Effects of intracranial and left atrial hypertension on lung fluid balance in sheep

1982 ◽  
Vol 52 (5) ◽  
pp. 1324-1329 ◽  
Author(s):  
T. A. Jones ◽  
M. I. Townsley ◽  
W. J. Weidner
Keyword(s):  
Surface Area ◽  
Left Atrial ◽  
Protein Concentration ◽  
Microvascular Permeability ◽  
Lung Fluid ◽  
Lung Fluid Balance ◽  
Primary Mechanism ◽  
Permeability Changes ◽  
Protein Rich ◽  
Filtration Surface

Elevation of intracranial pressure (ICP; 50–150 Torr) in sheep produces an increase in protein-rich lymph flow (QL) from the lung. This may be attributed to either microvascular permeability changes or increases in filtration surface area through recruitment. To eliminate increases in surface area, we recruited potential filtration beds by increasing left atrial pressure (Pla; 27–35 Torr) prior to elevating ICP in sheep anesthetized with pentobarbital sodium or halothane. Under these conditions, increased pulmonary microvascular permeability would be expected to produce an increased QL, lymphatic protein flux (CL), and plasma clearance of protein (CP). The results of ICP elevation following a period of steady-state Pla hypertension showed no such change in QL, CL or CP (n=8) compared with prior period of increased Pla. ICP elevation alone (n=6) produces a significant increase in CP manifested as an increase in QL (73%), with little change in the lymph-to-plasma ratio of protein concentration. These results suggest that a change in pulmonary microvascular surface area (not permeability) is the primary mechanism underlying increases in protein-rich QL following the elevation of ICP alone.

Effect of endotoxin on lung fluid balance in unanesthetized sheep

1984 ◽  
Vol 56 (2) ◽  
pp. 489-494 ◽  
Author(s):  
J. C. Gabel ◽  
T. N. Hansen ◽  
R. E. Drake
Keyword(s):  
Left Atrial ◽  
Capillary Permeability ◽  
Dry Weight ◽  
Base Line ◽  
Lung Fluid ◽  
Modified Method ◽  
Lung Fluid Balance ◽  
Extravascular Fluid ◽  
Pulmonary Capillary ◽  
Four Levels

We used a gravimetric technique to test for increased pulmonary capillary permeability after Escherichia coli endotoxin infusion in unanesthetized sheep. The sheep were chronically prepared with cannulas placed into the left atrium and pulmonary artery 1–2 wk before the experiments. We estimated pulmonary capillary pressure (Pc) as the average of pulmonary arterial and left atrial pressures, and used the modified method of Pierce to estimate the ratio of extravascular fluid weight (EVF) to blood-free dry weight. In 15 sheep we inflated a left atrial balloon to raise Pc to -10.7, 5, 10, or 15 mmHg above plasma oncotic pressure (IIc) for 3 h, then measured EVF. EVF averaged 4.0 +/- 0.2 (base line), 4.3 +/- 0.1, 4.5 +/- 0.1, and 5.1 +/- 0.5 (SD), respectively, for the four levels of Pc - IIc. We gave seven additional sheep 1 microgram/kg of E. coli endotoxin (0127:B8) and measured EVF after 3 h of stable Pc. Endotoxin increased Pc in each sheep. EVF was higher than control for the endotoxin sheep with Pc - IIc greater than -1. This finding is consistent with an increase in pulmonary capillary permeability caused by endotoxin. However, EVF was not elevated in the endotoxin sheep with Pc - IIc less than 1 mmHg. This shows that the increased permeability was insufficient to cause edema unless Pc was elevated. Thus endotoxin may cause edema by two mechanisms, 1) an increase in capillary permeability, and 2) an increase in Pc.

Adrenoceptor control of lung fluid and protein exchange

1981 ◽  
Vol 51 (1) ◽  
pp. 68-72 ◽  
Author(s):  
T. S. Hakim ◽  
F. L. Minnear ◽  
H. van der Zee ◽  
P. S. Barie ◽  
A. B. Malik
Keyword(s):  
Steady State ◽  
Surface Area ◽  
Left Atrial ◽  
Endothelial Permeability ◽  
Base Line ◽  
Adrenergic Blockade ◽  
Beta Adrenergic ◽  
Lung Fluid ◽  
Vascular Surface ◽  
Protein Exchange

We studied the effects of alpha- and beta-adrenergic antagonists on lung fluid and protein exchange in anesthetized sheep. alpha-Adrenergic blockade with 2 mg/kg phentolamine caused a transient and small decrease in lung lymph flow (Qlym), which was associated with a decrease in mean pulmonary arterial pressure (Ppa); but the steady-state Qlym and mean left atrial pressure were not different from base-line values. In contrast, beta-adrenergic blockade with propranolol (2 mg/kg) caused an increase in Qlym from a base-line value of 7.7 +/- 2.2 ml/h to a steady-state value of 10.6 +/-2.3 ml/h within 2 h (P less than 0.05), which was not associated with a change in Ppa. The increase in Qlym persisted for the 4-h duration of the study. The 39% increase in Qlym after propranolol was associated with a 50% increase in transvascular protein clearance (CL), whereas in control animals the 100% increase in Qlym after left atrial hypertension was associated with only a 36% increase in CL, indicating increased transvascular transport of proteins after propranolol. The transient decrease in Qlym after phentolamine may be due to the short-lasting decreased in pulmonary microvascular pressure and vascular surface area. However, the long-lasting increases in Qlym and CL after propranolol may be due to an increase in vascular surface area and to an increase in endothelial permeability of proteins. The results suggests that beta-adrenergic receptors regulate the transendothelial transport of fluid and proteins.

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.

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 arginine vasopressin on hemodynamics and lung fluid balance in lambs

1989 ◽  
Vol 256 (3) ◽  
pp. H641-H647 ◽  
Author(s):  
A. L. Gest ◽  
A. A. Moise ◽  
T. N. Hansen ◽  
S. Kaplan
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Fluid Balance ◽  
Arginine Vasopressin ◽  
Left Atrial ◽  
Plasma Concentrations ◽  
Base Line ◽  
Lung Fluid ◽  
Lung Fluid Balance ◽  
Lung Lymph

The purpose of this project was to study the effects of increased plasma concentrations of arginine vasopressin (AVP) on hemodynamics and lung fluid balance in lambs. We studied 16 unanesthetized newborn lambs during a base-line period and while infusing AVP into a hindlimb vein at 1.65 +/- 0.12 and 2.98 +/- 0.15 mU.kg-1.min-1. We measured aortic, pulmonary arterial, and left atrial pressures and heart rate continuously and cardiac output at frequent intervals. In five additional experiments, we collected samples of pure lung lymph during a base-line period and while infusing AVP at 2.02 +/- 0.15 mU.kg-1.min-1. AVP infusion increased plasma concentrations of AVP to 11.3 +/- 5.2 and 19.9 +/- 5.2 microU/ml at the low and high rates of infusion, respectively. Both aortic and left atrial pressures increased at the low rate of infusion (11 and 3 Torr, respectively) but remained unchanged at the higher rate. Systemic vascular resistance increased, and heart rate and cardiac output decreased at each rate of infusion. In fact, at the higher rate of infusion cardiac output decreased 38% when compared with base line. Neither pulmonary artery pressure nor pulmonary vascular resistance was affected by infusion of AVP. Despite the increase in left atrial pressure, the rate of lung lymph flow was not affected by the infusion of AVP, whereas the lymph-to-plasma protein ratio decreased slightly but significantly from 0.64 +/- 0.02 to 0.60 +/- 0.02.(ABSTRACT TRUNCATED AT 250 WORDS)

Aerosolized Pseudomonas elastase and lung fluid balance in anesthetized sheep

1992 ◽  
Vol 72 (5) ◽  
pp. 1927-1933 ◽  
Author(s):  
B. T. Peterson ◽  
M. L. Collins ◽  
L. D. Gray ◽  
A. O. Azghani
Keyword(s):  
Left Atrial ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Water Volume ◽  
Lung Epithelium ◽  
Lung Water ◽  
Lung Fluid ◽  
Lung Fluid Balance ◽  
Lung Epithelial ◽  
Lung Epithelial Permeability

The role of the lung epithelium in lung fluid balance was studied by ventilating anesthetized sheep with an aerosol of 20 mg of elastase from Pseudomonas aeruginosa (Ps. elastase) to increase lung epithelial permeability without affecting lung endothelial permeability or lung vascular pressures. Ps. elastase had no effect on the lung vascular pressures, the alveolar-arterial PO2 gradient (A-aPO2), the flow or protein concentration of the lung lymph, or the postmortem water volume of the lungs. The morphological alveolar flooding score in these sheep was 2.5 times the control level, but this was only marginally significant. Elevation of the left atrial pressure by 20 cmH2O alone increased the postmortem lung water volume but had no effect on A-aPO2, the alveolar flooding score, or the lung epithelial permeability assessed by the clearance of 99mTc-labeled human serum albumin. Addition of aerosolized Ps. elastase to these sheep had no effect on the total lung water volume, but it caused a redistribution of water into the air spaces, as evidenced by significant increases in the alveolar flooding score and A-aPO2 (P less than 0.01). Elevation of the left atrial pressure by 40 cmH2O without elastase caused the same response as elevation of the left atrial pressure by 20 cmH2O with elastase, except the higher pressure caused a greater increase in the total lung water volume. We conclude that alteration of the integrity of the lung epithelium with aerosolized Ps. elastase causes a redistribution of lung water into the alveoli without affecting the total lung water volume.(ABSTRACT TRUNCATED AT 250 WORDS)

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)

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)

Effects of manganese superoxide dismutase on lung fluid balance after smoke inhalation

1995 ◽  
Vol 78 (6) ◽  
pp. 2161-2168 ◽  
Author(s):  
T. T. Nguyen ◽  
C. S. Cox ◽  
D. N. Herndon ◽  
N. A. Biondo ◽  
L. D. Traber ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Fluid Balance ◽  
Manganese Superoxide Dismutase ◽  
Lymph Flow ◽  
Microvascular Permeability ◽  
Smoke Inhalation ◽  
Smoke Inhalation Injury ◽  
Lung Fluid ◽  
Lung Fluid Balance ◽  
Manganese Superoxide

There is evidence of increased oxygen free radical activity after smoke inhalation with and without concomitant burn injury. We determined the effects of manganese superoxide dismutase (Mn SOD) on lung fluid balance as measured by lung microvascular permeability coefficient (sigma), filtration coefficient (Kf), and lymph flow. Merino breed ewes (n = 6/group) were surgically prepared. The SOD group (SOD) received Mn SOD (9,000 U/kg) as an intravenous bolus and was insufflated with smoke. The control group (CON) received saline and smoke. sigma and Kf were determined 24 h before and 24 h after smoke injury. Lymph flow, arterial O2-to-inspired O2 fraction ratio, systemic hemodynamics, and pulmonary arterial and capillary pressures were measured. The sigma was significantly (P < 0.05) higher after smoke insufflation in SOD compared with CON (0.71 +/- 0.03 vs. 0.53 +/- 0.05). Kf was significantly lower after smoke insufflation in SOD compared with CON (0.038 +/- 0.010 vs. 0.061 +/- 0.010). Lymph flows were significantly lower during the 24 h after smoke insufflation in SOD compared with CON (33 +/- 7 vs. 55 +/- 8 ml/h at 24 h). Arterial O2-to-inspired O2 fraction ratio was significantly improved at 6 and 12 h after smoke insufflation in SOD compared with CON at the same time points. Mn SOD meliorates the lung microvascular permeability changes associated with smoke inhalation injury.

Effect of pulmonary perfusion on lung fluid filtration in young lambs

1988 ◽  
Vol 255 (6) ◽  
pp. H1336-H1341 ◽  
Author(s):  
W. G. Teague ◽  
M. E. Berner ◽  
R. D. Bland
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Surface Area ◽  
Left Atrial ◽  
Pulmonary Blood Flow ◽  
Balloon Catheter ◽  
Lymph Flow ◽  
Pulmonary Perfusion ◽  
Fluid Filtration ◽  
Lung Fluid

To study the effect of pulmonary perfusion on fluid filtration in the newborn lung, we measured pulmonary vascular pressures, cardiac output, lung lymph flow, and concentrations of protein in lymph and plasma of nine healthy, awake lambs, 2–3 wk old, before and during sustained alterations in pulmonary blood flow. A 12% reduction in cardiac output (from partial occlusion of the inferior vena cava) led to a corresponding decrease in lymph flow, consistent with a reduction in net lung fluid filtration. A 20% increase in pulmonary blood flow (from opening an external shunt between the carotid artery and jugular vein) increased lymph flow by approximately 40%, without a significant change in lymph protein concentration. These findings suggest that lung microvascular surface area expanded in response to increased perfusion, with little or no change in filtration pressure. In five lambs, lung microvascular pressure was increased by inflating a balloon catheter in the left atrium to establish full patency of the pulmonary microcirculation. In the presence of left atrial pressure elevation, increased perfusion through the arteriovenous shunt had no significant effect on pulmonary vascular pressures or lymph flow. Thus, in young lambs, modest changes in pulmonary blood flow may affect lung fluid filtration by altering perfused microvascular surface area; this response is inhibited in the presence of left atrial hypertension.

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