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

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.

1996 ◽  
Vol 271 (6) ◽  
pp. R1465-R1469 ◽  
Author(s):  
R. H. Stewart ◽  
D. A. Rohn ◽  
U. Mehlhorn ◽  
K. L. Davis ◽  
S. J. Allen ◽  
...  

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.


2020 ◽  
Vol 318 (4) ◽  
pp. R722-R729 ◽  
Author(s):  
Ranjeet M. Dongaonkar ◽  
Christopher M. Quick ◽  
Glen A. Laine ◽  
Karen Uray ◽  
Charles S. Cox ◽  
...  

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.


1981 ◽  
Vol 240 (5) ◽  
pp. R282-R288
Author(s):  
R. A. Brace ◽  
G. G. Power

Fluid and protein flux responses in the left thoracic duct and vasculature were measured in pentobarbital-anesthetized, nephrectomized, adult dogs before and after four successive intravascular saline infusions of 2% of body weight each. We found three main characteristics of the thoracic lymph flow and protein flux responses to the intravenous saline: 1) lymph flow reached a peak and then decreased by approximately 40% after each infusion; 2) the maximum lymph flow occurred 5-7 min after terminating each infusion; and 3) the lymph-to-plasma protein concentration ratio fell more than may be expected from the distribution of the infused saline. We were unable to explain these experimental data with a simple two-compartment mathematical model representing the vascular and interstitial spaces. To adequately explain the data, the model had to be expanded to four compartments representing a vascular compartment, two interstitial compartments each with different capillary protein permeabilities, and a lymphatic compartment. We also found it necessary to include interstitial stress relaxation, a nonlinear function curve for lymph flow versus interstitial fluid pressure, and a complaint lymphatic system.


1979 ◽  
Vol 46 (1) ◽  
pp. 146-151 ◽  
Author(s):  
T. Foy ◽  
J. Marion ◽  
K. L. Brigham ◽  
T. R. Harris

Pseudomonas bacteremia in sheep causes a prolonged increase in lung vascular permeability to protein. Isoproterenol and aminophylline could effect lung fluid balance after Pseudomonas by reducing vascular pressures or by blocking release of permeability mediators. We measured vascular pressures, lung lymph flow, and lymph and plasma protein concentrations in unanesthetized sheep under baseline conditions and during steady-state increased permeability after Pseudomonas. Pseudomonas caused pulmonary vascular pressures to rise and lung lymph flow to increase fivefold, but lymph/plasma protein concentration did not change. Pulmonary vascular pressures and lung lymph flow decreased during intravenous infusion of isoproterenol and aminophylline. The decrease in lymph flow after isoproterenol and isoproterenol plus aminophylline was linearly related to the decrease in microvascular pressure (r = 0.71). Lymph/plasma total protein concentration ratios and lymph clearance of proteins with molecular radii 36--96 A remained high during isoproterenol and aminophylline. These drugs can substantially reduce transvascular filtration primarily because they reduce lung vascular pressures.


1988 ◽  
Vol 65 (3) ◽  
pp. 1140-1146 ◽  
Author(s):  
F. Royer ◽  
D. J. Martin ◽  
G. Benchetrit ◽  
F. A. Grimbert

Changes in pulmonary capillary filtration induced by hyperoxia were investigated in 15 dogs. After 12 h of normobaric hyperoxic exposure, animals were anesthetized and artificially ventilated with 100% O2. A pulmonary lymphatic vessel was cannulated, and lymph flow and protein content were measured together with pulmonary and systemic hemodynamics. An increase in pulmonary capillary filtration was found when compared with reference data (normoxic dogs in similar conditions) gathered from available literature: lymph flow increased from 21.8 +/- 13.4 to 125.2 +/- 131.6 microliter/min, and the lymph-to-plasma protein concentration ratio increased from 0.67 +/- 0.08 to 0.78 +/- 0.08. To characterize the mechanisms involved, left atrial pressure was increased in two stages (approximately 10 and approximately 25 mmHg). The results clearly indicated an increase in pulmonary capillary permeability as evidenced by a decrease of the minimal estimate of the protein reflection coefficient from 0.62 +/- 0.05 to 0.42 +/- 0.05.


1983 ◽  
Vol 55 (5) ◽  
pp. 1514-1522 ◽  
Author(s):  
G. C. Kramer ◽  
B. A. Harms ◽  
B. I. Bodai ◽  
E. M. Renkin ◽  
R. H. Demling

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)


1986 ◽  
Vol 61 (3) ◽  
pp. 1139-1148 ◽  
Author(s):  
T. A. Hazinski ◽  
R. D. Bland ◽  
T. N. Hansen ◽  
E. G. Sedin ◽  
R. B. Goldberg

To study the influence of plasma protein concentration on fluid balance in the newborn lung, we measured pulmonary arterial and left atrial pressures, lung lymph flow, and concentrations of protein in lymph and plasma of eight lambs, 2–3 wk old, before and after we reduced their plasma protein concentration from 5.8 +/- 0.3 to 3.6 +/- 0.6 g/dl. Each lamb underwent two studies, interrupted by a 3-day period in which we drained protein-rich systemic lymph through a thoracic duct fistula and replaced fluid losses with feedings of a protein-free solution of electrolytes and glucose. Each study consisted of a 2-h control period followed by 4 h of increased lung microvascular pressure produced by inflation of a balloon in the left atrium. Body weight and vascular pressures did not differ significantly during the two studies, but lung lymph flow increased from 2.6 +/- 0.1 ml/h during normoproteinemia to 4.1 +/- 0.1 ml/h during hypoproteinemia. During development of hypoproteinemia, the average difference in protein osmotic pressure between plasma and lymph decreased by 1.6 +/- 2 Torr at normal left atrial pressure and by 4.9 +/- 2.2 Torr at elevated left atrial pressure. When applied to the Starling equation governing microvascular fluid balance, these changes in liquid driving pressure were sufficient to account for the observed increases in lung fluid filtration; reduction of plasma protein concentration did not cause a statistically significant change in calculated filtration coefficient. Protein loss did not influence net protein clearance from the lungs nor did it accentuate the increase in lymph flow associated with left atrial pressure elevation.(ABSTRACT TRUNCATED AT 250 WORDS)


1993 ◽  
Vol 75 (4) ◽  
pp. 1798-1806 ◽  
Author(s):  
G. Miserocchi ◽  
D. Venturoli ◽  
D. Negrini ◽  
M. Del Fabbro

A model of pleural fluid turnover, based on mass conservation law, was developed from experimental evidence that 1) pleural fluid filters through the parietal pleura and is drained by parietal lymphatics and 2) lymph flow increases after an increase in pleural liquid volume, attaining a maximum value 10 times greater than control. From the differential equation describing the time evolution of pleural liquid pressure, we obtained the equation for the steady-state condition ("set point") of pleural liquid pressure: Pss = (KfPi*+KlPzf)/Kf+Kl), where Kf is parietal pleura filtration coefficient, Kl is initial lymphatic conductance, Pzf is lymphatic potential absorption pressure, and Pi* is a factor accounting for the protein reflection coefficient of parietal mesothelium and hydraulic and colloid osmotic pressure of parietal interstitium and pleural liquid. Lymphatics act as a passive negative-feedback control tending to offset increases in pleural liquid volume. Some features of this control are summarized here: 1) lymphatics exert a tight control on pleural liquid volume or pressure so that the set point is maintained close to the potential absorption pressure of lymphatics; 2) a 10-fold increase in Kf would cause only a 2- and 5-fold increase in pleural liquid volume with normal (1.8 g/dl) and increased (3.4 g/dl) protein concentration of the pleural fluid, respectively; and 3) the reduction in maximum lymph flow greatly reduces the range of operation of the control with increased filtration and/or protein concentration of pleural fluid.


1980 ◽  
Vol 239 (6) ◽  
pp. G516-G523
Author(s):  
D. N. Granger ◽  
P. R. Kvietys ◽  
N. A. Mortillaro ◽  
A. E. Taylor

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.


1980 ◽  
Vol 239 (4) ◽  
pp. G300-G305 ◽  
Author(s):  
P. D. Richardson ◽  
D. N. Granger ◽  
D. Mailman ◽  
P. R. Kvietys

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.


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