Lung fluid balance in lambs before and after birth

1982 ◽  
Vol 53 (4) ◽  
pp. 992-1004 ◽  
Author(s):  
R. D. Bland ◽  
T. N. Hansen ◽  
C. M. Haberkern ◽  
M. A. Bressack ◽  
T. A. Hazinski ◽  
...  
Keyword(s):  
Fluid Balance ◽  
Endothelial Permeability ◽  
Lymph Flow ◽  
Lung Water ◽  
Fluid Exchange ◽  
Lung Fluid ◽  
Lung Fluid Balance ◽  
Before And After ◽  
Lung Lymph ◽  
Lung Lymph Flow

To study lung fluid balance before and after birth, we measured lung lymph flow and concentrations of protein in lymph and plasma of 22 unanesthetized fetal lambs and compared results with previous studies done on 26 newborn lambs, 1–2 wk old. Lymph flow, relative to lung mass, was less in fetuses than in newborns; lymph protein clearance was not significantly different. Less lymph flow before birth probably reflects less available surface area for fluid exchange in microcirculation of fetal lungs, compared with newborn lungs, with no difference in endothelial permeability to protein. Extravascular lung water, measured gravimetrically for 24 fetuses (10 without labor, nine in labor, five 6 h after vaginal birth), decreased by 45% (15 +/- 2 g/kg body wt) before birth and by an additional 38% (6 +/- 1 g/kg) after birth. In five lambs killed after birth, we measured lung lymph flow before and during labor and for 6 h after breathing began. Lymph flow was unaffected by labor but increased transiently after birth, accounting for 11% of the liquid removed from lungs postnatally. Liquid clearance studies performed in eight anesthetized 3-wk-old lambs confirmed the observation that lung lymphatics drain only a small fraction of liquid in potential air spaces. Most of that liquid probably leaves the lungs directly through pulmonary circulation.

Inspiratory airway obstruction does not affect lung fluid balance in lambs

1985 ◽  
Vol 58 (4) ◽  
pp. 1314-1318 ◽  
Author(s):  
T. N. Hansen ◽  
A. L. Gest ◽  
S. Landers
Keyword(s):  
Airway Obstruction ◽  
Endotracheal Tube ◽  
Fluid Balance ◽  
Left Atrial ◽  
Lymph Flow ◽  
Lung Fluid ◽  
Lung Fluid Balance ◽  
Pulmonary Arterial ◽  
Lung Lymph ◽  
Lung Lymph Flow

The purpose of this study was to examine the effects of inspiratory airway obstruction on lung fluid balance in newborn lambs. We studied seven 2- to 4-wk-old lambs that were sedated with chloral hydrate and allowed to breathe 30–40% O2 spontaneously through an endotracheal tube. We measured lung lymph flow, lymph and plasma protein concentrations, pulmonary arterial and left atrial pressures, mean and phasic pleural pressures and airway pressures, and cardiac output during a 2-h base-line period and then during a 2- to 3-h period of inspiratory airway obstruction produced by partially occluding the inspiratory limb of a nonrebreathing valve attached to the endotracheal tube. During inspiratory airway obstruction, both pleural and airway pressures decreased 5 Torr, whereas pulmonary arterial and left atrial pressures each decreased 4 Torr. As a result, calculated filtration pressure remained unchanged. Inspiratory airway obstruction had no effect on steady-state lung lymph flow or the lymph protein concentration relative to that of plasma. We conclude that in the spontaneously breathing lamb, any decrease in interstitial pressure resulting from inspiratory airway obstruction is offset by a decrease in microvascular hydrostatic pressure so that net fluid filtration remains unchanged.

Effect of progressive exercise on lung fluid balance in sheep

1988 ◽  
Vol 64 (5) ◽  
pp. 2125-2131 ◽  
Author(s):  
J. H. Newman ◽  
B. J. Butka ◽  
R. E. Parker ◽  
R. J. Roselli
Keyword(s):  
Cardiac Output ◽  
Fluid Balance ◽  
Lymph Flow ◽  
Base Line ◽  
Lung Fluid ◽  
Lung Fluid Balance ◽  
Progressive Exercise ◽  
Pulmonary Arterial ◽  
Lung Lymph ◽  
Lung Lymph Flow

The purpose of this study is to determine the roles of cardiac output and microvascular pressure on changes in lung fluid balance during exercise in awake sheep. We studied seven sheep during progressive treadmill exercise to exhaustion (10% grade), six sheep during prolonged constant-rate exercise for 45–60 min, and five sheep during hypoxia (fraction of inspired O2 = 0.12) and hypoxic exercise. We made continuous measurements of pulmonary arterial, left atrial, and systemic arterial pressures, lung lymph flow, and cardiac output. Exercise more than doubled cardiac output and increased pulmonary arterial pressures from 19.2 +/- 1 to 34.8 +/- 3.5 (SE) cmH2O. Lung lymph flow increased rapidly fivefold during progressive exercise and returned immediately to base-line levels when exercise was stopped. Lymph-to-plasma protein concentration ratios decreased slightly but steadily. Lymph flows correlated closely with changes in cardiac output and with calculated microvascular pressures. The drop in lymph-to-plasma protein ratio during exercise suggests that microvascular pressure rises during exercise, perhaps due to increased pulmonary venous pressure. Lymph flow and protein content were unaffected by hypoxia, and hypoxia did not alter the lymph changes seen during normoxic exercise. Lung lymph flow did not immediately return to base line after prolonged exercise, suggesting hydration of the lung interstitium.

Oleic acid lung injury in sheep

1986 ◽  
Vol 60 (2) ◽  
pp. 433-440 ◽  
Author(s):  
M. Julien ◽  
J. M. Hoeffel ◽  
M. R. Flick
Keyword(s):  
Oleic Acid ◽  
Lung Injury ◽  
Pulmonary Edema ◽  
Fluid Balance ◽  
Lymph Flow ◽  
Lung Fluid ◽  
Lung Fluid Balance ◽  
Pulmonary Arterial ◽  
Lung Lymph ◽  
Lung Lymph Flow

Intravenous infusion of oleic acid into experimental animals causes acute lung injury resulting in pulmonary edema. We investigated the mechanism of oleic acid lung injury in sheep. In experiments with anesthetized and unanesthetized sheep with lung lymph fistulas, we measured pulmonary arterial and left atrial pressures, cardiac output, lung lymph flow, and lymph and plasma protein concentrations. We injured the lungs with intravenous infusions of oleic acid at doses ranging from 0.015 to 0.120 ml/kg. We found that oleic acid caused reproducible dose-related increases in pulmonary arterial pressure and pulmonary vascular resistance, arterial hypoxemia, and increased protein-rich lung lymph flow and extravascular lung water. The lung fluid balance changes were characteristic of increased permeability pulmonary edema. Infusion of the esterified fat triolein had no hemodynamic or lung fluid balance effects. Depletion of leukocytes with a nitrogen mustard or platelets with an antiplatelet serum had no effect on oleic acid lung injury. Treatment of sheep before injury with methylprednisolone 30 mg/kg or ibuprofen 12.5–15.0 mg/kg also had no effects. Unlike other well-characterized sheep lung injuries, injury caused by oleic acid does not require participation of leukocytes.

Effects of inspiratory resistance loading on lung fluid balance in awake sheep

1986 ◽  
Vol 60 (1) ◽  
pp. 198-203 ◽  
Author(s):  
J. E. Loyd ◽  
K. B. Nolop ◽  
R. E. Parker ◽  
R. J. Roselli ◽  
K. L. Brigham
Keyword(s):  
Fluid Balance ◽  
Intrathoracic Pressure ◽  
Lymph Flow ◽  
Base Line ◽  
Plasma Protein Concentration ◽  
Lung Fluid ◽  
Mean Pulmonary Arterial Pressure ◽  
Lung Fluid Balance ◽  
Lung Lymph ◽  
Lung Lymph Flow

Because pulmonary edema has been associated clinically with airway obstruction, we sought to determine whether decreased intrathoracic pressure, created by selective inspiratory obstruction, would affect lung fluid balance. We reasoned that if decreased intrathoracic pressure caused an increase in the transvascular hydrostatic pressure gradient, then lung lymph flow would increase and the lymph-to-plasma protein concentration ratio (L/P) would decrease. We performed experiments in six awake sheep with chronic lung lymph cannulas. After a base-line period, we added an inspiratory load (20 cmH2O) and allowed normal expiration at atmospheric pressure. Inspiratory loading was associated with a 12-cmH2O decrease in mean central airway pressure. Mean left atrial pressure fell 11 cmH2O, and mean pulmonary arterial pressure was unchanged; calculated microvascular pressure decreased 8 cmH2O. The changes that occurred in lung lymph were characteristic of those seen after other causes of increased transvascular hydrostatic gradient, such as increased intravascular pressure. Lung lymph flow increased twice base line, and L/P decreased. We conclude that inspiratory loading is associated with an increase in the pulmonary transvascular hydrostatic gradient, possibly by causing a greater fall in interstitial perimicrovascular pressure than in microvascular pressure.

Effect of heparin or fibrinogen depletion on lung fluid balance in sheep after emboli

1979 ◽  
Vol 47 (1) ◽  
pp. 213-219 ◽  
Author(s):  
A. S. Binder ◽  
K. Nakahara ◽  
K. Ohkuda ◽  
W. Kageler ◽  
N. C. Staub
Keyword(s):  
Vascular Permeability ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Fluid Balance ◽  
Lymph Flow ◽  
Lung Fluid ◽  
Lung Fluid Balance ◽  
Lung Lymph ◽  
Lung Vascular Permeability ◽  
Lung Lymph Flow

Investigators have proposed that fibrinogen, fibrin, or their degradation products are essential for the increased lung vascular permeability to fluid and protein that may occur after microemboli. To test this hypothesis, we used 20 anesthetized ventilated sheep in which we measured lung lymph flow, pulmonary artery and left atrial pressures, thermodilution cardiac output, and lymph/plasma protein concentrations. We injected glass bead microemboli (200 micrometers diam) sufficient to raise pulmonary vascular resistance to three times base-line values and cause increased lung lymph flow with a parallel increase in protein clearance, which is characteristic of increased lung vascular permeability. Neither large doses of heparin (3,000 U/kg) nor fibrinogen depletion with viper venom (ancrod, 2 U/kg), by themselves, affected steady-state pulmonary hemodynamics or lung fluid balance. These treatments prior to giving sufficient amounts of emboli to triple the pulmonary vascular resistance did not prevent the increased lung vascular permeability. We conclude that neither fibrin deposition nor degradation are essential to microembolic lung vascular injury in sheep.

Isoproterenol and aminophylline reduce lung capillary filtration during high permeability

1979 ◽  
Vol 46 (1) ◽  
pp. 146-151 ◽  
Author(s):  
T. Foy ◽  
J. Marion ◽  
K. L. Brigham ◽  
T. R. Harris
Keyword(s):  
Plasma Protein ◽  
Protein Concentration ◽  
Lymph Flow ◽  
High Permeability ◽  
Plasma Protein Concentration ◽  
Lung Fluid ◽  
Lung Fluid Balance ◽  
Lung Lymph ◽  
Lung Vascular Permeability ◽  
Lung Lymph Flow

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.

Influence of opsonic fibronectin deficiency on lung fluid balance during bacterial sepsis

1980 ◽  
Vol 49 (4) ◽  
pp. 693-699 ◽  
Author(s):  
G. D. Niehaus ◽  
P. T. Schumacker ◽  
T. M. Saba
Keyword(s):  
Vascular Permeability ◽  
Fluid Balance ◽  
Lymph Flow ◽  
Plasma Protein Concentration ◽  
Pulmonary Hemodynamics ◽  
Lung Fluid ◽  
Protein Clearance ◽  
Lung Fluid Balance ◽  
Lung Lymph ◽  
Lung Vascular Permeability

Lung microvascular permeability in sheep increases during Pseudomonas bacteremia. The sheep's low plasma opsonic fibronectin concentration and associated inefficient reticuloendothelial clearance of blood-borne particulates may contribute to the response of increased lung vascular permeability during sepsis. The present study investigated the influence of sepsis on lung fluid balance in sheep with and without opsonic glycoprotein (plasma fibronectin) deficiency. Using the lung lymph fistula preparation in sheep, we made measurements of lung lymph flow (QLYM), lymph-to-plasma protein concentration ratios (L/P), pulmonary hemodynamics, and extravascular lung water content. Deficiency of opsonic fibronectin resulted in a minimal increase in lymph flow with no change in transvascular protein clearance (QLYM X L/P). Pseudomonas sepsis with or without fibronectin deficiency resulted in a stable L/P and a transient increase in pulmonary arterial pressure, which declined to a new steady state. Although sepsis resulted in a 100% elevation (P < 0.05) in lymph flow and transvascular protein clearance, sepsis in the presence of fibronectin deficiency induced a sustained 300--400% increase in lymph flow and a 300% increase in transvascular protein clearance. Thus opsonic fibronectin deficiency exaggerates the increased lung vascular permeability during sepsis.

Relationship between weight gain and lymph flow in dog lungs

1983 ◽  
Vol 245 (1) ◽  
pp. H125-H130 ◽  
Author(s):  
R. E. Drake ◽  
R. L. Scott ◽  
J. C. Gabel
Keyword(s):  
Weight Gain ◽  
Lymph Flow ◽  
Base Line ◽  
Lung Weight ◽  
Lung Fluid ◽  
Lung Fluid Balance ◽  
Extravascular Volume ◽  
Continuous Weight ◽  
Lung Lymph ◽  
Lung Lymph Flow

Lung weight is a useful indicator of increases in lung extravascular volume. In addition, the lung lymph flow rate (QL) is an important factor in lung fluid balance. We have studied the weight and QL responses to elevations in capillary pressure (Pc) in intact dog lung lower left lobes. We measured lobe weight continuously. We also measured QL from small lymph vessels from the same lobes. The base-line QL was 1.7 +/- 1.5 microliter/min, and the weight was constant. After we increased Pc by 8-20 cmH2O, both weight and QL increased transiently. In most lungs the weight reached a new steady state. When we increased Pc further, weight increased continuously; however, QL reached a plateau. The continuous weight gain was due to edema. These results show that weight and QL respond similarly in nonedematous lungs; however, the weight and QL responses in edematous lungs may be different.

Assessment of fluid balance in isolated sheep lungs

1985 ◽  
Vol 58 (3) ◽  
pp. 882-891 ◽  
Author(s):  
G. A. Patterson ◽  
W. A. Mitzner ◽  
J. T. Sylvester
Keyword(s):  
Fluid Balance ◽  
Autologous Blood ◽  
Pressure Ratio ◽  
Lymph Flow ◽  
Lung Water ◽  
Lung Weight ◽  
Superior Mediastinum ◽  
Lung Fluid ◽  
Lung Fluid Balance ◽  
Isolated Lung

In this study we demonstrate the validity and utility of an isolated lung preparation developed for the study of pulmonary fluid balance. Lungs of 2- to 3-mo-old sheep were perfused in situ with autologous blood treated with indomethacin (20 micrograms/ml). Lung lymph flow (QL), uncontaminated by systemic lymph, was measured from either the efferent duct of the caudomediastinal lymph node or the thoracic duct in the superior mediastinum. Lung weight change (delta W) was measured as the opposite of the change in weight of the extracorporeal blood reservoir. A unique feature of this experimental model is the ability to assess lung fluid balance from simultaneous measurements of delta W and QL. In addition, hemodynamic and blood gas variables can be tightly controlled. Our results show that changes in QL and the lymph-to-plasma oncotic pressure ratio caused by an increase in microvascular pressure were comparable with those seen previously in intact sheep. When microvascular pressure was returned to control levels, QL fell despite a sustained increase in the amount of extravascular lung water, suggesting compartmentalization of the filtrate and/or effects of intravascular volume on lymph-driving pressure or resistance. Lymph flow was directly proportional to respiratory frequency over the range of 0–30 min-1 when the change in frequency was maintained for periods as long as 30 min. This preparation should prove useful in the study of lung fluid balance, particularly when it is desired to use interventions which are precluded or difficult in intact animals.

Effect of increased bronchial venous pressure on lung lymph flow

1985 ◽  
Vol 59 (4) ◽  
pp. 1249-1253 ◽  
Author(s):  
N. B. Charan ◽  
G. M. Turk ◽  
D. H. Hey
Keyword(s):  
Evans Blue ◽  
Venous Pressure ◽  
Lymph Flow ◽  
Blue Dye ◽  
Protein Ratio ◽  
Evans Blue Dye ◽  
Lung Fluid ◽  
Lung Fluid Balance ◽  
Lung Lymph ◽  
Lung Lymph Flow

We postulated that if the bronchial circulation affects lung fluid balance, increases in bronchial venous pressures may influence lung lymph flow. This hypothesis was tested in eight anesthetized sheep prepared with acute lung lymph fistulas. After control data, we increased bronchial venous pressure by infusing saline directly into the bronchial vein at a controlled infusion pressure of 20–25 cmH2O. Evans blue dye (2.5 mg/ml) was added into the saline as a marker for assessing leakage that might occur from either the catheter or the ruptured bronchial veins. Lymph flow was measured every 15 min. Lymph as well as plasma samples were collected every 30 min for measurement of protein. In five sheep we also measured Evans blue dye content both in lymph and plasma to further characterize the role of bronchial circulation in lung fluid balance. The control lymph flow was 1.9 +/- 0.2 ml/15 min, and lymph-to-plasma protein ratio was 0.65 +/- 0.3 (mean +/- SE). With infusion of saline into the bronchial vein, the mean lung lymph flow and lymph-to-plasma protein ratio did not change significantly. There was a progressive increase in dye content both in lymph and plasma. The mean Evans blue dye content in lymph was 0.087, 0.16, and 0.26 microgram/ml, whereas in plasma it was 0.43, 1.15, and 1.45 microgram/ml in samples obtained at 30, 60, and 90 min, respectively. The dye content was significantly higher in the plasma compared with the lymph in all three samples (less than 0.05). Pulmonary arterial pressure, pulmonary capillary wedge pressure, and cardiac output did not change significantly throughout the experiment.

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