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)

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.

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.

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.

Effects of hypobaria on lung fluid balance in awake sheep

1988 ◽  
Vol 64 (1) ◽  
pp. 243-248 ◽  
Author(s):  
K. Hirai ◽  
T. Kobayashi ◽  
K. Kubo ◽  
T. Shibamoto
Keyword(s):  
Fluid Balance ◽  
Bubble Formation ◽  
Random Order ◽  
Barometric Pressure ◽  
Base Line ◽  
Plasma Protein Concentration ◽  
Pulmonary Vascular Permeability ◽  
Lung Fluid ◽  
Lung Fluid Balance ◽  
Lung Lymph

Effects of hypobaria on lung fluid balance were studied in five awake sheep with chronic lung lymph fistulas using a decompression chamber. Each sheep was exposed to three conditions of 6,600-m-simulated high altitude in random order as follows: 1) 6,600-m-simulated hypoxic hypobaria (barometric pressure 326 Torr, 21% inspired O2 fraction), 2) 6,600-m-simulated normoxic hypobaria (barometric pressure 326 Torr, 65% inspired O2 fraction), and 3) 6,600-m-simulated normoxic hypobaria (barometric pressure 326 Torr, 65% inspired O2 fraction) after pretreatment with a 2-h pure O2 inhalation (i.e., denitrogenation) to allow elimination of dissolved gases, especially N2, from the blood and tissues. We observed that under both hypoxic hypobaria and normoxic hypobaria, lung lymph flow (Qlym) significantly increased from the base-line values of 6.4 +/- 0.3 to 13.0 +/- 1.0 ml/h and 6.0 +/- 0.2 to 9.4 +/- 0.3 ml/h, respectively (P less than 0.05) and that the lymph-to-plasma protein concentration ratio remained unchanged. Moreover, pretreatment with a 2-h denitrogenation inhibited the increase in Qlym. These results suggest that rapid exposure to hypobaria causes an increase in pulmonary vascular permeability and that intravascular air bubble formation may account for this permeability change.

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.

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)

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.

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)

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.

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