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.

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 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.

Intestinal capillary filtration in acute and chronic portal hypertension

1988 ◽  
Vol 254 (3) ◽  
pp. G339-G345 ◽  
Author(s):  
R. J. Korthuis ◽  
D. A. Kinden ◽  
G. E. Brimer ◽  
K. A. Slattery ◽  
P. Stogsdill ◽  
...  
Keyword(s):  
Blood Flow ◽  
Portal Hypertension ◽  
Capillary Pressure ◽  
Vascular Resistance ◽  
Interstitial Fluid ◽  
Venous Pressure ◽  
Fluid Pressure ◽  
Lymph Flow ◽  
Interstitial Fluid Pressure ◽  
Capillary Filtration

The impact of acute and chronic portal hypertension on the dynamics of intestinal microvascular fluid exchange was examined in anesthetized, fasted, sham-operated control rats with normal portal pressures (CON), during acute elevations in portal pressure (APH) in control rats, and in rats in which chronic portal hypertension (CPH) was produced by calibrated stenosis of the portal vein 10 days prior to the experiments. Although intestinal blood flow and vascular resistance were not altered by APH in control rats, CPH was associated with an increased intestinal blood flow and reduced intestinal vascular resistance when compared with CON and APH. Intestinal capillary pressure and lymph flow were elevated in APH and CPH relative to control values. However, the increase in both variables was greater in CPH. The capillary filtration coefficient was elevated only in CPH. The transcapillary oncotic pressure gradient was not altered by APH or CPH. Interstitial fluid pressure was increased from -1.1 mmHg in CON to 3.9 mmHg during APH and to 5.0 mmHg in CPH. The results of this study indicate that chronic elevations in portal venous pressure produce larger increments in intestinal capillary pressure and filtration rate than do acute elevations in portal venous pressure of the same magnitude. However, the potential edemagenic effects of elevated capillary pressure in both acute and chronic portal hypertension are opposed by increases in lymph flow and interstitial fluid pressure.

Intestinal microvascular exchange during lipid absorption

1988 ◽  
Vol 255 (5) ◽  
pp. G690-G695 ◽  
Author(s):  
D. N. Granger ◽  
R. J. Korthuis ◽  
P. R. Kvietys ◽  
P. Tso
Keyword(s):  
Blood Flow ◽  
Interstitial Fluid ◽  
Fluid Pressure ◽  
Glucose Absorption ◽  
Lymph Flow ◽  
Interstitial Fluid Pressure ◽  
Lipid Absorption ◽  
Oncotic Pressure ◽  
Lymphatic Fluid ◽  
Flow Capillary

The forces and membrane coefficients governing transcapillary and lymphatic fluid fluxes were measured in the cat jejunum before and during perfusion of the gut lumen with oleic acid (5 mM) solubilized with taurocholic acid (10 mM). Net transmucosal fluid flux, lymph flow, capillary pressure (Pc), blood flow, capillary filtration coefficient (Kf,c), and lymph and plasma oncotic pressures were measured under absorptive and nonabsorptive conditions. Interstitial fluid pressure was calculated for the two conditions from measured parameters. Stimulation of lipid absorption resulted in a fivefold increase in lymph flow, a threefold increase in Kf,c, a doubling of blood flow, a 2.5 mmHg increase in Pc, and a 1.0 mmHg reduction in interstitial (lymph) oncotic pressure. Lipid absorption was associated with a 3.6 mmHg increase in interstitial fluid pressure. During lipid absorption, approximately 35% of the absorbed fluid is removed from the mucosal interstitium by lymphatics while capillaries remove the remaining 65%. The results of this study indicate that the effects of lipid absorption on microvascular and lymphatic fluid dynamics are quantitatively different than those produced by glucose absorption. These differences can be largely explained by lipid absorption-induced increases in blood flow and microvascular permeability.

Effects of bradykinin on intestinal transcapillary fluid exchange

1981 ◽  
Vol 59 (8) ◽  
pp. 786-789 ◽  
Author(s):  
J. A. Barrowman ◽  
M. A. Perry ◽  
P. R. Kvietys ◽  
M. Ulrich ◽  
D. N. Granger
Keyword(s):  
Pressure Gradient ◽  
Capillary Pressure ◽  
Protein Concentration ◽  
Fluid Pressure ◽  
Lymph Flow ◽  
Oncotic Pressure ◽  
Fluid Exchange ◽  
Intestinal Lymph ◽  
Pressure Exchange ◽  
Exchange Vessel

Bradykinin (50 μg∙L−1) increases intestinal lymph flow sixfold when infused intraarterially into the cat ileum. The capillary filtration coefficient and capillary pressure increase and interstitial fluid pressure rises from negative to positive values. A slight increase in lymph:plasma protein concentration occurs with a resulting fall in the transcapillary oncotic pressure gradient. These results indicate that the effect of bradykinin on intestinal lymph flow is attributable, at least in part, to increased capillary pressure, exchange vessel surface area, and a reduction in the effective transcapillary oncotic pressure gradient.

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.

Protein concentration of lymph and interstitial fluid in the rat tail

1984 ◽  
Vol 247 (1) ◽  
pp. H74-H79 ◽  
Author(s):  
K. Aukland ◽  
G. C. Kramer ◽  
E. M. Renkin
Keyword(s):  
Immunoglobulin G ◽  
Protein Concentration ◽  
Interstitial Fluid ◽  
Ethylenediaminetetraacetic Acid ◽  
Lymph Flow ◽  
Fluid Filtration ◽  
Flow Rates ◽  
Interstitial Volume ◽  
Rat Tail ◽  
Slow Turnover

Lymph was collected from tail lymphatics of anesthetized rats, subcutaneous interstitial fluid was obtained by implanting nylon wicks, and tendon interstitial fluid was obtained by centrifugation of pieces of tendon. Spontaneous lymph flow rates averaged 70 nl X min-1 X g skin-1. Protein concentrations and colloid osmotic pressures of sampled fluids differed significantly. Tail lymph had the highest protein concentration relative to plasma [lymph-to-plasma ratio 0.71 +/- 0.03 (SE) n = 10], followed by wick fluid (0.62 +/- 0.02, n = 9), with tendon fluid lowest (0.50 +/- 0.03, n = 10). Albumin and immunoglobulin G (IgG) concentrations in samples of tail skin and tendon were assayed by rocket immunoelectrophoresis. Comparison of their distribution volumes at lymph or tendon fluid concentrations, respectively, with interstitial fluid volumes measured as 2-h 51Cr-ethylenediaminetetraacetic acid space minus 5-min 125I-albumin space indicated that 50-60% of the interstitial volume in these tissues is not available for distribution of albumin or IgG. Low lymph flow and high interstitial protein content of rat tail indicate a slow turnover of interstitial protein. This suggests that interstitial washout of protein plays a role in limiting edema only after a sustained or chronic increase in fluid filtration.

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.

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)

scholarly journals Chronic lymph flow responses to hyperproteinemia

1998 ◽  
Vol 275 (1) ◽  
pp. R135-R140 ◽  
Author(s):  
R. Davis Manning
Keyword(s):  
Osmotic Pressure ◽  
Protein Concentration ◽  
Protein Transport ◽  
Colloid Osmotic Pressure ◽  
Lymph Flow ◽  
Plasma Protein Concentration ◽  
Autologous Plasma ◽  
Average Value ◽  
Permeability Surface

The long-term responses of lymph flow, lymph protein transport, and the permeability-surface area (PS) product to hyperproteinemia have been studied in conscious dogs. Plasma protein concentration (PPC) was increased by daily intravenous infusion of previously collected autologous plasma for 9 days. Lymph flow was determined by collecting lymph chronically from a lymphatic afferent to the popliteal node in the hind leg. Compared with the average value during the normal-PPC period, the following changes occurred during 10 days of high PPC: lymph flow decreased from 12.3 ± 1.1 to 3.8 ± 0.6 μl/min, lymph protein transport decreased from 241 ± 24 to 141 ± 21 μg/min, PS product decreased from 4.7 ± 0.5 to 3.0 ± 0.5 μl/min, PPC increased from 7.1 ± 0.1 to 8.8 ± 0.4 g/dl, lymph protein concentration increased from 1.9 ± 0.1 to 3.8 ± 0.1 g/dl, plasma colloid osmotic pressure increased from 18.6 ± 0.8 to 24.2 ± 2.1 mmHg, and lymph colloid osmotic pressure increased from 4.8 ± 0.2 to 10.4 ± 0.7 mmHg. In conclusion, long-term hyperproteinemia in dogs resulted in chronic decreases in lymph flow, lymph protein transport, and the PS product and chronic increases in lymph protein concentration and lymph colloid osmotic pressure. The marked decrease in lymph flow during hyperproteinemia decreased lymph protein transport and thus contributed to the increase in lymph protein concentration. In addition, the decreases in PS product and lymph protein transport suggest that transcapillary protein flux decreases during hyperproteinemia.

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