lymph Flow ◽  
Autologous Serum ◽  
Liquid Volume ◽  
Alveolar Wall ◽  
Ringer Lactate ◽  
Plasma Protein Concentration ◽  
Two Fluids ◽  
The Difference

We determined the clearance rates of 50 ml of isosmotic fluids from the lungs of anesthetized, ventilated sheep with lung lymph fistulas. The removal of the liquid volume followed a monoexponential process over 4 h for both Ringer lactate [half time (t 1/2) = 3 h] and autologous serum (t 1/2 = 6 h). Lymph flow did not increase with Ringer lactate, indicating that the alveolar fluid was cleared via the circulation. With serum, however, lymph flow increased 40%. In both groups the lymph-to-plasma protein concentration ratio fell slightly. Using protein tracers in the alveolar instillate, we found that less than 2% of the protein entered the lymph and plasma. Almost all of the protein remained in the air spaces and was concentrated in proportion to the amount of liquid volume that was cleared. Clearance of liquid volume from alveoli to interstitium could be due to subatmospheric interstitial fluid pressure or to active metabolic processes that cause small molecules to leave the alveolar fluid, or both. The results of the serum experiments tend to favor a metabolic process, but passive mechanisms are possible. The difference in lymph flow response between the two fluids must be due to the protein in the alveolar fluid. We believe Ringer lactate dilutes the alveolar wall interstitial protein concentration thereby decreasing local filtration, whereas serum concentrates alveolar wall interstitial fluids proteins thereby increasing local filtration.

Lymphatic and vascular responses to fluid infusion in castrated and noncastrated sheep

1987 ◽  
Vol 252 (6) ◽  
pp. R1114-R1118 ◽  
Author(s):  
G. J. Valenzuela ◽  
R. A. Brace ◽  
L. D. Longo
Keyword(s):  
Blood Volume ◽  
Thoracic Duct ◽  
Protein Concentration ◽  
Interstitial Fluid ◽  
Lymph Flow ◽  
Thoracic Duct Lymph ◽  
Base Line ◽  
Plasma Protein Concentration ◽  
Duct Lymph ◽  
Estrogen Withdrawal

Estrogen administration produces blood volume expansion and interstitial fluid retention. We decided to study the effect of estrogen withdrawal on blood volume and determine whether oophorectomy has an effect on lymph flow or protein concentration. The rate of left thoracic duct lymph flow averaged 0.041 +/- 0.005 (SE) and 0.071 +/- 0.008 ml X min-1 X kg-1 in castrated (n = 9) and noncastrated (n = 9) female sheep, respectively (P = 0.006). After three serial intravenous infusions of Ringer lactate solution (2% body wt/infusion) the thoracic duct lymph flow in the castrated animals increased 358, 457, and 498% over the base-line rate, compared with increase of 200, 235, and 353% in the nonpregnant ewes. However, with the lower control values in the castrated animals, the lymph flow rate reached the same absolute values as those seen in the noncastrated ewes. Lymph protein concentration and the lymph-to-plasma protein concentration ratio, as well as arterial and venous pressures, were unaltered by oophorectomy. Base-line whole blood volumes were 58.2 +/- 1.9 (n = 9) and 64.8 +/- 2.6 ml/kg (n = 9) in the castrated and noncastrated ewes, respectively (P less than 0.05). Systemic vascular compliance averaged 4.5 +/- 0.7 and 7.1 +/- 1.7 ml X kg-1 X mmHg-1 in the castrated and noncastrated ewes, respectively (P less than 0.05), whereas interstitial fluid compliance values were 12 and 32 ml X kg-1 X mmHg-1, respectively. The capillary filtration coefficients were not different in the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

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