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.

Microvascular, interstitial, and lymphatic interactions in normal heart

1985 ◽  
Vol 249 (4) ◽  
pp. H834-H842 ◽  
Author(s):  
G. A. Laine ◽  
H. J. Granger
Keyword(s):  
Plasma Protein ◽  
Protein Concentration ◽  
Venous Pressure ◽  
Left Ventricular ◽  
Lymph Flow ◽  
Normal Heart ◽  
Oncotic Pressure ◽  
Fluid Exchange ◽  
Edema Formation ◽  
Total Plasma Protein

Control of transmicrovascular fluid exchange in the heart is of critical importance in the prevention of myocardial edema formation. To quantify the absolute values for, and the interrelationships between, the forces and flows governing fluid balance within the normal heart, the following variables were measured: arterial pressure (Pa), coronary sinus pressure (Pcs), myocardial interstitial fluid pressure (Pint), plasma protein concentration (Cp), and oncotic pressure (tau cap) along with interstitial protein concentration (CL), interstitial oncotic pressure (tau int), and left ventricular lymph flow rate (Jv). All parameters were recorded under control conditions and during graded venous pressure elevations. Control values were Pa, 125 +/- 21 mmHg; Pcs, 7.3 +/- 1.3 mmHg; Pint, 14.9 +/- 3.1 mmHg; CL/Cp, 0.82 +/- 0.12; and Jv, 7.0 +/- 2.7 ml/h. As Pcs was elevated to eight times control, Pint increased from 15 to 50 mmHg and lymph flow rose sixfold. A filtration-independent value for CL/Cp could not be obtained for total plasma protein, although a washdown CL/Cp value for beta-lipoprotein of 0.04 was obtained. Our data indicate that a large surface area of myocardial exchange vessels coupled with lymphatics of relatively low sensitivity to extravascular volume expansion produce a system that relies on a large increase in interstitial hydrostatic pressure to limit edema formation.

Permeability characteristics of colonic capillaries

1980 ◽  
Vol 239 (4) ◽  
pp. G300-G305 ◽  
Author(s):  
P. D. Richardson ◽  
D. N. Granger ◽  
D. Mailman ◽  
P. R. Kvietys
Keyword(s):  
Pressure Gradient ◽  
Plasma Protein ◽  
Protein Concentration ◽  
Venous Pressure ◽  
Molecular Size ◽  
Lymph Flow ◽  
Oncotic Pressure ◽  
Plasma Protein Concentration ◽  
Permeability Characteristics ◽  
Pressure Elevation

Blood flow, lymph flow, lymph protein concentration (CL), lymph oncotic pressure, plasma protein concentration (CP), and plasma oncotic pressure were determined under steady-state conditions at venous pressures of 0, 10, 20, 30, and 40 mmHg in autoperfused segments of dog colon. Venous pressure elevation increased colonic vascular resistance, lymph flow, lymphatic protein flux, and the transcapillary oncotic pressure gradient, whereas the lymph-to-plasma protein concentration ratio (CL/CP) declined. The osmotic reflection coefficient (sigma d) was estimated using sigma d = 1-CL/CP when CL/CP is filtration independent (high lymph flows). For total protein sigma d = 0.85 +/- 0.02. Values of sigma d for plasma protein fractions with molecular radii ranging between 37 and 120 A increased as molecular radius increased. The results of this study suggest that 1) colonic capillaries selectively restrict macromolecules on the basis of molecular size, and 2) an increased lymph flow and transcapillary oncotic pressure gradient may play an important role in preventing interstitial edema subsequent to venous pressure elevation in the dog colon.

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.

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.

scholarly journals THE RELATIVE PRESSURES WITHIN CUTANEOUS LYMPHATIC CAPILLARIES AND THE TISSUES

1947 ◽  
Vol 86 (4) ◽  
pp. 293-308 ◽  
Author(s):  
Philip D. McMaster
Keyword(s):  
Pressure Gradient ◽  
Capillary Pressure ◽  
Lymph Flow ◽  
The Other ◽  
Interstitial Pressure ◽  
Edema Fluid

The pressure in the cutaneous lymphatic capillaries of normal mice anesthetized with nembutal ranged between 0.0 and 2.7 cm. of water. Measurements of the interstitial pressure in the tissue immediately next the lymphatics showed that, in more than half the instances studied, there was a slight gradient of pressure from the tissues to the lymph. In nearly all the other instances the pressures inside and outside the lymphatic capillaries were approximately equal. In two cases in which lymph flow in the capillaries was rapid, the lymph pressure may have been negative. Under these circumstances there must have been a considerable gradient of pressure from the tissues to the lymph. In skin which was rapidly becoming, or had recently become, edematous as result of the application of xylol or of heat, the intralymphatic capillary pressure generally was increased, yet when compared with the pressure prevailing in the edema fluid outside of the capillaries it was usually found to be relatively much lower, at times by as much as 5.9 cm. of water. The findings indicate that a pressure gradient is an important factor in lymph formation under normal and pathological circumstances.

Lymph flow, lymph protein concentration, and protein output from rat small intestine

1985 ◽  
Vol 248 (6) ◽  
pp. G670-G675
Author(s):  
J. S. Lee
Keyword(s):  
Small Intestine ◽  
Water Absorption ◽  
Protein Concentration ◽  
Capillary Permeability ◽  
Lymph Flow ◽  
Rat Small Intestine ◽  
Capillary Filtration ◽  
Intestinal Lymph ◽  
Lymph Duct ◽  
Protein Output

Lymph flow (JL), lymph protein concentration (CL), and protein output (JP) from the main intestinal lymph duct were determined. The basal JL from the mesenteric pedicle alone was the same as that from the mesenteric pedicle attached with a segment of the nonabsorbing intestine, indicating that the basal JL does not originate from the intestine but is totally from the region of the mesenteric pedicle. The basal CL was 3.5-3.8 g/100 ml. When the intestine was absorbing water, JL increased and CL decreased, but JP increased above the basal JP in the initial 20 min of water absorption and then decreased progressively with time. Furthermore, it was estimated that CL in the "excess lymph" (formed during water absorption) was 1.4 +/- 0.2 g/100 ml in the initial 10 min of water absorption and was zero or nearly so in the later periods. From this and other evidence, it is concluded that under various conditions without net water absorption rat small intestine does not produce lymph and that during water absorption there is no significant increase in capillary permeability or capillary filtration. Therefore, the excess lymph could be mostly derived from the fluid absorbed from the lumen of the intestine.

Effects of hypoproteinemia and increased vascular pressure on lung fluid balance in sheep

1983 ◽  
Vol 55 (5) ◽  
pp. 1514-1522 ◽  
Author(s):  
G. C. Kramer ◽  
B. A. Harms ◽  
B. I. Bodai ◽  
E. M. Renkin ◽  
R. H. Demling
Keyword(s):  
Plasma Protein ◽  
Fluid Balance ◽  
Protein Concentration ◽  
Lymph Flow ◽  
Base Line ◽  
Oncotic Pressure ◽  
Plasma Protein Concentration ◽  
Lung Fluid ◽  
Lung Fluid Balance ◽  
Normal Plasma

We compared the effects of a sustained decrease in plasma oncotic pressure on lung fluid balance with those of an increase in vascular pressure in six unanesthetized sheep. Initial plasma protein concentration of 58.0 +/- 2.2 (SE) mg/ml was quickly reduced to 34.0 +/- 1.4 mg/ml via plasmapheresis and held at this value for 24 h. Red cells were returned with lactated Ringer solution infused at a rate adjusted to maintain central venous pressure; cardiac output and pulmonary vascular pressures also remained at base line. Steady-state lymph flows increased from a base-line value of 8.8 +/- 3.2 to 20.1 +/- 5.6 ml/h, while the lymph-to-plasma protein concentration ratio ( [L/P] ) decreased from 0.65 +/- 0.03 to 0.44 +/- 0.04. Decreased lymph protein resulted in reestablishment of base-line plasma-to-lymph oncotic gradient. The increased lymph flow was not the result of increased filtration forces, since all vascular pressures and the oncotic gradient were unchanged; nor was it due entirely to increased surface area since [L/P] was decreased. The decrease in plasma oncotic pressure, delta pi P, was twice as effective at increasing lymph flow (1.66 ml X h-1 X mmHg-1, delta pi P) as an equivalent increase in microvascular pressure, delta PC, at normal plasma protein concentration (0.82 ml X h-1 X mmHg-1, delta PC). Elevation of microvascular pressure during hypoproteinemia had a greater effect on lymph flow (1.44 ml X h-1 X mmHg-1, delta PC) than at normal plasma protein concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

Modification of lymph by lymph nodes. III. Effect of increased lymph hydrostatic pressure

1985 ◽  
Vol 249 (4) ◽  
pp. H777-H782 ◽  
Author(s):  
T. H. Adair ◽  
A. C. Guyton
Keyword(s):  
Steady State ◽  
Hydrostatic Pressure ◽  
Blood Vessel ◽  
Lymph Nodes ◽  
Flow Rate ◽  
Protein Concentration ◽  
Lymph Flow ◽  
Blood Capillary ◽  
Fluid Exchange ◽  
Very High

Previous studies have shown that lymph nodes function as fluid exchange chambers in which the protein concentration of lymph is changed in the direction required to establish equilibrium of the Starling forces acting across the nodal blood-lymph barrier. We examined the effect of increased lymph hydrostatic pressure on efferent lymph by use of an isolated dog popliteal node preparation in which lymph having a protein concentration averaging 27.6 +/- 1.2% (SD) of that of plasma was infused into the node at a flow rate averaging 45.6 +/- 0.2 (SD) microliter/min. We compared steady-state values of prenodal and postnodal lymph flow and protein concentration following step increases in efferent lymph pressure from 0 to over 15 mmHg. Increasing efferent lymph pressure to values less than about 8 mmHg caused the efferent lymph protein concentration to increase; however, further increases in lymph pressure caused the lymph protein concentration to decrease to values approaching those attained at very low lymph pressures. We suggest that the failure of high lymph pressure to increase lymph protein concentration might be caused by blood vessel collapse within the node, a condition believed to increase nodal blood capillary pressure and to decrease blood-lymph barrier filtration coefficient. An important finding was that increasing efferent lymph pressure caused significant amounts of lymph proteins to be lost during nodal transit. Therefore, it appears that increasing efferent lymph pressure to very high values has little effect on lymph protein concentration but has great effect on postnodal lymph protein flux.

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.

Effect of luminal distension on intestinal transcapillary fluid exchange

1980 ◽  
Vol 239 (6) ◽  
pp. G516-G523
Author(s):  
D. N. Granger ◽  
P. R. Kvietys ◽  
N. A. Mortillaro ◽  
A. E. Taylor
Keyword(s):  
Blood Flow ◽  
Protein Concentration ◽  
Venous Pressure ◽  
Lymph Flow ◽  
Direct Effects ◽  
Fluid Exchange ◽  
Venous Outflow ◽  
Plasma Protein Concentration ◽  
Pressure Elevation ◽  
The Relationship

The direct effects of luminal distension pressure on intestinal transcapillary fluid exchange were studied in isolated autoperfused cat ileum preparations. Intestinal lymph flow, lymphatic pressure, lymph-to-plasma protein concentration ratio (L/P), blood flow, and perfusion pressures were allowed to reach a steady state at different luminal distension pressures (0–40 mmHg). Luminal distension was induced using a nonabsorbable silicone solution, thereby eliminating an influence of net water absorption. At a venous outflow pressure of 0 mmHg, lymph flow and lymphatic pressure increased, whereas blood flow and L/P decreased as luminal pressure was increased. The relationship between lymph flow, blood flow, and venous pressure was acquired at luminal pressures of 0 and 20 mmHg. When luminal pressure was 0, lymph flow increased and blood flow decreased progressively with venous pressure elevation; however, when luminal pressure was 20 mmHg, lymph flow and blood flow were unaffected until pressure exceeded 20 mmHg. The results of this study indicate that luminal pressure elevation enhances transcapillary fluid exchange and imposes a “waterfall” effect on the intestinal vasculature.

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