Changes in microvascular permeability with acceleration of edema in dog lungs

1990 ◽  
Vol 258 (2) ◽  
pp. H395-H399 ◽  
Author(s):  
B. D. Butler ◽  
R. E. Drake ◽  
W. D. Sneider ◽  
S. J. Allen ◽  
J. C. Gabel
Keyword(s):  
Weight Gain ◽  
Pulmonary Edema ◽  
Membrane Permeability ◽  
Left Atrial ◽  
Membrane Filtration ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Base Line ◽  
Edema Formation ◽  
Before And After

Elevation of left atrial pressure to 25–40 mmHg causes continuous pulmonary edema formation in dog lungs. However, after 5–120 min, the rate of edema formation often increases (acceleration of edema). Acceleration of edema could be associated with an increase in microvascular membrane permeability because an increase in permeability would cause fluid to filter through the microvascular membrane more rapidly. To test the hypothesis that acceleration is associated with increased permeability, we used the continuous weight-gain technique to estimate the pulmonary microvascular membrane filtration coefficient (Kf) before and after acceleration of edema in 10 dogs. Acceleration occurred 36 +/- 38 (SD) min after elevation of left atrial pressure to 35.2 +/- 5.4 mmHg. Rate of weight gain increased from 0.47 +/- 0.17 g/min before acceleration to 0.88 +/- 0.26 g/min (P less than 0.05) after acceleration of pulmonary edema. Kf was increased from initial values of 0.058 +/- 0.027 to 0.075 +/- 0.029 ml.min-1.mmHg-1 (P less than 0.05) after acceleration. In five additional dogs we cannulated lung lymphatics and determined the lymph to plasma protein concentration ratio (CL/CP) before and after acceleration. CL/CP increased from base-line values of 0.37 +/- 0.07 to 0.44 +/- 0.06 (P less than 0.05) after acceleration. Both the increase in Kf and CL/CP data support the hypothesis that acceleration of edema is due, in part, to a slight increase in microvascular membrane permeability. However, the findings could also have been caused by an increase in interstitial conductance, washout of interstitial proteins, or alveolar flooding.

β-Adrenergic agonist therapy accelerates the resolution of hydrostatic pulmonary edema in sheep and rats

2000 ◽  
Vol 89 (4) ◽  
pp. 1255-1265 ◽  
Author(s):  
James A. Frank ◽  
Yibing Wang ◽  
Oscar Osorio ◽  
Michael A. Matthay
Keyword(s):  
Pulmonary Edema ◽  
Left Atrial ◽  
Experimental Studies ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Adrenergic Agonist ◽  
Agonist Therapy ◽  
Arterial Blood ◽  
Alveolar Liquid Clearance ◽  
Alveolar Liquid

To determine whether β-adrenergic agonist therapy increases alveolar liquid clearance during the resolution phase of hydrostatic pulmonary edema, we studied alveolar and lung liquid clearance in two animal models of hydrostatic pulmonary edema. Hydrostatic pulmonary edema was induced in sheep by acutely elevating left atrial pressure to 25 cmH2O and instilling 6 ml/kg body wt isotonic 5% albumin (prepared from bovine albumin) in normal saline into the distal air spaces of each lung. After 1 h, sheep were treated with a nebulized β-agonist (salmeterol) or nebulized saline (controls), and left atrial pressure was then returned to normal. β-Agonist therapy resulted in a 60% increase in alveolar liquid clearance over 3 h ( P< 0.001). Because the rate of alveolar fluid clearance in rats is closer to human rates, we studied β-agonist therapy in rats, with hydrostatic pulmonary edema induced by volume overload (40% body wt infusion of Ringer lactate). β-Agonist therapy resulted in a significant decrease in excess lung water ( P < 0.01) and significant improvement in arterial blood gases by 2 h ( P < 0.03). These preclinical experimental studies support the need for controlled clinical trials to determine whether β-adrenergic agonist therapy would be of value in accelerating the resolution of hydrostatic pulmonary edema in patients.

Effect of thoracic duct drainage on hydrostatic pulmonary edema and pleural effusion in sheep

1991 ◽  
Vol 71 (1) ◽  
pp. 314-316 ◽  
Author(s):  
S. J. Allen ◽  
R. E. Drake ◽  
G. A. Laine ◽  
J. C. Gabel
Keyword(s):  
Pleural Effusion ◽  
Central Venous Pressure ◽  
Pulmonary Edema ◽  
Thoracic Duct ◽  
Left Atrial ◽  
Venous Pressure ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Central Venous ◽  
Pulmonary Arterial

Positive end-expiratory pressure (PEEP) increases central venous pressure, which in turn impedes return of systemic and pulmonary lymph, thereby favoring formation of pulmonary edema with increased microvascular pressure. In these experiments we examined the effect of thoracic duct drainage on pulmonary edema and hydrothorax associated with PEEP and increased left atrial pressure in unanesthetized sheep. The sheep were connected via a tracheostomy to a ventilator that supplied 20 Torr PEEP. By inflation of a previously inserted intracardiac balloon, left atrial pressure was increased to 35 mmHg for 3 h. Pulmonary arterial, systemic arterial, and central venous pressure as well as thoracic duct lymph flow rate were continuously monitored, and the findings were compared with those in sheep without thoracic duct cannulation (controls). At the end of the experiment we determined the severity of pulmonary edema and the volume of pleural effusion. With PEEP and left atrial balloon insufflation, central venous and pulmonary arterial pressure were increased approximately threefold (P less than 0.05). In sheep with a thoracic duct fistula, pulmonary edema was less (extra-vascular fluid-to-blood-free dry weight ratio 4.8 +/- 1.0 vs. 6.1 +/- 1.0; P less than 0.05), and the volume of pleural effusion was reduced (2.0 +/- 2.9 vs. 11.3 +/- 9.6 ml; P less than 0.05). Our data signify that, in the presence of increased pulmonary microvascular pressure and PEEP, thoracic duct drainage reduces pulmonary edema and hydrothorax.

Effect of airway and left atrial pressures on microvascular and interstitial pressures in adult lungs

1993 ◽  
Vol 74 (5) ◽  
pp. 2112-2120
Author(s):  
C. D. Fike ◽  
M. R. Kaplowitz
Keyword(s):  
Airway Pressure ◽  
Left Atrial ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Lower Airway ◽  
Fluid Flux ◽  
Edema Formation ◽  
Fluid Filtration ◽  
Lung Inflation ◽  
Micropuncture Technique

The purpose of this study was to determine the effect of lung inflation and left atrial pressure on the hydrostatic pressure gradient for fluid flux across 20- to 80-microns-diam arterioles and venules in isolated perfused lungs of adult rabbits. We used the micropuncture technique and measured microvascular or interstitial pressures at constant airway pressures of 5 and 15 cmH2O with left atrial pressure adjusted above (zone 3 conditions) or below (zone 2 conditions) airway pressure. Only in lungs inflated to the higher airway pressure did a reduction in left atrial pressure below airway pressure result in concomitant reductions in venular pressure. This suggests that the site of flow limitation in zone 2 shifted from venules > 80 microns diam toward vessels <20 microns diam with inflation from 5 to 15 cmH2O. With the lungs under zone 3 conditions, both transarteriolar and transvenular gradients (microvascular-interstitial pressures) were greater at the higher compared with the lower airway pressure. In contrast, transarteriolar and transvenular gradients changed in opposite directions when compared at the two inflation pressures under zone 2 conditions. Counteracting changes in transmicrovascular gradients make it difficult to predict the effect on fluid filtration from lung inflation under zone 2 conditions. When zone 3 conditions are maintained during inflation, the tendency for edema formation should increase.

Pulmonary neutrophil kinetics in sheep: effects of altered hemodynamics

1985 ◽  
Vol 59 (6) ◽  
pp. 1796-1801 ◽  
Author(s):  
J. A. Cooper ◽  
R. Bizios ◽  
A. B. Malik
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Left Atrial ◽  
Recovery Period ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Base Line ◽  
Pulmonary Hemodynamics ◽  
Pulmonary Blood Volume ◽  
Neutrophil Kinetics

We investigated the effect of elevated left atrial pressure and reduced cardiac output on pulmonary neutrophil kinetics in the sheep. Sheep neutrophils were isolated, labeled with 111In-oxine, and reinfused. Erythrocytes were labeled with [99mTc]pertechnetate. A gamma camera measured the lung activities of the labeled neutrophils and erythrocytes. The results indicated that 38.5% of the total injected neutrophils marginated in the lung. Pulmonary hemodynamics were altered by inflating a left atrial balloon three times in each sheep for 15–30 min to achieve 5- to 25-mmHg increments in pulmonary arterial wedge pressure. At least a 30-min recovery period was allowed between inflations. After each left atrial balloon inflation, neutrophil uptake remained unchanged from base line, despite decreased mean cardiac output to 0.67 +/- 0.24 (+/- SD) 1/min and increased pulmonary blood volume. The absence of pulmonary neutrophil uptake was confirmed by arterial-venous measurements. Increased pulmonary blood volume had little effect on lung neutrophil uptake, suggesting that most of the pulmonary neutrophils are marginated. We conclude that the lungs have a large marginated neutrophil pool compared with the circulating pool and that reduced cardiac output and elevated left atrial pressure have no effect on pulmonary neutrophil kinetics in the sheep.

Pulmonary Edema and Elevated Left Atrial Pressure: Four Hours and Beyond

Physiology ◽  
2002 ◽  
Vol 17 (6) ◽  
pp. 223-226 ◽  
Author(s):  
R. E. Drake ◽  
M. F. Doursout
Keyword(s):  
Connective Tissue ◽  
Pulmonary Edema ◽  
Left Atrial ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Cardiogenic Pulmonary Edema ◽  
Left Heart ◽  
Fluid Accumulation ◽  
Increased Pressure

Cardiogenic pulmonary edema is caused by the increase in left atrial pressure when the left heart fails. The increased pressure causes rapid fluid accumulation within the lung interstitial spaces. However, over the following days to weeks, additional fluid may accumulate due to the deposition of excess lung connective tissue.

Pulmonary hypertension, pulmonary edema, and decreased pulmonary compliance produced by increased ICP in cats

1984 ◽  
Vol 60 (6) ◽  
pp. 1207-1213 ◽  
Author(s):  
Melvin M. Newman ◽  
Marta Kligerman ◽  
Mary Willcox
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Edema ◽  
Left Atrial ◽  
Pulmonary Ventilation ◽  
Systolic Pressure ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Sodium Pentobarbital ◽  
Left Heart Failure ◽  
Pulmonary Compliance

✓ Cats, anesthetized with sodium pentobarbital, were cannulated to measure pulmonary, systemic, and left atrial pressures and pulmonary ventilation, compliance, and resistance. Intracranial pressure was elevated to 30 mm Hg by injecting silicone oil into the extradural space. After an average time of 56 minutes, pulmonary systolic and diastolic pressures more than doubled, systemic systolic pressure sometimes rose and sometimes fell, and diastolic pressure rose 5%. Left atrial pressure never exceeded 8 cm of saline. Pulmonary compliance decreased by one-half, but airway resistance was unchanged. Pulmonary edema was estimated from histological sections. The pulmonary hypertension may be the result of a sympathetic discharge confined to the lung, since no remarkable changes in heart rate or systemic blood pressure occurred. The decrease in pulmonary compliance followed the rise in pulmonary arterial pressure, and is interpreted as the result of interstitial edema. There was no evidence that left heart failure or elevated left atrial pressure caused the pulmonary edema.

Assessment of alveolar-capillary membrane permeability of dogs by aerosolization

1981 ◽  
Vol 51 (4) ◽  
pp. 955-962 ◽  
Author(s):  
G. J. Huchon ◽  
J. W. Little ◽  
J. F. Murray
Keyword(s):  
Membrane Permeability ◽  
Left Atrial ◽  
Volume Of Distribution ◽  
The Body ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Pressure Groups ◽  
Capillary Membrane ◽  
Anesthetized Dogs ◽  
Alveolar Capillary

We developed a method for measuring an index of alveolar-capillary membrane permeability (PI) by aerosolizing a mixture of 99mTc-diethylenetriaminepentaacetic acid (Tc-DTPA) and 125I-antipyrine (I-AP) and injecting 111In-DTPA (In-DTPA). The I-AP was used to compute the quantity of Tc-DTPA delivered and the In-DTPA the quantity of Tc-DTPA in the body. The PI was the ratio of the uptake of Tc-DTPA per minute to the amount deposited at the end of aerosolization. In 14 anesthetized dogs we measured the volume of distribution of I-AP (0.54 +/- 0.034 l/kg body wt) and/or showed that the volumes of distribution of Tc-DTPA and In-DTPA were similar. We measured PI in four groups of dogs: control (n = 5), oleic acid (n = 5), hydrochloric acid (n = 6), and high left atrial pressure (n = 5). The PI increased significantly in both groups with acid-induced increased permeability compared with the control and high left atrial pressure groups, which did not differ from each other. We conclude that the aerosolization method is suitable for differentiating increased from normal permeability.

Effects of coronary flow reduction on lung vascular tissue transport in sheep

1983 ◽  
Vol 55 (6) ◽  
pp. 1906-1915 ◽  
Author(s):  
T. R. Harris ◽  
J. C. Collins ◽  
R. J. Roselli
Keyword(s):  
Left Atrial ◽  
Coronary Flow ◽  
Vascular Tissue ◽  
Lymph Flow ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Base Line ◽  
Flow Reduction ◽  
Second Period ◽  
Increased Pressure

This study was performed to measure the effects of a sustained reduction in coronary flow on lung lymph flow and protein content. Ten halothane-anesthetized sheep with cannulated lymphatic vessels were provided with a carotid-to-left anterior descending coronary artery cannula containing an electromagnetic flowmeter. One group of five animals was observed at base line and after coronary flow was reduced to 38% of base line. A second group of five animals acted as controls and was observed at base line, for 111 min of increased left atrial pressure, and a second period of normal pressures. Sustained coronary flow reduction led to significant increases in pulmonary arterial pressure, left atrial pressure, lymph flow, total protein lymph-to-plasma concentration ratio (L/P), and protein lymph clearance (L/P X lymph flow). Analysis of the pressure, lymph, protein, and indicator data with a two-pore model of the microvascular barrier showed that the observations were consistent with the concept that coronary flow reduction decreased functioning lung capillary surface but increased the size of the large pore and the number of small pores relative to the number of larger pores. Control studies showed increases in lymph flow and decreases in L/P with increased pressure but no significant changes in any variable between the first and second period of normal pressures. We conclude that coronary flow reduction increases lung vascular-tissue transport by decreasing the resistance of the microvascular barrier to protein and fluid movement. However, increased pressure secondary to left ventricular dysfunction plays a role in the magnitude of this response.

Longitudinal distribution of pulmonary vascular resistance with very high pulmonary blood flow

1987 ◽  
Vol 62 (1) ◽  
pp. 344-358 ◽  
Author(s):  
M. Younes ◽  
Z. Bshouty ◽  
J. Ali
Keyword(s):  
Blood Flow ◽  
Weight Gain ◽  
Left Atrial ◽  
Pulmonary Blood Flow ◽  
Lower Lobe ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Longitudinal Distribution ◽  
Flow Rates ◽  
Flow Threshold

Dog left upper lobes (LUL) were perfused in situ via the left lower lobe artery. Lobe weight was continuously monitored. Increasing lobar flow from normal to 10 times normal had little effect on left atrial pressure, which ranged from 1 to 5 mmHg. There was a flow threshold (Qth) below which lobar weight was stable. Qth ranged from 1.1 to 1.55 l/min (mean 1.27) corresponding to four times normal LUL blood flow. Above Qth, step increases in lobar flow resulted in progressive weight gain at a constant rate that was proportional to flow. The effective pressure at the filtration site (EFP) at different flow rates was estimated from the static vascular pressure that resulted in the same rate of weight gain. From this value and from mean pulmonary arterial (PA) and left atrial (LA) pressures, we calculated resistance upstream (Rus) and downstream (Rds) from filtration site. At Qth, Rds accounted for 60% of total resistance. This fraction increased progressively with flow, reaching 83% at Q of 10 times normal. We conclude that during high pulmonary blood flow EFP is closer to PA pressure than it is to LA pressure, and that this becomes progressively more so as a function of flow. As a result, the lung accumulates water at flow rates in excess of four times normal despite a normal left atrial pressure.

Effects of prolonged elevated microvascular pressure on lung fluid balance in sheep

1985 ◽  
Vol 58 (3) ◽  
pp. 869-875 ◽  
Author(s):  
R. E. Parker ◽  
R. J. Roselli ◽  
K. L. Brigham
Keyword(s):  
Arterial Pressure ◽  
Left Atrial ◽  
Systemic Arterial Pressure ◽  
Protein Fractions ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Base Line ◽  
Total Proteins ◽  
Lung Fluid ◽  
Osmotic Reflection Coefficient

Experiments were conducted in seven chronically instrumented unanesthetized sheep to estimate the osmotic reflection coefficient (sigma d) for total proteins and the solvent-drag reflection coefficients (sigma f) for six endogenous protein fractions. We measured the lymph-to-plasma ratio of total proteins (CL/CP) and six protein fractions during base-line conditions and after left atrial pressure elevations of 24–26 h per elevation. We also monitored pulmonary arterial pressure, left atrial pressure, systemic arterial pressure, and lung lymph flow at the various levels of pulmonary microvascular pressure. Our results indicate the CL/CP may require up to 24 h to reach a true steady state. It was found that sigma d is at least 0.89 for total proteins and sigma f is at least 0.84, 0.87, 0.86, 0.92, 0.95, and 0.96 for protein fractions with effective molecular radii of 36, 39.5, 44, 66, 105, and 123 A, respectively. In addition, the sigma f values for various protein fractions obtained from this investigation are compared with the predicted values of various mathematical models of the lung microcirculation.

Sign in / Sign up

Export Citation Format

Share Document