Parenchymal stress affects interstitial and pleural pressures in in situ lung

1991 ◽  
Vol 71 (5) ◽  
pp. 1967-1972 ◽  
Author(s):  
G. Miserocchi ◽  
D. Negrini ◽  
C. Gonano

After resecting the intercostal muscles and thinning the endothoracic fascia, we micropunctured the lung tissue through the intact pleural space at functional residual capacity (FRC) and at volumes above FRC to evaluate the effect of increasing parenchymal stresses on pulmonary interstitial pressure (Pip). Pip was measured at a depth of approximately 230 microns from the pleural surface, at 50% lung height, in 12 anesthetized paralyzed rabbits oxygenated via a tracheal tube with 50% humidified O2. Pip was -10 +/- 1.5 cmH2O at FRC. At alveolar pressure of 5 and 10 cmH2O, lung volume increased by 8.5 and 19 ml and Pip decreased to -12.4 +/- 1.6 and -12.3 +/- 5 cmH2O, respectively. For the same lung volumes held by decreasing pleural surface pressure to about -5 and -8.5 cmH2O, Pip decreased to -17.4 +/- 1.6 and -23.8 +/- 5 cmH2O, respectively. Because Pip is more negative than pleural pressure, the data suggest that in intact pulmonary interstitium the pressure of the liquid phase is primarily set by the mechanisms controlling interstitial fluid turnover.

1980 ◽  
Vol 48 (6) ◽  
pp. 939-946 ◽  
Author(s):  
S. J. Lai-Fook ◽  
B. Toporoff

Pulmonary perivascular interstitial fluid pressure (Px) was measured as a function of extravascular water accumulation (W). Px was measured directly by wick catheters and open-ended needles inserted in the interstitium near the hilus of isolated perfused dog lobes. Lobes were studied at constant transpulmonary pressure (Ptp) and vascular pressure (Pv, arterial equal to venous pressure). Px-W behavior had two distinct phases: an initial low compliance phase interpreted as perivascular filling, followed sometimes by an abrupt transition to a high compliance phase interpreted as alveolar flooding. W at transition was between 20 and 50% of the initial lung weight. Perivascular compliance during filling at a Ptp of 6 cmH2O was 0.1 g.g wet lobe wt-1.cmH2O-1, which was one-sixth that during alveolar flooding and 2.5 times that at a Ptp of 25 cmH2O. At the start of alveolar flooding, estimated alveolar interstitial fluid pressure was slightly (2 cmH2O) below alveolar pressure (PAlv) at a Ptp of 6 cmH2O but considerably belov PAlv at high lung volumes. These findings support the concept that alveolar surface tension reduces the interstitial fluid pressure below PAlv.


2004 ◽  
Vol 84 (2) ◽  
pp. 385-410 ◽  
Author(s):  
STEPHEN J. LAI-FOOK

Lai-Fook, Stephen J. Pleural Mechanics and Fluid Exchange. Physiol Rev 84: 385–410, 2004; 10.1152/physrev.00026.2003.—The pleural space separating the lung and chest wall of mammals contains a small amount of liquid that lubricates the pleural surfaces during breathing. Recent studies have pointed to a conceptual understanding of the pleural space that is different from the one advocated some 30 years ago in this journal (Agostoni E. Physiol Rev 52: 57–128, 1972). The fundamental concept is that pleural surface pressure, the result of the opposing recoils of the lung and chest wall, is the major determinant of the pressure in the pleural liquid. Pleural liquid is not in hydrostatic equilibrium because the vertical gradient in pleural liquid pressure, determined by the vertical gradient in pleural surface pressure, does not equal the hydrostatic gradient. As a result, a viscous flow of pleural liquid occurs in the pleural space. Ventilatory and cardiogenic motions serve to redistribute pleural liquid and minimize contact between the pleural surfaces. Pleural liquid is a microvascular filtrate from parietal pleural capillaries in the chest wall. Homeostasis in pleural liquid volume is achieved by an adjustment of the pleural liquid thickness to the filtration rate that is matched by an outflow via lymphatic stomata.


1983 ◽  
Vol 55 (4) ◽  
pp. 1098-1102
Author(s):  
J. P. Kohler ◽  
C. L. Rice ◽  
G. S. Moss ◽  
J. P. Szidon

In a model of increased hydrostatic pressure pulmonary edema Parker et al. (J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 44: 267-276, 1978) demonstrated that alveolar pressure in occluded fluid-filled lung segments was determined primarily by interstitial fluid pressure. Alveolar pressure was subatmospheric at base line and rose with time as hydrostatic pressure was increased and pulmonary edema developed. To further test the hypothesis that fluid-filled alveolar pressure is determined by interstitial pressure we produced permeability pulmonary edema-constant hydrostatic pressure. After intravenous injection of oleic acid in dogs (0.01 mg/kg) the alveolar pressure rose from -6.85 +/- 0.8 to +4.60 +/- 2.28 Torr (P less than 0.001) after 1 h and +6.68 +/- 2.67 Torr (P less than 0.01) after 3 h. This rise in alveolar fluid pressure coincided with the onset of pulmonary edema. Our experiments demonstrate that during permeability pulmonary edema with constant capillary hydrostatic pressures, as with hemodynamic edema, alveolar pressure of fluid-filled segments seems to be determined by interstitial pressures.


1979 ◽  
Vol 46 (5) ◽  
pp. 950-955 ◽  
Author(s):  
M. Goshy ◽  
S. J. Lai-Fook ◽  
R. E. Hyatt

Saline-filled wick catheters were inserted intraparenchymally in the loose connective tissue separating the bronchus and pulmonary artery of unperfused isolated dog lobes. Px, the difference between perivascular pressure and pleural surface pressure (which was atmospheric pressure), was measured by the wick for arterial pressures (Pa) of 10 and 25 cmH2O at lobe transpulmonary pressures (Ptp) of 25, 15, 10, 5, and 2 cmH2O during a deflation pressure-volume maneuver. The response time of Px to step changes in Pa was relatively short, a pressure plateau always occurring in less than 3 min. For Pa of 25 cmH2O, mean Px in five lobes was -2 cmH2O at Ptp of 2 cmH2O and decreased almost linearly to -9 cmH2O at Ptp of 25 cmH2O. Reducing Pa from 25 to 10 cmH2O resulted in a mean decrease in Px of 1 cmH2O at Ptp of 2 cmH2O and 2 cmH2O at Ptp of 25 cmH2O. These results are generally consistent with predictions from a continuum-mechanics analysis of pulmonary vascular interdependence and do not support the concept that perivascular interstitial fluid pressure is different from surface pressure.


1987 ◽  
Vol 62 (5) ◽  
pp. 1826-1831 ◽  
Author(s):  
P. Gustin ◽  
F. Lomba ◽  
J. Bakima ◽  
P. Lekeux ◽  
K. P. Van de Woestijne

Nine right apical lobes of healthy Friesian calves and 10 right apical lobes of double-muscled calves of Belgian White and Blue (BWB) breed were suspended in an airtight box, inflated at a constant transpulmonary pressure (Ptp), and subjected to quasi-sinusoidal pressure changes (amplitude: 0.5 kPa) at a frequency of 30 cycles/min. Lobar resistance (RL) was partitioned at six different lung volumes into three components: central airway resistance (Rc), small airway resistance (Rp), and tissue resistance (Rt). Pressure in small airways (2–3 mm ID) was measured with a retrograde catheter. Alveolar pressure was sampled in capsules glued onto the punctured pleural surface. RL was minimal at values of Ptp comprised between 0.5 and 0.7 kPa and increased at higher and lower values of Ptp. At a Ptp of 0.5 kPa, Rc, Rp, and Rt represented 30, 15, and 55% of RL, respectively, in Friesian calves and 25, 25, and 50% in BWB calves. Rp increased markedly at low lung volumes. Rt was responsible for the increase of RL at high Ptp. Rc tended to decrease at high Ptp. The significantly higher values of Rp in BWB calves (P less than 0.05) might explain the sensitivity of this breed to severe bronchopneumonia.


1984 ◽  
Vol 57 (1) ◽  
pp. 262-270 ◽  
Author(s):  
W. Hida ◽  
J. Hildebrandt

Peribronchoarterial interstitial fluid pressure [Px(f)] was measured by wicks inserted between bronchus and artery of dog lobes filled with air, saline, 6% dextran in saline, or mineral oil. Five inflations were made to total lung capacity, with one min stops at eight selected volume levels in each cycle. Deflation recoil (measured as transpulmonary pressure, Ptp) was largest for air and least for saline and dextran, and it fell between these extremes for mineral oil. Correspondingly, Px(f) was most negative for air, slightly less negative for mineral oil, and least for saline and dextran. On the first cycle, the Px(f) for saline and dextran were nearly equal, but in later cycles Px(f) with saline drifted fairly rapidly toward alveolar pressure. By plotting Px(f) vs. Ptp, all first-cycle curves were brought toward a single line. During later cycles, Ptp and Px(f) always changed together along this line, except for saline. We conclude that 1) at fixed vascular pressure, Px(f) depends mainly on Ptp and less on lung volume; 2) large changes in Px(f) with saline suggest that at least some fluid can enter this interstitial space quite rapidly; and 3) peripheral tissue swelling with saline causes some reduction in Ptp, and both swelling and lower recoil contribute to increased trapping of saline.


1990 ◽  
Vol 69 (6) ◽  
pp. 2168-2174 ◽  
Author(s):  
G. Miserocchi ◽  
D. Negrini ◽  
C. Gonano

We developed an experimental approach to measure the pulmonary interstitial pressure with the micropuncture technique in in situ lungs with an intact pleural space. Experiments were done in anesthetized paralyzed rabbits that were oxygenated via an endotracheal tube with 50% humidified oxygen and kept in either the supine or the lateral position. A small area of an intercostal space was cleared of the intercostal muscles down to the endothoracic fascia. Subsequently a "pleural window" was opened by stripping the endothoracic fascia over a 0.2-cm2 surface and leaving the parietal pleura (approximately 10 microns thick). Direct micropuncture through the pleural window was performed with 2- to 3-microns-tip pipettes connected to a servo-null pressure-measuring system. We recorded pleural liquid pressure and, after inserting the pipette tip into the lung, we recorded interstitial pressure from subpleural lung tissue. Depth of recording for interstitial pressure averaged 263 +/- 122 (SD) microns. We report data gathered at 26, 53, and 84% lung height (relative to the most dependent portion of the lung). For the three heights, interstitial pressure was -9.8 +/- 3, -10.1 +/- 1.6, and -12.5 +/- 3.7 cmH2O, respectively, whereas the corresponding pleural liquid pressure was -3.4 +/- 0.5, -4.4 +/- 1, and -5.2 +/- 0.3 cmH2O, respectively.


1994 ◽  
Vol 76 (4) ◽  
pp. 1411-1416 ◽  
Author(s):  
S. Stick ◽  
D. Turner ◽  
P. LeSouef

During the rapid thoracic compression maneuver in infants, the transmission of pressure from compression jacket to pleural space and airway is less at functional residual capacity than at end inspiration. To examine whether reduced pressure transmission at functional residual capacity vs. higher lung volumes is explained by passive characteristics of the chest wall rather than by respiratory muscle activity, we assessed the pressure transmitted across the chest wall in nine anesthetized infants and young children after muscle relaxation. We measured esophageal and airway occlusion pressure during chest compressions at different lung volumes determined by varying distending pressure. In six subjects studied under static conditions, there was an approximately linear relationship between distending pressure and the proportion of pressure transmitted to the airway and esophagus from the compression jacket. The mean r2 value (95% confidence interval) was 0.80 (0.09) for pressure transmission to the airway and 0.85 (0.04) for pressure transmission to the esophagus. This relationship between lung volume and pressure transmission observed under static conditions was also demonstrated dynamically. Thus the reduced transmission of pressure from compression jacket to airway and pleural space at low lung volumes occurs independently of respiratory muscle activity.


1989 ◽  
Vol 67 (4) ◽  
pp. 1371-1376 ◽  
Author(s):  
Q. H. Yang ◽  
M. R. Kaplowitz ◽  
S. J. Lai-Fook

We studied the vertical gradient in lung expansion in rabbits in the prone and supine body positions. Postmortem, we used videomicroscopy to measure the size of surface alveoli through transparent parietal pleural windows at dependent and nondependent sites separated in height by 2–3 cm at functional residual capacity (FRC). We compared the alveolar size measured in situ with that measured in the isolated lungs at different deflationary transpulmonary pressures to obtain transpulmonary pressure (pleural surface pressure) in situ. The vertical gradient in transpulmonary pressure averaged 0.48 +/- 0.16 (SD) cmH2O/cm height (n = 10) in the supine position and 0.022 +/- 0.014 (SD) cmH2O/cm (n = 5) in the prone position. In mechanically ventilated rabbits, we used the rib capsule technique to measure pleural liquid pressure at different heights of the chest in prone and supine positions. At FRC, the vertical gradient in pleural liquid pressure averaged 0.63 cmH2O/cm in the supine position and 0.091 cmH2O/cm in the prone position. The vertical gradients in pleural liquid pressure were all less than the hydrostatic value (1 cmH2O/cm), which indicates that pleural liquid is not generally in hydrostatic equilibrium. Both pleural surface pressure and pleural liquid pressure measurements show a greater vertical gradient in the supine than in the prone position. This suggests a close relationship between pleural surface pressure and pleural liquid pressure. Previous results in the dog and pony showed relatively high vertical gradients in the supine position and relatively small gradients in the prone position. This behavior is similar to the present results in rabbits. Thus the vertical gradient is independent of animal size and might be related to chest shape and weight of heart and abdominal contents.


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