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.

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.

Factors affecting perfusion distribution in canine oleic acid pulmonary edema

1986 ◽  
Vol 60 (5) ◽  
pp. 1498-1503 ◽  
Author(s):  
J. Ali ◽  
L. D. Wood
Keyword(s):  
Oleic Acid ◽  
Pulmonary Edema ◽  
Venous Blood ◽  
Lower Lobe ◽  
Acid Group ◽  
Left Lower Lobe ◽  
Base Line ◽  
Positive End Expiratory Pressure ◽  
Vascular Effects ◽  
Factors Affecting

Factors affecting perfusion distribution in oleic acid pulmonary edema were examined in 28 anesthetized open-chest dogs. Sixteen had unilobar oleic acid edema produced by left lower lobe pulmonary artery infusion of 0.03 ml/kg of oleic acid, and 12 had the same amount of edema produced by left lower lobe endobronchial instillation of hypotonic plasma. Lobar perfusion (determined from flow probes) and lobar shunt (determined from mixed venous and lobar venous blood) were measured at base line, 1.5 h after edema, and 10 min after 10 cmH2O positive end-expiratory pressure (PEEP). Fourteen dogs (8 oleic acid, 6 plasma) received sodium nitroprusside (11.72 +/- 7.10 micrograms X kg-1 X min-1). Total and lobar shunts increased to the same extent in all animals. Lobar perfusion decreased by 49.8 +/- 4.8% without nitroprusside and 34.0 +/- 3.6% with nitroprusside in the oleic acid group, corresponding values being 40.3 +/- 0.8% and 26.4 +/- 1.7% in the hypotonic plasma group. PEEP returned perfusion and shunt to base line. In oleic acid edema, most of the decreased perfusion results from mechanical effects of the edema, a smaller fraction results from other vascular effects of the oleic acid, and approximately 30% is reversible by nitroprusside. PEEP normalizes the perfusion distribution.

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.

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.

A model of unsteady-state transvascular fluid and protein transport in the lung

1984 ◽  
Vol 56 (5) ◽  
pp. 1389-1402 ◽  
Author(s):  
R. J. Roselli ◽  
R. E. Parker ◽  
T. R. Harris
Keyword(s):  
Steady State ◽  
Interstitial Fluid ◽  
Transport Theory ◽  
Fluid Pressure ◽  
Water Volume ◽  
Free Fluid ◽  
Base Line ◽  
Unsteady State ◽  
Total Change ◽  
Organ Systems

Models of steady-state fluid and solute transport in the microcirculation are used primarily to characterize filtration and permeability properties of the transport barrier. Important transient relationships, such as the rate of fluid accumulation in the tissue, cannot be predicted with steady-state models. In this paper we present three simple models of unsteady-state fluid and protein exchange between blood plasma and interstitial fluid. The first treats the interstitium as a homogeneous well-mixed compliant compartment, the second includes an interstitial gel, and the third allows for both gel and free fluid in the interstitium. Because we are primarily interested in lung transvascular exchange we used the multiple-pore model and pore sizes described by Harris and Roselli (J. Appl. Physiol.: Respirat . Environ. Exercise Physiol. 50: 1–14, 1981) to characterize the microvascular barrier. However, the unsteady-state transport theory presented here should apply to other organ systems and can be used with different conceptual models of the blood-lymph barrier. For a step increase in microvascular pressure we found good agreement between theoretical and experimental lymph flow and lymph concentrations in the sheep lung when the following parameter ranges were used: base-line interstitial volume, 150–190 ml; interstitial compliance, 7–10 ml/Torr; initial interstitial fluid pressure, -1 Torr; pressure in initial lymphatics, -5 to -6 Torr; and conductivity of the interstitium and lymphatic barrier, 4.25 X 10(-4) ml X s-1 X Torr-1. Based on these values the model predicts 50% of the total change in interstitial water volume occurs in the first 45 min after a step change in microvascular pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

scholarly journals Ventilation inhomogeneity in oleic acid-induced pulmonary edema

1997 ◽  
Vol 82 (4) ◽  
pp. 1040-1045 ◽  
Author(s):  
John Y. C. Tsang ◽  
Michael J. Emery ◽  
Michael P. Hlastala
Keyword(s):  
Oleic Acid ◽  
Pulmonary Edema ◽  
Phase Iii ◽  
Lung Water ◽  
Peripheral Airways ◽  
Ventilation Inhomogeneity ◽  
Distal Airway ◽  
Tissue Compliance ◽  
Permeability Pulmonary Edema ◽  
The Right

Tsang, John Y. C., Michael J. Emery, and Michael P. Hlastala. Ventilation inhomogeneity in oleic acid-induced pulmonary edema. J. Appl. Physiol.82(4): 1040–1045, 1997.—Oleic acid causes permeability pulmonary edema in the lung, resulting in impairment of gas-exchange and ventilation-perfusion heterogeneity and mismatch. Previous studies have shown that by using the multiple-breath helium washout (MBHW) technique, ventilation inhomogeneity (VI) can be quantitatively partitioned into two components, i.e., convective-dependent inhomogeneity (cdi) and diffusive-convective-dependent inhomogeneity (dcdi). Changes in VI, as represented by the normalized slope of the phase III alveolar plateau, were studied for 120 min in five anesthetized mongrel dogs that were ventilated under paralysis by a constant-flow linear motor ventilator. These animals received oleic acid (0.1 mg/kg) infusion into the right atrium at t = 0. MBHWs were done in duplicate for 18 breaths every 40 min afterward. Three other dogs that received only normal saline served as controls. The data show that, after oleic acid infusion, dcdi, which represents VI in peripheral airways, is responsible for the increasing total VI as lung water accumulates progressively over time. The cdi, which represents VI between larger conductive airways, remains relatively constant throughout. This observation can be explained by increases in the heterogeneity of tissue compliance in the periphery, distal airway closure, or by decreases in ventilation through collateral channels.

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
Keyword(s):  
Liquid Phase ◽  
Surface Pressure ◽  
Interstitial Fluid ◽  
Pleural Space ◽  
Interstitial Pressure ◽  
Alveolar Pressure ◽  
Lung Volumes ◽  
Pleural Surface ◽  
Residual Capacity

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.

Lobe weight gain and vascular, alveolar, and peribronchial interstitial fluid pressures

1982 ◽  
Vol 52 (1) ◽  
pp. 173-183 ◽  
Author(s):  
W. Hida ◽  
H. Inoue ◽  
J. Hildebrandt
Keyword(s):  
Weight Gain ◽  
Filtration Rate ◽  
Interstitial Fluid ◽  
Time Lag ◽  
Fluid Pressure ◽  
Steady Increase ◽  
Pressure Gradients ◽  
Alveolar Pressure ◽  
Interstitial Edema ◽  
Lobar Bronchus

Interstitial fluid movements in acute pulmonary edema were studied by recording interstitial fluid pressure [Px (f)] relative to pleural pressure (atmospheric), together with lobe weight gain or loss (delta W). Px (f) was measured by wicks inserted between lobar bronchus and artery while alveolar pressure (PA) was fixed at either 5 or 20 cmH2O. When vascular pressure (Pvas) was raised abruptly from -5 to +25 cmH2O by air inflation for 60 min, Px (f) became abruptly less negative, then remained stable. However, during vascular inflation with plasma, delta W began a steady increase, but plotted against delta W, Px(f) became less negative in several phases. After an immediate rise due to interdependence effects following vascular distension, Px (f) remained almost unchanged for 4–7 min as delta W increased 15–80% of initial lobe weight (Wi), representing a transport lag between leakage and measuring sites and suggesting that interstitial edema was not homogeneous. Next, Px (f) increased progressively as weight increased a further 70–200% of Wi and finally slowed its rise near zero pressure. When Pvas was lowered, Px (f) became abruptly more negative, again by interdependence; however, as delta W then decreased 20–50% of Wi over 30 min, Px (f) did not change consistently. It was possible to relate the rate of weight gain occurring between 2 and 5 min after Pvas was raised to two pressure gradients, Pvas - Px (f) and Pvas - PA, and to relate the time lag to filtration rate and Pvas - Px (f).

Rebreathing lung tissue volume of sheep with normal and edematous lungs

1986 ◽  
Vol 61 (3) ◽  
pp. 1132-1138 ◽  
Author(s):  
G. J. Huchon ◽  
A. Lipavsky ◽  
J. M. Hoeffel ◽  
J. F. Murray
Keyword(s):  
Oleic Acid ◽  
Pulmonary Edema ◽  
Blood Volume ◽  
Lung Tissue ◽  
Extravascular Lung Water ◽  
Lung Water ◽  
Lung Weight ◽  
Tissue Volume ◽  
Accuracy Of Measurements ◽  
Permeability Pulmonary Edema

To determine the accuracy of measurements of lung tissue volume (Vlt) by rebreathing acetylene in normal and edematous lungs, we compared gravimetric values of total lung weight (Ql) and extravascular lung water (Qwl) with Vlt in anesthetized control sheep (C) and sheep with hydrostatic pulmonary edema (HPE) or oleic acid-induced permeability pulmonary edema (PPE), five animals each. In eight additional sheep we determined that acetylene solubility in blood (0.117 +/- 0.010 ml X 100 ml-1 X Torr-1) differed significantly from that in lung-blood homogenates (0.095 +/- 0.009 ml X 100 ml-1 X Torr-1, P = 0.0017). The latter value was used in all calculations. In C, Vlt was 194% of Qwl and 98% of Ql; in HPE, Vlt was 144% of Qwl and 87% of Ql; and in PPE, Vlt was 112% of Qwl and 77% of Ql. We conclude that when the lungs are normal, Vlt reasonably measures Ql not Qwl. However in both HPE and PPE, Vlt progressively underestimates Ql and cannot differentiate between increased blood volume and increased Qwl.

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