Inhomogeneity during deflation of excised canine lungs. I. Alveolar pressures

1988 ◽  
Vol 65 (4) ◽  
pp. 1757-1765 ◽  
Author(s):  
D. O. Warner ◽  
R. E. Hyatt ◽  
K. Rehder
Keyword(s):  
Pressure Gradient ◽  
Vertical Gradient ◽  
Pleural Pressure ◽  
Alveolar Pressure ◽  
Limiting Value

Factors both intrinsic and extrinsic to the lung may cause inhomogeneity of alveolar pressures during deflation. Wilson et al. (J. Appl. Physiol. 59: 1924-1928, 1985) predicted that any such inhomogeneity would be limited by interdependence of regional expiratory flows. To test this hypothesis and to explore how the pleural pressure gradient might affect inhomogeneity of alveolar pressures, we deflated at submaximal flows excised canine lobes that first were suspended in air and then were immersed in foams that simulated the vertical gradient of pleural pressure. Interregional inhomogeneity of regional transpulmonary pressures was measured with use of an alveolar capsule technique. Flow-dependent inhomogeneity of alveolar pressures was present, with differences in alveolar pressure quickly relaxing to a constant limiting value at each flow. Foam immersion increased inhomogeneity at a given flow. We conclude that factors intrinsic to the lung cause significant inhomogeneity of alveolar pressures at submaximal expiratory flows and that this inhomogeneity is enhanced by the extrinsic gradient of pleural pressure. These observations are consistent with the interdependence of flow proposed by Wilson et al.

Determinants of transvascular fluid shifts in zone I lungs

1980 ◽  
Vol 48 (2) ◽  
pp. 256-264 ◽  
Author(s):  
G. Nicolaysen ◽  
A. Hauge
Keyword(s):  
Lung Volume ◽  
Transmural Pressure ◽  
Pleural Pressure ◽  
Alveolar Pressure ◽  
Fluid Filtration ◽  
Fluid Shifts ◽  
Transvascular Fluid Shifts

We studied the fluid shifts in isolated, plasma-perfused rabbit lungs kept completely within zone I. The rate of fluid filtration or reabsorption was determined gravimetrically. A rise in alveolar pressure at constant pleural and vascular pressures reduced th rate of filtration or increased the rate of reabsorption in seven of eight lungs. In seven of seven lungs a reduction in pleural pressure at constant alveolar and vascular pressures increased the rate of filtration or decreased the rate of reabsorption. Thus, a given rise in lung volume had opposite effects depending on whether this rise was caused by an increased alveolar or reduced pleural pressure. Therefore, the exchange vessels studied cannot be true extra-alveolar vessels, which always expand (reflecting a rise in transmural pressure) with a rise in lung volume. When alveolar and pleural pressures were equally increased at constant vascular pressure, the rate of filtration was reduced in four of four lungs. The results can be explained through the existence of exchange vessels situated neither in the alveolar septae proper nor among the true extra-alveolar vessels. The vessels in the alveolar junctions are the most likely candidates.

Effect of vascular pressure on interstitial pressures in the isolated dog lung

1993 ◽  
Vol 75 (1) ◽  
pp. 268-272 ◽  
Author(s):  
M. R. Glucksberg ◽  
J. Bhattacharya
Keyword(s):  
Pressure Gradient ◽  
Airway Pressure ◽  
Pleural Pressure ◽  
Interstitial Pressure ◽  
Direct Measurements ◽  
Intravascular Pressure

We report the first direct measurements of the effect of pulmonary vascular pressures on perialveolar interstitial pressures. In seven experiments we varied the intravascular pressure (Pvas) in isolated dog lungs held at constant airway pressure (PA). By the micropuncture servo-null technique, we recorded perialveolar interstitial pressures with respect to pleural pressure (0 cmH2O) at the alveolar junctions (Pjct) and in microvascular adventitia (Padv). At PA = 7 cmH2O, increase from 5 to 15 cmH2O did not affect Pjct, although it decreased Padv by 1.2 +/- 0.4 cmH2O. The Pjct-Padv gradient increased by 77%. Increasing Pvas to 25 cmH2O had no further effect on either interstitial pressure. In four experiments we also determined interstitial pressure in the hilum (Phil). When Pvas was increased from 5 to 15 cmH2O, Phil increased by 4.5 +/- 0.9 cmH2O. Further elevation of Pvas to 25 cmH2O increased Phil further by 2.4 +/- 0.4 cmH2O. At PA = 15 cmH2O, all interstitial pressures decreased, but their responses to Pvas were similar. We conclude that increase of Pvas 1) increases Phil but not perialveolar interstitial pressures and 2) increases the perialveolar interstitial pressure gradient, which may promote local liquid clearance.

Measurement of Lung Water Content and Pleural Pressure Gradient with Magnetic Resonance Imaging

1995 ◽  
Vol 10 (1) ◽  
pp. 73-81 ◽  
Author(s):  
John R. Mayo ◽  
Alex L. MacKay ◽  
Ken P. Whittall ◽  
Elisabeth M. Baile ◽  
Peter D. Paré
Keyword(s):  
Magnetic Resonance Imaging ◽  
Magnetic Resonance ◽  
Pressure Gradient ◽  
Water Content ◽  
Pleural Pressure ◽  
Resonance Imaging ◽  
Lung Water ◽  
Lung Water Content

Interstitial fluid pressure gradient measured by micropuncture in excised dog lung

1984 ◽  
Vol 56 (2) ◽  
pp. 271-277 ◽  
Author(s):  
J. Bhattacharya ◽  
M. A. Gropper ◽  
N. C. Staub
Keyword(s):  
Fluid Flow ◽  
Pressure Gradient ◽  
Pressure Difference ◽  
Airway Pressure ◽  
Interstitial Fluid ◽  
Fluid Pressure ◽  
Interstitial Fluid Pressure ◽  
Pleural Pressure ◽  
Alveolar Wall ◽  
Fluid Filtration

We have directly measured lung interstitial fluid pressure at sites of fluid filtration by micropuncturing excised left lower lobes of dog lung. We blood-perfused each lobe after cannulating its artery, vein, and bronchus to produce a desired amount of edema. Then, to stop further edema, we air-embolized the lobe. Holding the lobe at a constant airway pressure of 5 cmH2O, we measured interstitial fluid pressure using beveled glass micropipettes and the servo-null method. In 31 lobes, divided into 6 groups according to severity of edema, we micropunctured the subpleural interstitium in alveolar wall junctions, in adventitia around 50-micron venules, and in the hilum. In all groups an interstitial fluid pressure gradient existed from the junctions to the hilum. Junctional, adventitial, and hilar pressures, which were (relative to pleural pressure) 1.3 +/- 0.2, 0.3 +/- 0.5, and -1.8 +/- 0.2 cmH2O, respectively, in nonedematous lobes, rose with edema to plateau at 4.1 +/- 0.4, 2.0 +/- 0.2, and 0.4 +/- 0.3 cmH2O, respectively. We also measured junctional and adventitial pressures near the base and apex in each of 10 lobes. The pressures were identical, indicating no vertical interstitial fluid pressure gradient in uniformly expanded nonedematous lobes which lack a vertical pleural pressure gradient. In edematous lobes basal pressure exceeded apical but the pressure difference was entirely attributable to greater basal edema. We conclude that the presence of an alveolohilar gradient of lung interstitial fluid pressure, without a base-apex gradient, represents the mechanism for driving fluid flow from alveoli toward the hilum.

Voluntary changes of thoracoabdominal shape and regional lung volumes in humans

1975 ◽  
Vol 39 (6) ◽  
pp. 997-1003 ◽  
Author(s):  
A. E. Grassino ◽  
B. Bake ◽  
R. R. Martin ◽  
R. Anthonisen
Keyword(s):  
Pressure Gradient ◽  
Negative Pressure ◽  
Degree Of Freedom ◽  
Pleural Pressure ◽  
Abdominal Pressure ◽  
Volume Distribution ◽  
Lung Volumes ◽  
Rib Cage ◽  
Regional Lung

We measured regional lung volumes from apex to base in humans during changes in thoracoabdominal shape which we monitored with magnetometers. In erect subjects, voluntary changes of shape at FRC did not change regional volume distribution. In supine subjects, the effect of negative pressure applied to the abdomen and a similar thoracoabdominal configuration achieved by voluntary means were studied. The distribution of regional volumes in both situations was the same as that measured during relaxation at the same overall lung volumes. We concluded that neither voluntary changes in shape nor negative abdominal pressure influenced the human pleural pressure gradient. This result, which differed from findings in animals, was probably because the human chest was relatively stiff and behaved with one degree of freedom; all parts of the human rib cage changed dimensions proportionally while negative abdominal pressure distorted the rib cage of animals.

Elevation gradient of intrathoracic pressure

1961 ◽  
Vol 16 (3) ◽  
pp. 465-468 ◽  
Author(s):  
John J. Krueger ◽  
Thomas Bain ◽  
John L. Patterson
Keyword(s):  
Pressure Gradient ◽  
Lung Tissue ◽  
Regional Differences ◽  
Work Of Breathing ◽  
Elevation Gradient ◽  
Intrathoracic Pressure ◽  
Vertical Gradient ◽  
Vertical Position ◽  
Horizontal Position ◽  
The Mean

Intrathoracic (intrapleural) pressure was measured in 15 anesthetized mongrel dogs held in the vertical position. A small balloon attached to a polyethylene catheter was inserted, without admission of air, into the chest through the 3rd intercostal space, or above the first rib, and passed down to the costophrenic sulcus. Along the lateral, anterolateral, and posterolateral aspects of the lung surface a vertical gradient of pressure was found, amounting to an increase of +0.21 cm H2O/cm descent, which was absent when the animal was in the horizontal position. This pressure gradient agrees closely with the gradient predicted on the basis of the mean density of lung tissue at end expiration in these animals. Among the implications of these findings is the possible existence of regional differences in the elastic work of breathing, based on differences in vertical distance between parts of the lung. Submitted on May 2, 1960

Lung expansion and the perialveolar interstitial pressure gradient

1989 ◽  
Vol 66 (6) ◽  
pp. 2600-2605 ◽  
Author(s):  
J. Bhattacharya ◽  
M. A. Gropper ◽  
J. M. Shepard
Keyword(s):  
Blood Flow ◽  
Pressure Gradient ◽  
Lung Volume ◽  
Extravascular Lung Water ◽  
Combined Effects ◽  
Interstitial Pressure ◽  
Alveolar Pressure ◽  
Lung Water ◽  
Interstitial Liquid ◽  
Lung Expansion

We have determined the combined effects of lung expansion and increased extravascular lung water (EVLW) on the perialveolar interstitial pressure gradient. In the isolated perfused lobe of dog lung, we measured interstitial pressures by micropuncture at alveolar junctions (Pjct) and in adventitia of 30- to 50-microns microvessels (Padv) with stopped blood flow at vascular pressure of 3–5 cmH2O. We induced edema by raising vascular pressures. In nonedematous lobes (n = 6, EVLW = 3.1 +/- 0.3 g/g dry wt) at alveolar pressure of 7 cmH2O, Pjct averaged 0.5 +/- 0.8 (SD) cmH2O and the Pjct-Padv gradient averaged 0.9 +/- 0.5 cmH2O. After increase of alveolar pressure to 23 cmH2O the gradient was abolished in nonedematous lobes, did not change in moderately edematous lobes (n = 9, EVLW = 4.9 +/- 0.6 g/g dry wt), and increased in severely edematous lobes (n = 6, EVLW = 7.6 +/- 1.4 g/g dry wt). Perialveolar interstitial compliance decreased with increase of alveolar pressure. We conclude that increase of lung volume may reduce perialveolar interstitial liquid clearance by abolishing the Pjct-Padv gradient in nonedematous lungs and by compressing interstitial liquid channels in edematous lungs.

Positive airway pressure and vertical transpulmonary pressure gradient in man

1975 ◽  
Vol 38 (5) ◽  
pp. 896-899 ◽  
Author(s):  
K. Rehder ◽  
N. Abboud ◽  
J. R. Rodarte ◽  
R. E. Hyatt
Keyword(s):  
Continuous Positive Airway Pressure ◽  
Pressure Gradient ◽  
Airway Pressure ◽  
Positive Airway Pressure ◽  
Transpulmonary Pressure ◽  
Vertical Gradient ◽  
Normal Subjects ◽  
Volume Curve ◽  
Pressure Volume Curve ◽  
Consistent Change

Static transpulmonary pressure (Pao-Pes) and the vertical gradient of transpulmonary pressure were determined in five sitting conscious normal subjects at mean airway pressures of 0 (ambient), 11, and 21 cmH2O. All subjects exhibited a nonuniform transpulmonary pressure gradient down the esophagus. The vertical pressure gradient was consistently larger in the lower (8–20cm below esophageal artifact) than in the middle region (0–8cm) of the esophagus. The gradient was not significantly altered by continuous positive airway pressure (11 and 21 cmH2O) or by changes in lung volume (60, 70, and 80% of total lung capacity (TLC)). Continuous positive airway pressure also did not result in a consistent change of the overall static pressure-volume curve of the lung. There was a small but statistically significant increase in TLC with each increase in airway pressure.

Liquid thickness vs. vertical pressure gradient in a model of the pleural space

1987 ◽  
Vol 62 (4) ◽  
pp. 1747-1754 ◽  
Author(s):  
S. J. Lai-Fook ◽  
D. C. Price ◽  
N. C. Staub
Keyword(s):  
Body Position ◽  
Vertical Gradient ◽  
Radioactive Tracer ◽  
Pleural Space ◽  
Pleural Pressure ◽  
Cylindrical Shape ◽  
Liquid Pressure ◽  
Rubber Balloon ◽  
Plastic Cylinder ◽  
Pleural Liquid Pressure

In recent studies using relatively noninvasive techniques, the vertical gradient in pleural liquid pressure was 0.2–0.5 cmH2O/cm ht, depending on body position, and pleural liquid pressure closely approximated lung recoil (J. Appl. Physiol. 59: 597–602, 1985). We built a model to discover why the vertical gradient in pleural pressure is less than hydrostatic (1 cmH2O/cm). A long rubber balloon of cylindrical shape was inflated in a plastic cylinder. The “pleural” space between the balloon and cylinder was filled with blue-dyed water. With the cylinder vertical, we measured pleural pressure by a transducer through side taps at 2-cm intervals up the cylinder. The pressure was measured with different amounts of water in the pleural space. With a clear separation between the balloon and the container, the vertical gradient in pleural liquid pressure was hydrostatic. As water was withdrawn from the pleural space, the balloon approached the wall of the container. Over an 8-cm-long midregion of the model where the balloon diameter matched the cylinder diameter, the vertical gradient was not hydrostatic and was virtually absent. In this region, the pleural liquid pressure was uniform and equal to the recoil of the balloon. In this section we could not see any pleural space. By scintillation imaging using 99mTc-diethylenetriamine pentaacetic acid in the water, we estimated the thickness of this flat “costal” pleural space to be approximately 20 microns. Radioactive tracer injected at the top of the pleural space appeared by 24 h at the bottom, which indicated a slow drainage of liquid by gravity.(ABSTRACT TRUNCATED AT 250 WORDS)

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