Effects of different-size microemboli on lung fluid and protein exchange

1981 ◽  
Vol 51 (2) ◽  
pp. 461-464 ◽  
Author(s):  
A. Johnson ◽  
A. B. Malik
Keyword(s):  
Hydrostatic Pressure ◽  
Pulmonary Arteries ◽  
Plasma Protein Concentration ◽  
Fluid Filtration ◽  
Lung Fluid ◽  
Collateral Arteries ◽  
Branching Points ◽  
Micron Diameter ◽  
Lung Lymph ◽  
Protein Exchange

We examined the effects of embolization with different-size glass-bead microemboli on pulmonary transvascular fluid and protein exchange in the sheep lung lymph fistula preparation. Embolization with either 200- or 500-micron-diameter glass beads caused comparable increases in pulmonary vascular resistance, which were sustained for the duration of the study. The 200-micron beads increased pulmonary lymph flow (Qlym) and did not affect the lymph-to-plasma protein concentration ratio (L/P), whereas injection with 500-micron beads increased Qlym and decreased L/P. The latter changes were comparable to those observed after an increase in pulmonary microvascular pressure induced by left atrial hypertension, suggesting that the 500-micron beads increase the Qlym by raising the microvascular hydrostatic pressure. In contrast, the 200-micron beads increased the transvascular clearance of proteins to a greater extent, since L/P did not decrease as Qlym increased. These findings suggest that lung vascular permeability increases after embolization with smaller (200-micron) but not with larger (500-micron) emboli. The increased permeability after embolization with small beads may be due to transmission of the permeability-increasing substances to the downstream capillaries via the collateral pulmonary arteries. This would not occur after embolization with larger emboli if these obstructed the pulmonary arteries upstream from branching points of the collateral arteries. The ultrafiltration of protein-poor plasma after embolization with the 500-micron beads may reflect increased fluid filtration in unobstructed microvessels due to increase in the microvascular hydrostatic pressure.

Does ADP-Induced Platelet Aggregation Mediate Lung Vascular Injury?

1981 ◽  
Author(s):  
A B Malik ◽  
F L Minnear ◽  
M V Tahamont ◽  
D G Moon ◽  
J E Kaplan
Keyword(s):  
Platelet Aggregation ◽  
Vascular Injury ◽  
Protein Concentration ◽  
Control Group ◽  
Plasma Protein Concentration ◽  
Fluid Filtration ◽  
Lung Fluid ◽  
Protein Clearance ◽  
Pulmonary Arterial ◽  
Protein Exchange

We determined the effects of ADP-induced platelet aggregation on lung fluid and protein exchange to examine whether platelet aggregation mediates lung vascular injury. The studies were made in intact sheep in which pulmonary lymph was obtained, and the protein concentration of lymph was compared to that of plasma. Two groups were studied: Control sheep receiving i.v. infusion of 10 mg/kg of ADP and experimental sheep in which platelets were depleted with anti-platelet serum prior to ADP infusion. In the control group, ADP decreased the platelet count from 178,554 ± 62,750 to 103,500 ± 47,828 cells/mm3, suggesting the entrapment of platelet in the pulmonary circulation. The pulmonary arterial pressure (Ppa) increased from 13.1 ± 1.8 to 15.9 ± 1.2 mmHg. Lung lymph flow (Qlym) increased from 8.4 ± 1.8 to 11.4 ± 2.3ml/hr (p < 0.05) and transvascular protein clearance (Qlym x lymph/plasma protein concentration), a measure of protein exchange, increased from 6.7 ± 1.3 to 9.4 ± 3.0 ml/hr (p < 0.05). These increases could be explained by an increase in microvascular pressure (Pmv) and ultrafiltration since mechanically elevation of Pmv produced the same changes in Qlym and clearance. Platelet depletion prevented the ADP-induced increases in platelet aggregation does not mediate lung vascular injury, but increases fluid filtration by increasing the microvascular pressure. This effect may be mediated by release of pulmonary vasoconstrictor substances such as thromboxane A2 and serotonin after platelet aggregation.

Effect of pulmonary arterial occlusion on lung fluid and protein exchange

1982 ◽  
Vol 53 (3) ◽  
pp. 543-548 ◽  
Author(s):  
P. S. Barie ◽  
A. B. Malik
Keyword(s):  
Protein Concentration ◽  
Arterial Occlusion ◽  
Base Line ◽  
Plasma Protein Concentration ◽  
Lung Fluid ◽  
Mean Pulmonary Arterial Pressure ◽  
Protein Clearance ◽  
Pulmonary Arterial ◽  
Lung Lymph ◽  
Protein Exchange

We examined the effects of left pulmonary arterial occlusion and reperfusion on pulmonary transvascular fluid and protein exchange in the sheep lung lymph fistula preparation. Pulmonary lymph flow (Qlym) increased from the base-line value of 5.0 +/- 0.8 to 10.0 +/- 2.1 ml/h after occlusion (P less than 0.05); the steady-state value of 11.9 +/- 2.2 ml/h during reperfusion was not significantly different from the value during occlusion. The lymph-to-plasma protein concentration ratio (L/P) did not change significantly during either occlusion or reperfusion. Transvascular protein clearance (Qlym X L/P) increased from 3.7 +/- 0.6 to 8.4 +/- 2.1 ml/h during occlusion (P less than 0.05) and remained elevated at 8.6 +/- 1.7 ml/h during reperfusion. The sustained increases in Qlym and protein clearance could not be explained by the 3-Torr increase in mean pulmonary arterial pressure during the occlusion period or by an increase in the interstitial protein concentration caused by a period of decreased filtration during occlusion. The increases in protein clearance that occurred with increased Qlym during occlusion and reperfusion were greater than the increases in protein clearance with comparably increased Qlym during left atrial hypertension. The results suggest that occlusion of a pulmonary artery increases vascular permeability to plasma proteins in the lung.

Hypobaric hypoxia does not affect lung fluid or protein exchange in awake adult sheep at rest

1983 ◽  
Vol 61 (7) ◽  
pp. 714-716
Author(s):  
G. Coates ◽  
L. W. Belbeck ◽  
G. W. Gray
Keyword(s):  
Pulmonary Artery ◽  
Left Atrial ◽  
Hypobaric Hypoxia ◽  
Barometric Pressure ◽  
Lymph Flow ◽  
Adult Sheep ◽  
Lung Fluid ◽  
Lung Lymph ◽  
Lung Lymph Flow ◽  
Protein Exchange

We measured pulmonary artery [Formula: see text] and left atrial [Formula: see text] pressures, lung lymph flow, and lymph/plasma protein concentrations in four adult sheep at a barometric pressure of 380 Torr (1 Torr = 133.322 Pa) for 22 h. Hypobaric hypoxia caused an immediate increase in [Formula: see text] from 20 to 39 Torr. There was no significant change in [Formula: see text], lymph flow, or lymph protein concentrations. We conclude that hypobaric hypoxia does not affect lung fluid or protein exchange in awake adult sheep at rest.

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.

CVF-induced decomplementation: effect on lung transvascular protein flux after thrombin

1987 ◽  
Vol 62 (3) ◽  
pp. 863-869 ◽  
Author(s):  
A. Johnson ◽  
S. K. Lo ◽  
F. B. Blumenstock ◽  
A. B. Malik
Keyword(s):  
Plasma Protein Concentration ◽  
Pulmonary Hemodynamics ◽  
Mean Pulmonary Arterial Pressure ◽  
Protein Clearance ◽  
Pulmonary Arterial ◽  
Hemolytic Complement Activity ◽  
The Mean ◽  
Lung Lymph ◽  
Made In ◽  
Protein Exchange

We examined the effects of cobra venom factor (CVF) on the changes in pulmonary hemodynamics and transvascular fluid and protein exchange following thrombin-induced pulmonary microembolism. Studies were made in unanesthetized sheep prepared with lung lymph fistulas. The animals received tranexamic acid (100 mg) to suppress fibrinolysis and were then challenged with an intravenous infusion of alpha-thrombin (80 U/kg). Control-thrombin challenged sheep were compared with the CVF-treated sheep challenged with the same thrombin dosage. CVF treatment (187 U X kg-1 X day-1 for 4 days) decreased the total hemolytic complement activity by 45% of control. Thrombin infusion in control sheep increased the mean pulmonary arterial pressure (Ppa), pulmonary vascular resistance (PVR), and lymph protein clearance (pulmonary lymph flow X lymph-to-plasma protein concentration ratio, Clym). Thrombin infusion in CVF-treated sheep produced smaller increments in Ppa, PVR, and Clym. Pulmonary lymph obtained from control-thrombin and CVF-thrombin sheep induced migration of granulocytes obtained from normal unchallenged sheep. The granulocytes obtained from CVF-treated sheep responded relatively less to the migratory and O-2-generating stimuli (i.e., zymosan-treated serum, pulmonary lymph from sheep after thrombin challenge, and plasma from sheep after CVF treatment) compared with normal granulocytes. The attenuation of the thrombin-induced increases in Ppa, PVR, and lung transvascular fluid and protein exchange by CVF treatment may be the result of impaired function of granulocytes.

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.

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.

Lung fluid balance, vascular permeability, and gas exchange after acid aspiration in awake goats

1984 ◽  
Vol 56 (4) ◽  
pp. 979-985 ◽  
Author(s):  
R. Winn ◽  
J. Stothert ◽  
B. Nadir ◽  
J. Hildebrandt
Keyword(s):  
Protein Concentration ◽  
Base Line ◽  
Lung Water ◽  
Plasma Protein Concentration ◽  
Acid Aspiration ◽  
Lung Fluid ◽  
Lung Fluid Balance ◽  
Lung Injuries ◽  
Pulmonary Arterial ◽  
Lung Lymph

Lung injuries were produced by instilling 2.5 ml/kg of 0.1 N HCl into the trachea of lightly anesthetized goats with previously implanted lung lymph fistulas. Lymph flow (QL), lymph-to-plasma protein concentration ratio (L/P), pulmonary arterial and wedge pressures (Ppa, Pw), percent shunt (Qs/QT), and postmortem extravascular lung water (EVLW) were then measured for up to 48 h. QL began to increase within 15 min of injury from a baseline value of 7.2 ml/h to reach a peak of 231% of base line by 1.5 h, then decreased to 160% at 24 h and returned to base line by 48 h. Average L/P increased from 0.66 to a peak of 0.73 at 2 h. Ppa increased from 17.0 cmH2O to a first peak of 25.3 cmH2O at 15 min, then decreased to base line by 75 min. There was a second rise that peaked at 3 h before returning to base line at 24–48 h; Pw was unchanged throughout. Qs/QT increased from 8.5 to a peak of 34% at 1 h, then decreased to 15% at 4 h, and stabilized at 17–20% at 48 h. EVLW was 237% of base line at 4 h and declined somewhat but remained elevated at 194% of base line at 24 and 48 h. Qs/QT was less than expected based on the reduction in lung volume after aspiration. We conclude that microvascular permeability was increased after acid and that a protective vasoconstriction, probably due to local hypoxia, directed blood away from nonventilated alveoli.

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