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.

Continuity of arterial and venous extra-alveolar interstitium in excised rabbit lungs

1987 ◽  
Vol 63 (2) ◽  
pp. 634-638 ◽  
Author(s):  
W. J. Lamm ◽  
R. K. Albert
Keyword(s):  
Weight Gain ◽  
Filtration Rate ◽  
Hydrostatic Stress ◽  
Alveolar Pressure ◽  
Initial Weight ◽  
Lung Weight ◽  
Fluid Filtration ◽  
Single Compartment ◽  
Pulmonary Arterial ◽  
Lung Base

We studied the interdependence of arterial and venous extra-alveolar vessel (EAV) leakage on the rate of pulmonary vascular fluid filtration (measured as the change in lung weight over time). Edema was produced in continually weighed, excised rabbit lungs kept in zone 1 (alveolar pressure = 25 cmH2O) by increasing pulmonary arterial (Ppa) and/or venous (Ppv) pressure from 5 to 20 cmH2O (relative to the lung base) and continuing this hydrostatic stress for 3–5 h. Raising Ppa and Ppv simultaneously produced a lower filtration rate than the sum of the filtration rates obtained when Ppa and Ppv were raised separately, while the lung gained from 20 to 95% of its initial weight. When vascular pressure was elevated in either EAV segment, fluid filtration always decreased rapidly as the lung gained up to 30–45% of its initial weight. Filtration then decreased more slowly. The lungs became isogravimetric at 60 and 85% weight gain when the Ppa or Ppv was elevated, respectively; when Ppa and Ppv were raised simultaneously substantial fluid filtration continued even after 140% weight gain. We conclude that the arterial and venous EAV's share a common interstitium in the zone 1 condition, this interstitium cannot be represented as a single compartment with a fixed resistance and compliance, and arterial and venous EAV leakage influences leakage from the other segment.

Effect of surface tension on circulation in the excised lungs of dogs

1964 ◽  
Vol 19 (4) ◽  
pp. 707-712 ◽  
Author(s):  
I. Bruderman ◽  
K. Somers ◽  
W. K. Hamilton ◽  
W. H. Tooley ◽  
J. Butler
Keyword(s):  
Surface Tension ◽  
Arterial Pressure ◽  
Pulmonary Vascular Resistance ◽  
Lung Volume ◽  
Pulmonary Circulation ◽  
Pulmonary Arterial Pressure ◽  
Alveolar Pressure ◽  
Pulmonary Arterial ◽  
Air Liquid Interface ◽  
Effect Of Surface

The hypothesis that the surface tension of the fluid film which lines the lung alveoli reduces the pericapillary pressure in air-filled lungs was tested by perfusing the excised lungs of dogs with saline, 6% dextran in saline, and blood. After almost maximal inflation with air from low volumes or the degassed state (inflation state) the pulmonary arterial pressure, relative to the base of the lungs, was lower than the alveolar pressure with flows up to 50 ml/min. It was higher than the alveolar pressure at any flow when the air-liquid interface had been abolished by filling the lungs to the same volume with fluid. The pulmonary arterial pressure at the same flow and alveolar pressure was lower in the inflation state than after deflation from higher volumes (the deflation state). However, lung volume was larger in the deflation state. The possibility of some low resistance channels in the inflation state could not be excluded. However, histological examinations showed that the alveolar capillaries were patent and failed to show any airless lung. pulmonary circulation; pericapillary pressure in lungs; surface tension and pulmonary vascular resistance Submitted on July 29, 1963

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 lung inflation on fluid flux in zone 1 lungs

1988 ◽  
Vol 64 (1) ◽  
pp. 285-290 ◽  
Author(s):  
R. K. Albert ◽  
W. J. Lamm ◽  
D. L. Luchtel
Keyword(s):  
Positive Pressure ◽  
Alveolar Pressure ◽  
Fluid Flux ◽  
Lung Weight ◽  
Fluid Filtration ◽  
Lung Inflation ◽  
Dependent Part ◽  
Autologous Whole Blood ◽  
New Zealand White Rabbits ◽  
Pulmonary Arterial

Because of conflicting data in the literature, we studied the effect of positive-pressure inflation on transvascular fluid filtration in zone 1 lungs. Lungs from New Zealand White rabbits (n = 10) were excised, perfused with saline and autologous whole blood (1:1), ventilated, and continuously weighed. Pulmonary arterial and venous pressures (Pvas) were referenced to the most dependent part of the lung. A change in vascular volume (delta Vvas) and a fluid filtration rate (FFR) were calculated from the change in lung weight that occurred from 0 to 30 s and from 3 to 5 and 5 to 10 min, respectively, after changing alveolar pressure (PA). FFR's and delta Vvas's were measured with Pvas equal to 2 or 10 cmH2O and PA changing from 15 to 30 cmH2O when the lungs were normal and after they were made edematous. When Pvas = 2 cmH2O, increasing PA increased the Vvas and the FFR in both normal and edematous lungs. However, when Pvas = 10 cmH2O, increasing PA only slightly changed the Vvas and reduced the FFR in the normal lungs, and decreased Vvas and markedly decreased the FFR in the presence of edema. Inflating zone 1 lungs by positive pressure has an effect on transvascular fluid flux that depends on the Pvas. The results suggest that the sites of leakage in zone 1 also vary depending on Pvas and PA.

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.

Extra-alveolar veins are contiguous with, and leak fluid into, periarterial cuffs in rabbit lungs

1991 ◽  
Vol 71 (4) ◽  
pp. 1606-1613 ◽  
Author(s):  
D. L. Luchtel ◽  
L. Embree ◽  
R. Guest ◽  
R. K. Albert
Keyword(s):  
Electron Microscopy ◽  
Scanning Electron Microscopy ◽  
Interstitial Fluid ◽  
Blue Dye ◽  
Alveolar Pressure ◽  
Vessel Lumen ◽  
Freeze Dried ◽  
Orange G ◽  
Pulmonary Arterial ◽  
Scanning Electron

We previously observed physiological evidence that arterial and venous extra-alveolar vessels shared a common interstitial space. The purpose of the present investigation was to determine the site of this continuity to improve our understanding of interstitial fluid movement in the lung. Orange G and Evans blue dyes were added to the arterial and venous reservoirs, respectively, of excised rabbit lungs as they were placed 20 cmH2O into zone 1 (pulmonary arterial and venous pressures = 5 cmH2O, alveolar pressure = 25 cmH2O). After 10 s or 4 h the lungs were fixed by immersion in liquid N2, freeze-dried, cut into 5-mm serial slices, and examined by light macroscopy. Serial sections of 0.25–0.5 mm were subsequently examined by scanning electron microscopy. In the animals subjected to the zone 1 stress for 4 h, arterial and venous extra-alveolar vessels were surrounded by cuffs of edema. The edema ratio (cuff area divided by vessel lumen area) was greater around arteries than veins and decreased with increasing vessel size. Periarterial cuffs usually contained orange dye and frequently contained both orange and blue dye. Lymphatics containing orange or blue dye were frequently seen in periarterial cuffs. Scanning electron microscopy demonstrated that extra-alveolar veins of approximately 100 microns diameter were anatomically contiguous with arterial extra-alveolar vessel cuffs. In rabbit lungs, both arterial and venous extra-alveolar vessels (and/or alveolar corner vessels) leak fluid into perivascular cuffs surrounding arterial extra-alveolar vessels, and lymphatics located in the periarterial cuff contain fluid that originates from both the arterial and venous extra-alveolar vessels.

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.

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.

Cytochalasin D induces edema formation and lowering of interstitial fluid pressure in rat dermis

2001 ◽  
Vol 281 (1) ◽  
pp. H7-H13 ◽  
Author(s):  
Ansgar Berg ◽  
Kristofer Rubin ◽  
Rolf K. Reed
Keyword(s):  
Extracellular Matrix ◽  
Interstitial Fluid ◽  
Acute Inflammation ◽  
Cultured Cells ◽  
Circulatory Arrest ◽  
Fluid Pressure ◽  
Cytochalasin D ◽  
Interstitial Fluid Pressure ◽  
Edema Formation ◽  
Fluid Filtration

The increased capillary fluid filtration required to create a rapid edema formation in acute inflammation can be generated by lowering the interstitial fluid pressure (PIF). The lowering of PIF appears to involve dynamic β1-integrin-mediated interactions between dermal cells and extracellular matrix fibers. The present study specifically investigates the role of the cell cytoskeleton, i.e., the contractile apparatus of cells, in controlling PIF in rat skin as the integrins are linked to both the cytoskeleton and the extracellular matrix. PIF was measured using a micropuncture technique in the dorsal skin of the hind paw at a depth of 0.2–0.5 mm and following the induction of circulatory arrest with the intravenous injection of KCl in pentobarbital anesthesia. This procedure prevented the transcapillary flux of fluid and protein leading to edema formation in acute inflammation, which in turn can increase the PIF and therefore potentially mask a decrease of PIF. Control PIF ( n = 42) averaged −0.8 ± 0.5 (means ± SD) mmHg. In the first group of experiments, subdermal injection of 2 μl cytochalasin D, a microfilament-disrupting drug, lowered PIF to an average of −2.8 ± 0.7 mmHg within 40 min postinjection ( P< 0.05 compared with control). Subdermal injection of vehicle (10% DMSO in PBS or PBS alone) did not change the PIF( P > 0.05). Lowering of the PIF was not observed after the injection of colchicine or nocodazole, which specifically disrupts microtubuli in cultured cells. In the second group of experiments, 2 μl of cytochalasin D injected subdermally into rats with intact circulation increased the total tissue water (TTW) and albumin extravasation rate ( E ALB) by 0.7 ± 0.2 and 0.4 ± 0.3 ml/g dry wt, respectively ( P < 0.05 compared with vehicle). Nocodazole and colchicine did not significantly alter the TTW or E ALB compared with the vehicle ( P > 0.05). Taken together, these findings strongly suggest that the connective tissue cells can participate in control of PIF via the actin filament system. In addition, the observation that subdermal injection of cytochalasin D lowered PIF indicates that a dynamic assembly and disassembly of actin filaments also occurs in the cells of dermal tissues in vivo.

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).

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