Alveolar surface tension, lung inflation, and hydration affect interstitial pressure [Px(f)]

1984 ◽  
Vol 57 (1) ◽  
pp. 262-270 ◽  
Author(s):  
W. Hida ◽  
J. Hildebrandt
Keyword(s):  
Interstitial Fluid ◽  
Total Lung Capacity ◽  
Fluid Pressure ◽  
Transpulmonary Pressure ◽  
Mineral Oil ◽  
Interstitial Pressure ◽  
Alveolar Pressure ◽  
Lung Inflation ◽  
Lung Capacity ◽  
Alveolar Surface

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.

Alveolar liquid pressure measured by micropipettes in isolated dog lung

1982 ◽  
Vol 53 (3) ◽  
pp. 737-743 ◽  
Author(s):  
S. J. Lai-Fook ◽  
K. C. Beck
Keyword(s):  
Interstitial Fluid ◽  
Total Lung Capacity ◽  
Fluid Pressure ◽  
Transpulmonary Pressure ◽  
Initial Weight ◽  
Liquid Pressure ◽  
Lung Inflation ◽  
Main Determinant ◽  
Lung Capacity ◽  
Alveolar Surface

Micropipettes (2–5 microns), in conjunction with a servo-nulling system, were used to measure liquid pressure (Pliq) in subpleural alveoli of lobes of dog lungs made edematous by perfusing with plasma to a constant extravascular weight gain (W). Pliq was measured at fixed transpulmonary pressure (Ptp) in lungs whose W was more than 0.5 that of the initial weight (Wi). In six lobes at W/Wi = 0.6, Pliq, relative to alveolar pressure (Palv), was -2.6 +/- 0.4 cmH2O (mean +/- SE), -11.8 +/- 0.6, and -17.5 +/- 1.7 at deflation Ptp values of 5, 15, and 25 cmH2O, respectively. The Pliq increased to -2, -7, and -13.7, respectively, at W/Wi = 2.8. Based on a mean alveolar radius of 50 micron at Ptp at 25 cmH2O and values of Palv - Pliq, values for alveolar surface tension (tau) at W/Wi = 0.6 were 6, 30, and 44 dyn/cm at Ptp of 5, 15, and 25 cmH2O, respectively. In five other lobes at W/Wi = 0.5 and at 65 and 84% total lung capacity, tau was much higher on lung inflation than on deflation. If pericapillary interstitial fluid pressure (Pi) and Pliq were identical under edematous conditions, tau would be the main determinant of Pi.

Perivascular interstitial fluid pressure measured by micropipettes in isolated dog lung

1982 ◽  
Vol 52 (1) ◽  
pp. 9-15 ◽  
Author(s):  
S. J. Lai-Fook
Keyword(s):  
Interstitial Fluid ◽  
Fluid Pressure ◽  
Transpulmonary Pressure ◽  
Alveolar Pressure ◽  
Lung Weight ◽  
Lung Inflation ◽  
Water Accumulation ◽  
The Right ◽  
Alveolar Surface ◽  
Lung Lobes

Micropipettes in conjunction with a servo-nulling system were used to measure fluid pressure (Pf) in the interstitium around the partially exposed vein near the hilus of the right upper lung lobes of the dog. Lobes were studied at constant transpulmonary pressure (Ptp). In the absence of extravascular water accumulation, Pf was -1.5 cmH2O relative to pleural pressure at Ptp of 6 cmH2O and vascular pressure (Pv) of 0 cmH2O and was more negative in lobes tested at higher Ptp values. In five lobes made edematous with plasma at Ptp of 6 cmH2O and Pv of 15 cmH2O, mean Pf increased from -1 to 4.4 cmH2O as lung weight increased up to 400% of the initial excised weight. In four other lobes, at Ptp of 15 cmH2O and Pv of 20 cmH2O, Pf increased from -2.4 to 8.8 for a similar increase in weight. In lobes degassed and filled with saline or plasma, Pf always equilibrated to alveolar pressure (PA). Results suggest that alveolar surface tension (tau) in air-filled lobes with gross edema prevented Pf from reaching PA. Reduction in Pf below PA was larger at higher Ptp, consistent with increased tau with lung inflation.

Pressure-volume behavior of perivascular interstitium measured in isolated dog lung

1980 ◽  
Vol 48 (6) ◽  
pp. 939-946 ◽  
Author(s):  
S. J. Lai-Fook ◽  
B. Toporoff
Keyword(s):  
Interstitial Fluid ◽  
Venous Pressure ◽  
Fluid Pressure ◽  
Transpulmonary Pressure ◽  
Interstitial Fluid Pressure ◽  
Alveolar Pressure ◽  
Lung Weight ◽  
Lung Volumes ◽  
Water Accumulation ◽  
Alveolar Surface

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.

Alveolar pressure in fluid-filled occluded lung segments during permeability edema

1983 ◽  
Vol 55 (4) ◽  
pp. 1098-1102
Author(s):  
J. P. Kohler ◽  
C. L. Rice ◽  
G. S. Moss ◽  
J. P. Szidon
Keyword(s):  
Oleic Acid ◽  
Hydrostatic Pressure ◽  
Pulmonary Edema ◽  
Intravenous Injection ◽  
Interstitial Fluid ◽  
Fluid Pressure ◽  
Base Line ◽  
Interstitial Pressure ◽  
Alveolar Pressure ◽  
Permeability Pulmonary Edema

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.

Effect of lung inflation in vivo on airways with smooth muscle tone or edema

1997 ◽  
Vol 82 (2) ◽  
pp. 491-499 ◽  
Author(s):  
Robert H. Brown ◽  
Wayne Mitzner ◽  
Yonca Bulut ◽  
Elizabeth M. Wagner
Keyword(s):  
Smooth Muscle ◽  
Total Lung Capacity ◽  
Muscle Tone ◽  
Transpulmonary Pressure ◽  
Airway Wall ◽  
Lung Inflation ◽  
Airway Narrowing ◽  
Lung Capacity ◽  
Luminal Area

Brown, Robert H., Wayne Mitzner, Yonca Bulut, and Elizabeth M. Wagner. Effect of lung inflation in vivo on airways with smooth muscle tone or edema. J. Appl. Physiol. 82(2): 491–499, 1997.—Fibrous attachments to the airway wall and a subpleural surrounding pressure can create an external load against which airway smooth muscle must contract. A decrease in this load has been proposed as a possible cause of increased airway narrowing in asthmatic individuals. To study the interaction between the airways and the surrounding lung parenchyma, we investigated the effect of lung inflation on relaxed airways, airways contracted with methacholine, and airways made edematous by infusion of bradykinin into the bronchial artery. Measurements were made in anesthetized sheep by using high-resolution computed tomography to visualize changes in individual airways. During methacholine infusion, airway area was decreased but increased minimally with increases in transpulmonary pressure. Bradykinin infusion caused a 50% increase in airway wall area and a small decrease in airway luminal area. In contrast to airways contracted with methacholine, the luminal area after bradykinin increased substantially with increases in transpulmonary pressure, reaching 99% of the relaxed area at total lung capacity. Thus airway edema by itself did not prevent full distension of the airway at lung volumes approaching total lung capacity. Therefore, we speculate that if a deep inspiration fails to relieve airway narrowing in vivo, this must be a manifestation of airway smooth muscle contraction and not airway wall edema.

Effects of surfactant on the in vivo alveolar surface-to-volume ratio

1996 ◽  
Vol 80 (1) ◽  
pp. 86-90 ◽  
Author(s):  
N. Miyazawa ◽  
S. Suzuki ◽  
T. Akahori ◽  
T. Okubo
Keyword(s):  
Surface Tension ◽  
Pulmonary Surfactant ◽  
Total Lung Capacity ◽  
Volume Ratio ◽  
Transpulmonary Pressure ◽  
Mean Free Path ◽  
Lung Capacity ◽  
Alveolar Surface ◽  
Saline Lavage

To investigate how pulmonary surfactant influences alveolar structure in vivo, we examined the alveolar surface area-to-lung volume (S/V) ratio of the lung parenchyma of a live dog by light-scattering stereology before and after saline lavage. We measured the backscattered light pattern produced by applying a laser beam to the pleural surface of a ventilated animal and obtained the S/V [equivalent to the inverse of the optical mean free path (lambda)]. After saline lavage, V at transpulmonary pressure (P) of 30 cmH2O (defined as total lung capacity) decreased by 11.1 +/- 3.1% (SD) and the P-V curve shifted to a lower V. The lambda-V curve was shifted to a higher lambda and to a lower V after saline lavage. S/V decreased after saline lavage (lambda increased by 38 +/- 27% on the deflation limb at a V of 80% of control total lung capacity). The alveolar surface tension increased after saline lavage, and the increase in surface tension was greater on inflation than on deflation. We conclude that depletion of pulmonary surfactant increases the alveolar surface tension in vivo, resulting in a decrease in S/V.

Dynamics of Interstitial Fluid Pressure in Extracellular Matrix Hydrogels in Microfluidic Devices

2015 ◽  
Vol 137 (9) ◽  
Author(s):  
Joe Tien ◽  
Le Li ◽  
Ozgur Ozsun ◽  
Kamil L. Ekinci
Keyword(s):  
Extracellular Matrix ◽  
Pressure Distribution ◽  
Interstitial Fluid ◽  
Scaling Laws ◽  
Fluid Pressure ◽  
Interstitial Fluid Pressure ◽  
External Loading ◽  
Interstitial Pressure ◽  
Time Resolved ◽  
Long Time

In order to understand how interstitial fluid pressure and flow affect cell behavior, many studies use microfluidic approaches to apply externally controlled pressures to the boundary of a cell-containing gel. It is generally assumed that the resulting interstitial pressure distribution quickly reaches a steady-state, but this assumption has not been rigorously tested. Here, we demonstrate experimentally and computationally that the interstitial fluid pressure within an extracellular matrix gel in a microfluidic device can, in some cases, react with a long time delay to external loading. Remarkably, the source of this delay is the slight (∼100 nm in the cases examined here) distension of the walls of the device under pressure. Finite-element models show that the dynamics of interstitial pressure can be described as an instantaneous jump, followed by axial and transverse diffusion, until the steady pressure distribution is reached. The dynamics follow scaling laws that enable estimation of a gel's poroelastic constants from time-resolved measurements of interstitial fluid pressure.

Effect of volume and volume history of the lungs on pulmonary shunt flow

1964 ◽  
Vol 207 (1) ◽  
pp. 235-238 ◽  
Author(s):  
Nicholas R. Anthonisen
Keyword(s):  
Lung Volume ◽  
Total Lung Capacity ◽  
Full Range ◽  
Transpulmonary Pressure ◽  
Pulmonary Shunt ◽  
Shunt Flow ◽  
Lung Capacity ◽  
Surface Active Properties ◽  
History Of ◽  
Surface Active

Relative pulmonary shunt flow (Qs/Qt), was measured in denitrogenated open-chested cats during apnea over the full range of lung volumes. The particular lung volume and transpulmonary pressure were also measured. When completely collapsed lungs were inflated, Qs/Qt decreased sharply to 3% at total lung capacity (TLC). During deflation from TLC Qs/Qt was insensitive to changes in lung volume. Qs/Qt remained low during reinflation after deflation from TLC. These changes in shunt flow can be interpreted as due to either recruitment or collapse of gas exchange units during lung volume change. It appears that completely collapsed lungs inflate very unevenly but that deflation from TLC proceeds remarkably evenly. Reinflation after deflation from TLC also seems to proceed evenly, and the manifest pressure-volume hysteresis is most likely due to hysteresis of the surface-active properties of the alveolar lining material.

Alveolar pressure and lung volume as determinants of net transvascular fluid filtration

1977 ◽  
Vol 42 (4) ◽  
pp. 476-482 ◽  
Author(s):  
G. Bo ◽  
A. Hauge ◽  
G. Nicolaysen
Keyword(s):  
Lung Volume ◽  
Continuous Monitoring ◽  
Interstitial Fluid ◽  
Positive Airway Pressure ◽  
Fluid Pressure ◽  
Alveolar Pressure ◽  
Experimental Conditions ◽  
Fluid Filtration ◽  
Pulmonary Arterial ◽  
Relative Change

We have investigated the influence of changes in alveolar pressure (PAlv) and in lung volume on the net transvascular fluid filtration rate (FFR). The preparation was isolated, perfused zone III rabbit lungs. In observation periods the outflow pressure was kept constant at a level generally causing net filtration. All pressures were measured relative to atmospheric. FFR was measured by continuous monitoring of preparation weight. Elevation of Palv at constant lung volume caused reversible reductions in FFR, also at constant capillary hydrostatic pressure (Pa-V less than 2 Torr). Increases in lung volume at constant PAlv caused reversible increases in FFR. When both PAlv and Ptp were increased a reduction in FFR was seen in the majority of cases. We conclude that at constant pulmonary arterial pressure, the size and the direction of the influence of positive airway pressure on FFR depend on the relative change in lung volume and in alveolar pressure per se. Under the present experimental conditions a rise in PAlv will be transmitted to interstitial fluid pressure and affect the transvascular fluid balance.

Lung inflation distends small arteries (< 1 mm) in excised dog lungs

1993 ◽  
Vol 75 (6) ◽  
pp. 2595-2601 ◽  
Author(s):  
R. K. Albert ◽  
W. J. Lamm ◽  
D. A. Rickaby ◽  
A. al-Tinawi ◽  
C. A. Dawson
Keyword(s):  
Pulmonary Arteries ◽  
Transpulmonary Pressure ◽  
Alveolar Pressure ◽  
Flow Conditions ◽  
Lung Inflation ◽  
Small Arteries ◽  
Diameter Range ◽  
Unit Increase

We utilized microfocal fluoroscopic angiography to study the influence of lung inflation on small (0.2- to 1.3-mm-diam) pulmonary arteries in isolated left lower lobes from dog lungs during both flow and no-flow conditions. Alveolar pressure, which in this preparation was equal to transpulmonary pressure, was set at 2, 8, or 14 mmHg while vascular pressure was varied from 0 to 24 mmHg. The diameters of these small arterial vessels increased with lung inflation. No differences were observed between the results obtained during flow and no-flow conditions. Thus, arteries in this diameter range can be considered as extra-alveolar, and the effect of lung inflation on these small extra-alveolar arteries was qualitatively similar to that previously described for larger extra-alveolar vessels. Quantitatively, the degree of vessel distension was about the same per unit increase in transpulmonary pressure at constant vascular pressure as for a change in vascular pressure at constant transpulmonary pressure. Accordingly, inflation produced a decrease in perivascular pressure surrounding these small arteries that was approximately equal to the increase in transpulmonary pressure.

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