Effect of hypoproteinemia on lung fluid balance in awake newborn lambs

1986 ◽  
Vol 61 (3) ◽  
pp. 1139-1148 ◽  
Author(s):  
T. A. Hazinski ◽  
R. D. Bland ◽  
T. N. Hansen ◽  
E. G. Sedin ◽  
R. B. Goldberg
Keyword(s):  
Plasma Protein ◽  
Fluid Balance ◽  
Left Atrial ◽  
Protein Concentration ◽  
Lymph Flow ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Plasma Protein Concentration ◽  
Lung Fluid ◽  
Lung Lymph

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)

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.

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)

scholarly journals Effect of Elevated Left Atrial Pressure and Decreased Plasma Protein Concentration on the Development of Pulmonary Edema

1959 ◽  
Vol 7 (4) ◽  
pp. 649-657 ◽  
Author(s):  
ARTHUR C. GUYTON ◽  
ARTHUR W. LINDSEY ◽  
HOWELL, JOHNNIE O. ◽  
WILLIAMS JOHN W. ◽  
FRANKLIN MALCOLM A.
Keyword(s):  
Pulmonary Edema ◽  
Plasma Protein ◽  
Left Atrial ◽  
Protein Concentration ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Plasma Protein Concentration

Furosemide reduces lung fluid filtration in lambs with lung microvascular injury from air emboli

1989 ◽  
Vol 67 (5) ◽  
pp. 1990-1996 ◽  
Author(s):  
M. E. Berner ◽  
W. G. Teague ◽  
R. G. Scheerer ◽  
R. D. Bland
Keyword(s):  
Cardiac Output ◽  
Left Atrial ◽  
Balloon Catheter ◽  
Lymph Flow ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Protein Ratio ◽  
Fluid Filtration ◽  
Lung Lymph ◽  
Lung Lymph Flow

To study the effects of furosemide on the neonatal pulmonary circulation in the presence of lung injury, we measured pulmonary arterial and left atrial pressures, cardiac output, lung lymph flow, and concentrations of protein in lymph and plasma of nine lambs that received furosemide, 2 mg/kg iv, during a continuous 8-h intravenous infusion of air. Air embolism increased pulmonary vascular resistance by 71% and nearly tripled steady-state lung lymph flow, with no change in lymph-to-plasma protein ratio. These findings reflect an increase in lung vascular protein permeability. During sustained lung endothelial injury, diuresis from furosemide led to a rapid reduction in cardiac output (average 29%) and a 2-Torr decrease in left atrial pressure. Diuresis also led to hemoconcentration, with a 15% increase in both plasma and lymph protein concentrations. These changes were associated with a 27% reduction in lung lymph flow. In a second set of studies, we prevented the reduction in left atrial pressure after furosemide by inflating a balloon catheter in the left atrium. Nevertheless, lymph flow decreased by 25%, commensurate with the reduction in cardiac output that occurred after furosemide. In a third series of experiments, we minimized the furosemide-related decrease in cardiac output by opening an external fistula between the carotid artery and jugular vein immediately after injection of furosemide. In these studies, the reduction in lung lymph flow (average 17%) paralleled the smaller (17%) decrease in cardiac output. These results suggest that changes in lung vascular filtration pressure probably do not account for the reduction in lung lymph flow after furosemide in the presence of lung vascular injury.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Left atrial pressure elevation recreates the altered lung lymph flow of seizures

1982 ◽  
Vol 53 (2) ◽  
pp. 432-435 ◽  
Author(s):  
R. P. Simon ◽  
L. L. Bayne ◽  
M. P. Naughton
Keyword(s):  
Left Atrial ◽  
Pressor Response ◽  
Lymph Flow ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Pressure Elevation ◽  
Generalized Seizures ◽  
Neural Interactions ◽  
Lung Lymph ◽  
Lung Lymph Flow

We compared the effects of elevated left atrial pressure of central nervous system origin (bicuculline-induced seizures) with an identical pulmonary vascular pressure elevation induced in six sheep by inflation of a balloon in the left atrium. The degree and duration of the consequent elevation in pulmonary lymph flow and the alteration in protein movement in the two groups was identical. Alterations in pulmonary fluid and protein flux resulting from generalized seizures can be explained by the pressor response alone; specific brain-lung neural interactions need not be postulated.

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.

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 hypoxia on lung lymph flow in newborn lambs with left atrial hypertension

1988 ◽  
Vol 254 (3) ◽  
pp. H487-H493
Author(s):  
J. U. Raj ◽  
T. A. Hazinski ◽  
R. D. Bland
Keyword(s):  
Blood Flow ◽  
Left Atrial ◽  
Control Period ◽  
Lymph Flow ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Fluid Filtration ◽  
Alveolar Hypoxia ◽  
Lung Lymph ◽  
Lung Lymph Flow

To determine the effect of left atrial hypertension on the vascular response to hypoxia in the newborn lung, we measured pulmonary artery and left atrial pressures, lung blood flow and lymph flow, and concentrations of protein in lymph and plasma of 13 lambs that spontaneously breathed air for 2-6 h (control period), followed by 8-11% O2 mixed with 3-5% CO2 and N2 for 2-4 h (experimental period). In eight studies, the lambs were made hypoxic first, after which we elevated their left atrial pressure by 10-12 Torr for 2-3 h. In 10 additional studies, we reversed the sequence by raising left atrial pressure first followed by addition of hypoxia. In lambs with normal left atrial pressure, alveolar hypoxia increased both pulmonary blood flow and lymph flow, with an associated reduction in lymph-to-plasma protein ratio (L/P). When left atrial pressure was increased in the presence of hypoxia, lymph flow increased by a small amount and L/P decreased further. In lambs with preexisting left atrial pressure elevation, addition of alveolar hypoxia increased both blood flow and lymph flow with no significant change in L/P. These results suggest that in newborn lambs with normal left atrial pressure, alveolar hypoxia increases lung lymph flow mainly by increasing microvascular filtration pressure, whereas in lambs with elevated left atrial pressure, hypoxia increases lymph flow by another mechanism, perhaps by increasing the perfused surface area for fluid filtration.

Lymph flow from edematous dog lungs

1987 ◽  
Vol 62 (6) ◽  
pp. 2416-2420 ◽  
Author(s):  
R. E. Drake ◽  
S. J. Allen ◽  
J. P. Williams ◽  
G. A. Laine ◽  
J. C. Gabel
Keyword(s):  
Flow Rate ◽  
Left Atrial ◽  
Lymph Flow ◽  
Effective Resistance ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Base Line ◽  
Lymph Vessels ◽  
Lymph System ◽  
Lung Lymph

We measured the flow rate (QLV) from cannulated lung lymph vessels in anesthetized dogs. Low-resistance lymph cannulas were used and the vessels were cannulated at the lung hilus. When we increased left atrial pressure to 42.9 +/- 5.7 (SD) cmH2O (base line = 6.6 +/- 4.6 cmH2O), the lungs became edematous and QLV increased from a base line of 20.4 +/- 21.5 microliters/min to 388 +/- 185 microliters/min. QLV plateaued at the higher level. We also measured the relationship between lymph flow rate and the height of the outflow end of the lymph cannula. From this relationship, determined at the end of the period of elevated left atrial pressure, we calculated the effective resistance and pressure driving lymph from the lungs. We also cannulated lymph vessels in the downstream direction and estimated the effective resistance and pressure opposing flow into the part of the lymphatic system between the lung hilus and the veins (extrapulmonary lymph vessels). We found that the effective resistance of the extrapulmonary part of the lymph system (0.042 +/- 0.030 (SD) cmH2O X min X microliter-1) was large compared with the resistance of the lymph vessels from the lungs (0.026 +/- 0.027). These data indicate that the resistance of the extrapulmonary part of the lung lymph system limits the maximum flow of lymph from edematous lungs.

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