Perivascular interstitial fluid pressure measured by micropipettes in isolated dog lung

1982 ◽  
Vol 52 (1) ◽  
pp. 9-15 ◽  
Author(s):  
S. J. Lai-Fook

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.

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.


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.


1982 ◽  
Vol 53 (3) ◽  
pp. 737-743 ◽  
Author(s):  
S. J. Lai-Fook ◽  
K. C. Beck

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.


1977 ◽  
Vol 42 (4) ◽  
pp. 476-482 ◽  
Author(s):  
G. Bo ◽  
A. Hauge ◽  
G. Nicolaysen

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.


1988 ◽  
Vol 64 (6) ◽  
pp. 2357-2365 ◽  
Author(s):  
D. P. Schuster ◽  
J. W. Haller ◽  
M. Velazquez

We tested whether severity of injury measured from the pulmonary transcapillary escape rate for transferrin (PTCER), lung water accumulation, and changes in regional pulmonary blood flow (PBF) would be similar after oleic acid (OA) injection into either all lung lobes or directly into the pulmonary artery feeding the left caudal lobe (LCL) only. Measurements were made with positron emission tomography. After 0.015 ml/kg OA was injected into the LCL (Lobar, n = 5), lung water increased in the left dorsal region from 37 +/- 5 to 50 +/- 8 ml/100 ml lung (P less than 0.05), PTCER was 533 +/- 59 10(-4)/min, and regional PBF decreased 62%. No significant change occurred in the uninjured right dorsal lung where PTCER was 85 +/- 32. In the left ventral region PTCER was 357 +/- 60, PBF decreased only 31%, and the increase in lung water was less (25 +/- 3 to 30 +/- 6). In contrast after 0.08 ml/kg OA was injected via the right atrium (Diffuse, n = 6), PTCER (283 +/- 94) was lower in the left dorsal region of this group than in the corresponding region of the Lobar group (P less than 0.05). The increase in lung water, however, was the same, but no change occurred in PBF distribution. These results indicate important differences between the two methods of causing lung injury with OA. After injury lung water accumulates primarily in dependent portions of lung and is not always accompanied by a decrease in regional PBF. These decreases, when they occur, may instead indicate severe vascular injury.


1993 ◽  
Vol 75 (6) ◽  
pp. 2595-2601 ◽  
Author(s):  
R. K. Albert ◽  
W. J. Lamm ◽  
D. A. Rickaby ◽  
A. al-Tinawi ◽  
C. A. Dawson

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.


1988 ◽  
Vol 64 (1) ◽  
pp. 285-290 ◽  
Author(s):  
R. K. Albert ◽  
W. J. Lamm ◽  
D. L. Luchtel

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.


1986 ◽  
Vol 20 (3) ◽  
pp. 189-194 ◽  
Author(s):  
S. I. Tillery ◽  
B. E. Lehnert

Measurements of the total lung weights and the individual weights of the lung lobes of male F344 rats ranging in age from about 30 days to 140 days or more were made in order to determine how lung growth and the growths of the individual lung lobes relate to bodyweight over the course of maturation of this species. Additionally, in this study we also (1) compared how each lung lobe grows relative to total lung growth, (2) evaluated the ratios of lung dry weight to wet weight and (3) obtained information on the weights of the trachea and extra-hilar main-stem bronchi as the F344 rat matures. The wet weights WLT of the trachea-lung preparations and the pooled lobe weights WPL as functions of rat bodyweight WB could be readily described by the following logarithmic expressions: WLT = 0·596 ln WB - 1·923, r = 0·95; WPL = 0·464 ln WB - 1·566, r = 0·96. Expressed as percentages of the pooled lobe weights, the individual lobes remained at constant values as the animals grew with the exception of the right caudal lobe which decreased between bodyweights of 72 and 96 g; absolute wet weight measurements of the individual lobes indicated that the right cranial, right middle and right intermediate lobes actually decreased in weight between bodyweights of 300 and 385 g. The dry weights of the lobes consistently represented approximately 22% of the wet weights regardless of animal age or bodyweight, and on average the airways represented about 20% of the weights of the intact airway-lung preparations over the course of animal maturation.


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 47 (4) ◽  
pp. 666-669 ◽  
Author(s):  
S. J. Lai-Fook ◽  
R. E. Hyatt

At several transpulmonary pressures (Ptp), the pressure-diameter (PD) behavior of the largest intraparenchymal arterial segment in the isolated pig lung was compared with the behavior of the segment after its excision from the parenchyma and its extension to lengths equivalent to those in the intact state. For physiological changes in length, as may occur with lung inflation during Ptp changes from 4 to 25 cmH2O, excised-vessel diameters did not change significantly at a constant transmural pressure. The excised-vessel PD behavior was not significantly different from the intact-vessel PD behavior at a Ptp of 4 cmH2O. At any constant arterial pressure, intact-vessel diameters became larger as Ptp increased. Estimates of the perivascular pressure (Px) obtained by directly comparing intact-vessel and excised-vessel PD curves were as follows: 1) Px was equal to pleural pressure at a Ptp approximating the functional residual capacity; 2) Px decreased almost linearly as Ptp increased; and 3) Px decreased with a fall in arterial pressure. These results are consistent with direct measurements of the perivascular interstitial fluid pressure.


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