Permeability of parietal pleura to liquid and proteins

1994 ◽  
Vol 76 (2) ◽  
pp. 627-633 ◽  
Author(s):  
D. Negrini ◽  
D. Venturoli ◽  
M. I. Townsley ◽  
R. K. Reed

The permselectivity of the parietal pleura was determined in spontaneously breathing anesthetized rabbits and dogs. In rabbits, we injected intrapleurally 5 ml of 1-g/dl albumin solution containing 100 microCi of 131I-labeled albumin plus 100 microCi of either lactate dehydrogenase (LDH) or alpha 2–125I-macroglobulin. Dogs received 100 ml of 1-g/dl albumin solution containing 100 microCi of 131I-albumin plus 100 microCi of alpha 2–125I-macroglobulin. A transpleural pressure gradient was set, lowering the intracapsular pressure to -30 cmH2O. The solvent drag reflection coefficients (sigma f) were calculated as the ratio between tracer concentrations in capsular and pleural liquid collected at 60–180 min. In rabbits sigma f was 0.44 +/- 0.2 (SD) for albumin, 0.84 +/- 0.1 for LDH, and 0.93 +/- 0.05 for alpha 2-macroglobulin. In dogs sigma f was 0.30 +/- 0.19 for albumin and 0.53 +/- 0.15 for alpha 2-macroglobulin. The hydraulic conductivity of the parietal pleura was 2.18 +/- 1.54 microliters.h-1.cmH2O-1.cm-2 in rabbits and 1.22 +/- 1.13 microliters.h-1.cmH2O-1.cm-2 in dogs. The parietal pleura could be modeled by two pore populations with radii of 83–89 and 156-222 A. The permeability coefficient averaged 0.08–0.21 x 10(-6) cm/s for albumin, 0.06–0.09 x 10(-6) cm/s for LDH, and 0.01-0.03 x 10(-6) cm/s for alpha 2-macroglobulin.

1990 ◽  
Vol 69 (2) ◽  
pp. 438-442 ◽  
Author(s):  
D. Negrini ◽  
M. I. Townsley ◽  
A. E. Taylor

The hydraulic conductivity (Lp) of the parietal pleura was measured in vivo in spontaneously breathing anesthetized dogs in either the supine (n = 8) or the prone (n = 7) position and in an excised portion of the chest wall in which the pleura and its adjacent tissue were intact (n = 3). A capsule was glued to the exposed parietal pleura after the intercostal muscles were removed. The capsule was filled with either autologous plasma or isotonic saline. Transpleural fluid flow (V) was measured at several transpleural hydrostatic pressures (delta P) from the rate of meniscus movement within a graduated pipette connected to the capsule. Delta P was defined as the measured difference between capsule and pleural liquid pressures. The Lp of the parietal pleura was calculated from the slope of the line relating V to delta P by use of linear regression analysis. Lp in vivo averaged 1.36 X 10(-3) +/- 0.45 X 10(-3) (SD) ml.h-1.cmH2O-1.cm-2, regardless of whether the capsule was filled with plasma or saline and irrespective of body position. This value was not significantly different from that measured in the excised chest wall preparation (1.43 X 10(-3) +/- 1.1 X 10(-3) ml.h-1.cmH2O-1.cm-2). The parietal pleura offers little resistance to transpleural protein movement, because there was no observed difference between plasma and saline. We conclude that because the Lp for intact parietal pleura and extrapleural interstitium is approximately 100 times smaller than that previously measured in isolated stripped pleural preparations, removal of parietal pleural results in a damaged preparation.


2004 ◽  
Vol 286 (2) ◽  
pp. H731-H741 ◽  
Author(s):  
Lucas DeMaio ◽  
John M. Tarbell ◽  
Russell C. Scaduto ◽  
Thomas W. Gardner ◽  
David A. Antonetti

A sudden increase in the transmural pressure gradient across endothelial monolayers reduces hydraulic conductivity ( Lp), a phenomenon known as the sealing effect. To further characterize this endothelial adaptive response, we measured bovine aortic endothelial cell (BAEC) permeability to albumin and 70-kDa dextran, Lp, and the solvent-drag reflection coefficients (σ) during the sealing process. The diffusional permeability coefficients for albumin (1.33 ± 0.18 × 10–6 cm/s) and dextran (0.60 ± 0.16 × 10–6 cm/s) were measured before pressure application. The effective permeabilities (measured when solvent drag contributes to solute transport) of albumin and dextran ( Pealb and Pedex) were measured after the application of a 10 cmH2O pressure gradient; during the first 2 h of pressure application, Pealb, Pedex, and Lp were significantly reduced by 2.0 ± 0.3-, 2.1 ± 0.3-, and 3.7 ± 0.3-fold, respectively. Immunostaining of the tight junction (TJ) protein zonula occludens-1 (ZO-1) was significantly increased at cell-cell contacts after the application of transmural pressure. Cytochalasin D treatment significantly elevated transport but did not inhibit the adaptive response, whereas colchicine treatment had no effect on diffusive permeability but inhibited the adaptive response. Neither cytoskeletal inhibitor altered σ despite significantly elevating both Lp and effective permeability. Our data suggest that BAECs actively adapt to elevated transmural pressure by mobilizing ZO-1 to intercellular junctions via microtubules. A mechanical (passive) component of the sealing effect appears to reduce the size of a small pore system that allows the transport of water but not dextran or albumin. Furthermore, the structures of the TJ determine transport rates but do not define the selectivity of the monolayer to solutes (σ).


1997 ◽  
Vol 273 (2) ◽  
pp. H997-H1002 ◽  
Author(s):  
R. E. Drake ◽  
S. Dhother ◽  
R. A. Teague ◽  
J. C. Gabel

Microvascular membranes are heteroporous, so the mean osmotic reflection coefficient for a microvascular membrane (sigma d) is a function of the reflection coefficient for each pore. Investigators have derived equations for sigma d based on the assumption that the protein osmotic pressure gradient across the membrane (delta II) does not vary from pore to pore. However, for most microvascular membranes, delta II probably does vary from pore to pore. In this study, we derived a new equation for sigma d. According to our equation, pore-to-pore differences in delta II increase the effect of small pores and decrease the effect of large pores on the overall membrane osmotic reflection coefficient. Thus sigma d for a heteroporous membrane may be much higher than previously derived equations indicate. Furthermore, pore-to-pore delta II differences increase the effect of plasma protein osmotic pressure to oppose microvascular fluid filtration.


1987 ◽  
Vol 63 (5) ◽  
pp. 1912-1918 ◽  
Author(s):  
D. Negrini ◽  
C. Capelli ◽  
M. Morini ◽  
G. Miserocchi

Using liquid-filled catheters, we recorded, in 30 anesthetized, spontaneously breathing supine rabbits, the hydraulic pressure from the parietal subpleural interstitial space (Pspl). Through a small exposed area of parietal pleura a plastic catheter (1 mm ED), with a closed and smooth tip and several holes on the last centimeter, was carefully advanced between the muscular layer and the parietal pleura, tangentially to the pleural surface to reach the submesothelial layer. Simultaneous measurements of pleural liquid pressure (Pliq) were obtained from intrapleurally placed cannulas. End-expiratory Pspl decreased (became more negative) with increasing height (LH) according to the following: Pspl (cmH2O) = -1 - 0.4 LH (cm), the corresponding equation for Pliq being Pliq (cmH2O) = -1.5 – 0.7 LH (cm). Thus at end expiration a transpleural hydraulic pressure difference (Pliq-Pspl) developed at any height, increasing from the bottom to the top of the cavity as Pliq - Pspl (cmH2O) = -0.5 – 0.3 LH (cm). The Pliq-Pspl difference increased during inspiration due to the much smaller tidal change in Pspl than in Pliq. By considering the gravity-dependent distribution of the functional hydrostatic pressure in the systemic capillaries of the pleura (Pc) and the Pspl and Pliq values integrated over the respiratory cycle we estimated that on the average, the Pc-Pspl difference is sevenfold larger than the Pspl-Pliq difference.


1993 ◽  
Vol 264 (5) ◽  
pp. H1428-H1437 ◽  
Author(s):  
V. H. Huxley ◽  
F. E. Curry ◽  
M. R. Powers ◽  
B. Thipakorn

We tested two hypotheses to account for the reduction in coupling of anionic solute to water flow (solvent drag) in microvessels during perfusion with plasma compared with albumin. Solvent drag is determined by both hydraulic conductivity (Lp) and solute reflection coefficient (sigma). Accordingly, decreased solvent drag during plasma perfusion must be the result of an increase in sigma (hypothesis 1) or reduction of Lp (hypothesis 2) or some combination of both mechanisms. These hypotheses were assessed by measuring Lp, sigma, and diffusive solute permeability (Psd) to the anionic protein alpha-lactalbumin in frog mesenteric exchange microvessels during plasma or albumin perfusion. The solute permeability coefficient to alpha-lactalbumin (Ps alpha-lactalbumin) was lower during exposure to plasma than bovine serum albumin (BSA) [(Ps alpha-lactalbumin)plasma/(Ps alpha-lactalbumin)BSA = 0.31 +/- 0.11 (means +/- SE, n = 9)]. Solute reflection coefficient to alpha-lactalbumin (sigma alpha-lactalbumin) was 0.69 +/- 0.02 in plasma and 0.34 +/- 0.03 in BSA (n = 7). Lp was not significantly influenced by perfusate protein composition (Lp plasma/Lp BSA = 1.02 +/- 0.11; n = 20). These data lead to the conclusion that the actions of plasma are to confer charge selectivity for anionic solute and, to a lesser extent, modify the porous pathways of the microvessel wall. Taken together, these results indicate that porous pathways contribute significantly to macromolecular flux in plasma-perfused vessels.


1985 ◽  
Vol 59 (2) ◽  
pp. 597-602 ◽  
Author(s):  
J. P. Wiener-Kronish ◽  
M. A. Gropper ◽  
S. J. Lai-Fook

We have developed a minimally invasive method for measuring the hydrostatic pressure in the pleural space liquid. A liquid-filled capsule is bonded into a rib and a small hole is cut in the parietal pleura to allow direct communication between the liquid in the capsule and the pleural space. The pressure can be measured continuously by a strain gauge transducer connected to the capsule. The rib capsule does not distort the pleural space or require removal of intercostal muscle. Pneumothoraces are easily detected when they occur inadvertently on puncturing the parietal pleura. We examined the effect of height on pleural pressure in 15 anesthetized spontaneously breathing dogs. The vertical gradients in pleural pressure were 0.53, 0.42, 0.46, and 0.23 cmH2O/cm height for the head-up, head-down, supine, and prone body positions, respectively. These vertical gradients were much less than the hydrostatic value (1 cmH2O/cm), indicating that the pleural liquid is not in hydrostatic equilibrium. In most body positions the magnitudes of pleural liquid pressure interpolated to midchest level were similar to the mean transpulmonary (surface) pressure determined postmortem. This suggests that pleural liquid pressure is closely related to the lung static recoil.


1990 ◽  
Vol 258 (2) ◽  
pp. H587-H598 ◽  
Author(s):  
F. E. Curry ◽  
W. L. Joyner ◽  
J. C. Rutledge

We investigated the exchange of water and macromolecules across venular microvessels after permeability was increased. Quantitative fluorescence microscopy was used to measure albumin permeability coefficients in individually perfused microvessels of decerebrate frogs. Control permeability coefficient was 2.3 +/- 0.25 X 10(-7) cm/s. Solvent drag increased the apparent solute permeability coefficient (Ps) by 0.57 +/- 0.05 X 10(-7) cm/s for each cmH2O increase in microvessel pressure. The divalent cation ionophore A23187 (0.1–5 microM) produced a transient increase in Ps to a peak value (within 1–3 min), followed (after 4–8 min) by a sustained increase in permeability (16–34% of peak values). Peak values of Ps were 13 and 80 times control for 0.1 and 5 microM A23187, respectively. Both diffusion and solvent drag contributed to the sustained increase in Ps. The equivalent pore radius of the structures determining diffusion and solvent drag was less than or equal to 25 nm during the sustained increase in permeability, smaller than observed gaps between adjacent endothelial cells. The basement membrane and a fibrous matrix secreted by endothelial cells into the gaps may offer resistance to exchange in the high permeability state.


During transpiration the hydrostatic tension which develops in the xylem conducting elements of the root draws water from the soil through the intervening tissues of the cortex, etc. It is uncertain whether this movement is entirely diffusional or in part a mass flow. To detect any such mass flow tomato plants grown in water culture were decapitated and placed in a canister through the lid of which the cut stem protruded and in which the pressure on the culture medium could be raised. The resulting rate of exudation (flux) was measured, and compared with the flux caused by an equivalent difference in osmotic potential obtained by measuring the ∆ f. p. of the medium and sap exuded. If these values of flux were equal, movement was by diffusion alone, but if pressure caused a greater flux, an additional mass flow was indicated. Preliminary experiments indicated a much greater flux in response to differences of pressure than osmotic potential, but accurate assessment of the effect was precluded by difficulties inherent in this straightforward approach. A less direct technique was therefore devised; the change in flux caused by changing the osmotic potential of the external medium (the hydrostatic pressure being maintained constant) was compared with the change in flux caused by changing the external pressure (the osmotic potential of the external medium being kept constant). The changes in flux were measured in such a way as to minimize changes in the osmotic potential in the xylem and in resistances to diffusion or mass flow respectively. In this way the change in flux per unit change in osmotic potential difference across the cortex (osmotic permeability coefficient, k 0 ) and the change in flux per unit change in pressure difference across the cortex (pressure permeability coefficient, k p ) could be compared under the same pressure gradient and in addition the effects of pressure gradients on k 0 could be studied. Thus, the effects of a pressure gradient on the diffusional movement of water could be assessed, as well as any mass flow component of the flux detected and measured.


1997 ◽  
Vol 273 (6) ◽  
pp. H2774-H2782 ◽  
Author(s):  
El Rasheid Zakaria ◽  
Joanne Lofthouse ◽  
Michael F. Flessner

We and others have shown that the loss of fluid and macromolecules from the peritoneal cavity is directly dependent on intraperitoneal hydrostatic pressure (Pip). Measurements of the interstitial pressure gradient in the abdominal wall demonstrated minimal change when Pipwas increased from 0 to 8 mmHg. Because flow through tissue is governed by both interstitial pressure gradient and hydraulic conductivity ( K), we hypothesized that K of these tissues varies with Pip. To test this hypothesis, we dialyzed rats with Krebs-Ringer solution at constant Pipof 0.7, 1.5, 2.2, 3, 4.4, 6, or 8 mmHg. Tracer amounts of125I-labeled immunoglobulin G were added to the dialysis fluid as a marker of fluid movement into the abdominal wall. Tracer deposition was corrected for adsorption to the tissue surface and for local loss into lymphatics. The hydrostatic pressure gradient in the wall was measured using a micropipette and a servo-null system. The technique requires immobilization of the tissue by a porous Plexiglas plate, and therefore a portion of the tissue is supported. In agreement with previous results, fluid flux into the unrestrained abdominal wall was directly related to the overall hydrostatic pressure difference across the abdominal wall (Pip= 0), but the interstitial pressure gradient near the peritoneum increased only ∼40% over the range of Pip= 1.5–8 mmHg (20–28 mmHg/cm). K of the abdominal wall varied from 0.90 ± 0.1 × 10−5cm2⋅ min−1⋅ mmHg−1at Pip= 1.5 mmHg to 4.7 ± 0.43 ×10−5cm2⋅ min−1⋅ mmHg−1on elevation of Pipto 8 mmHg. In contrast, for the same change in Pip, abdominal muscle supported on the skin side had a significantly lower range of fluid flux (0.89–1.7 × 10−4vs. 1.9–10.1 × 10−4ml ⋅ min−1⋅ cm−2in unsupported tissue). The differences between supported and unsupported tissues are likely explained in part by a reduced pressure gradient across the supported tissue. In conclusion, the in vivo hydraulic conductivity of the unsupported abdominal wall muscle in anesthetized rats varies with the superimposed hydrostatic pressure within the peritoneal cavity.


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