Lung inflation can cause pulmonary edema in zone I of in situ dog lungs

1980 ◽  
Vol 49 (5) ◽  
pp. 815-819 ◽  
Author(s):  
R. K. Albert ◽  
S. Lakshminarayan ◽  
W. Kirk ◽  
J. Butler
Keyword(s):  
Weight Gain ◽  
Venous Pressure ◽  
Lower Lobe ◽  
Alveolar Pressure ◽  
Weight Changes ◽  
Lung Water ◽  
Lung Weight ◽  
Lung Inflation ◽  
Pulmonary Arterial

We investigated whether increases in lung water can occur due to lung inflation in zone I when alveolar vessels are collapsed. Static left lower lobe alveolar pressure, pulmonary arterial pressure, and pulmonary venous pressure were controlled in living, anesthetized, open-chested dogs. The lobe was inflated with 6% CO2 in air and suspended from a strain gauge, which allowed continual weight recording. The lung was held in zone I conditions. Arterial and venous pressures were equal at either 1 or 5 cmH2O, relative to the base of the 10- to 14-cm-high lobes. Weight changes were measured for 5 min after 5-cmH2O increments of alveolar pressure from 0 or 5 to 30 cmH2O. Lung weight gain due to edema occurred with inflation to alveolar pressures above 10 cmH2O. Greater lung distension resulted in greater rates of weight gain. Weight loss occurred on deflation. The fluid may have leaked from distended extra-alveolar vessels. This mechanism could explain the increased lung water seen with mechanical ventilation and/or positive end-expiratory pressure breathing.

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 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.

Effects of imidazole and indomethacin on fluid balance in isolated sheep lungs

1985 ◽  
Vol 58 (3) ◽  
pp. 892-898 ◽  
Author(s):  
G. A. Patterson ◽  
P. Rock ◽  
W. A. Mitzner ◽  
N. F. Adkinson ◽  
J. T. Sylvester
Keyword(s):  
Weight Gain ◽  
Fluid Balance ◽  
Autologous Blood ◽  
Lung Weight ◽  
Similar Time ◽  
Platelet Counts ◽  
Pulmonary Arterial ◽  
Time Courses ◽  
Lung Lymph

We determined the effects of extracorporeal perfusion with a constant flow (75 ml . min-1 . kg-1) of autologous blood on hemodynamics and fluid balance in sheep lungs isolated in situ. After 5 min, perfusate leukocyte and platelet counts fell by two-thirds. Pulmonary arterial pressure (Ppa) increased to a maximum of 32.0 +/- 3.4 Torr at 30 min and thereafter fell. Lung lymph flow (QL), measured from the superior thoracic duct, and perfusate thromboxane B2 (TXB2) concentrations followed similar time courses but lagged behind Ppa, reaching maxima of 4.1 +/- 1.2 ml/h and 2.22 +/- 0.02 ng/ml at 60 min. Lung weight gain, measured as the opposite of the weight change of the extracorporeal reservoir, and perfusate 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) concentration increased rapidly during the first 60 min and then more gradually. After 210 min, weight gain was 224 +/- 40 g and 6-keto-PGF1 alpha concentration, 4.99 +/- 0.01 ng/ml. The ratio of lymph to plasma oncotic pressure (pi L/pi P) at 30 min was 0.61 +/- 0.06 and did not change significantly. Imidazole (5 mM) reduced the changes in TXB2, Ppa, QL, and weight and platelet count but did not alter 6-keto-PGF1 alpha, pi L/pi P, or leukocyte count. Indomethacin (0.056 mM) reduced TXB2, 6-keto-PGF1 alpha, and the early increases in weight, Ppa, and QL but did not alter the time courses of leukocyte or platelet counts. Late in perfusion, however, Ppa and QL were greater than in either untreated or imidazole-treated lungs.

Effects of lung volume and alveolar surface tension on pulmonary vascular resistance

1987 ◽  
Vol 62 (4) ◽  
pp. 1622-1626 ◽  
Author(s):  
R. Y. Sun ◽  
G. F. Nieman ◽  
T. S. Hakim ◽  
H. K. Chang
Keyword(s):  
Surface Tension ◽  
Lung Volume ◽  
Pulmonary Arterial Pressure ◽  
Lower Lobe ◽  
Venous Occlusion ◽  
Alveolar Pressure ◽  
Lung Inflation ◽  
Occlusion Technique ◽  
Pulmonary Arterial ◽  
Alveolar Surface

Utilizing the arterial and venous occlusion technique, the effects of lung inflation and deflation on the resistance of alveolar and extraalveolar vessels were measured in the dog in an isolated left lower lobe preparation. The lobe was inflated and deflated slowly (45 s) at constant speed. Two volumes at equal alveolar pressure (Palv = 9.9 +/- 0.6 mmHg) and two pressures (13.8 +/- 0.8 mmHg, inflation; 4.8 +/- 0.5 mmHg, deflation) at equal volumes during inflation and deflation were studied. The total vascular pressure drop was divided into three segments: arterial (delta Pa), middle (delta Pm), and venous (delta Pv). During inflation and deflation the changes in pulmonary arterial pressure were primarily due to changes in the resistance of the alveolar vessels. At equal Palv (9.9 mmHg), delta Pm was 10.3 +/- 1.2 mmHg during deflation compared with 6.8 +/- 1.1 mmHg during inflation. At equal lung volume, delta Pm was 10.2 +/- 1.5 mmHg during inflation (Palv = 13.8 mmHg) and 5.0 +/- 0.7 mmHg during deflation (Palv = 4.8 mmHg). These measurements suggest that the alveolar pressure was transmitted more effectively to the alveolar vessels during deflation due to a lower alveolar surface tension. It was estimated that at midlung volume, the perimicrovascular pressure was 3.5–3.8 mmHg greater during deflation than during inflation.

Lymph flow and lung weight in isolated sheep lungs

1986 ◽  
Vol 61 (5) ◽  
pp. 1830-1835 ◽  
Author(s):  
W. Mitzner ◽  
J. T. Sylvester
Keyword(s):  
Weight Gain ◽  
Arterial Pressure ◽  
Left Atrial ◽  
Pulmonary Arterial Pressure ◽  
Lymph Flow ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Lung Water ◽  
Lung Weight ◽  
Pulmonary Arterial

To study the relationship between lung weight and lymph flow, we used an in situ, isolated sheep lung preparation that allowed these two variables to be measured simultaneously. All lungs were perfused for 4.5 h at a constant rate of 100 ml X min-1 X kg-1. In control lungs, the left atrial pressure (Pla) was kept at atmospheric pressure. In experimental lungs, Pla was kept atmospheric except for a 50-min elevation to 18 mmHg midway through the perfusion. During this period of left atrial hypertension, pulmonary arterial pressure rose from 18 to 31 mmHg, lymph flow rose from 3 to 12 ml/h, and the lymph-to-plasma oncotic pressure ratio (pi L/pi P) fell from 0.7 to 0.48. After left atrial pressure was returned to control, pulmonary arterial pressure, lymph flow, and pi L/pi P all returned to control levels. The rate of weight gain after the return of left atrial pressure to control was also the same as that in the control group. However, during the period of left atrial hypertension 135 ml of fluid were filtered into the lung, and this large increase in lung weight remained after the pressure was lowered. The presence of this substantial excess lung water despite control values for vascular pressures, lymph flow, rate of weight gain, and pi L/pi P suggests that the absolute amount of lung water has little influence on the dynamic aspects of lung fluid balance. These results are consistent with a two-compartment model of the interstitial space, where only one of the compartments is readily drained by the lymphatics.

Fluid leaks from extra-alveolar vessels in living dog lungs

1978 ◽  
Vol 44 (5) ◽  
pp. 759-762 ◽  
Author(s):  
R. K. Albert ◽  
S. Lakshminarayan ◽  
T. W. Huang ◽  
J. Butler
Keyword(s):  
Venous Pressure ◽  
Blood Gases ◽  
Alveolar Pressure ◽  
Arterial Blood Gases ◽  
Fluid Accumulation ◽  
Lung Weight ◽  
Arterial Blood ◽  
Pulmonary Arterial ◽  
The Right ◽  
Lung Base

Edema transudation from extra-alveolar vessels was investigated in anesthetized, open-chested dogs. Fluid accumulation at different alveolar and extra-alveolar vascular pressures was assessed by continuous lung weighing and microscopy. The left (experimental) lung was distended with 6% CO2 and air while normal arterial blood gases were maintained by separately ventilating the right lung. Extra-alveolar vessels were isolated by compressing alveolar vessels with alveolar pressures high enough to stop blood flow. Weight increased steadily (edemogenesis) when pulmonary arterial and/or pulmonary venous pressure was 1 cmH2O below this pressure. Because some alveolar vessels at the lung base could have remained open and leaked, extra-alveolar vessels were also separated from alveolar vessels by glass bead embolization sufficient to stop perfusion. Lung weight gains followed selective pulmonary arterial or venous pressure elevations. Electron microscopy demonstrated edema in experimental lobes which was not present in control lobes with undistended extra-alveolar vessels at the same alveolar pressure. Thus pulmonary edema can be caused by fluid leaking from extra-alveolar vessels.

Perfusion through vessels open in zone 1 contributes to gas exchange in rabbit lungs in situ

1995 ◽  
Vol 79 (6) ◽  
pp. 1895-1899 ◽  
Author(s):  
W. J. Lamm ◽  
T. Obermiller ◽  
M. P. Hlastala ◽  
R. K. Albert
Keyword(s):  
High Frequency ◽  
Pulmonary Arterial Pressure ◽  
Venous Pressure ◽  
High Frequency Oscillation ◽  
Bias Flow ◽  
Flow Through ◽  
Pulmonary Arterial ◽  
Zero Reference ◽  
The Mean

We previously found that up to 15% of the normal cardiac output can flow through lungs that are entirely in zone 1 and that the zone 1 pathway utilizes alveolar corner vessels. Because of the proximity of these vessels to alveoli, we hypothesized that lungs perfused under zone 1 conditions would exchange gas. We used the multiple inert gas elimination technique to assess the ventilation-perfusion (VA/Q) distribution under zones 1 and 2 in six rabbit lungs perfused with tris(hydroxymethyl)aminomethane-buffered Tyrode solution containing 1% albumin, 4% dextran, and papaverine (25 mg/l). High-frequency oscillation (tidal volume = 2.8 ml at 20 Hz, bias flow = 1 l/min) kept alveolar pressure (PA) nearly constant at 10 or 20 cmH2O. Pulmonary arterial pressure was set 2.5 cmH2O below or 5 cmH2O above PA (zones 1 and 2, respectively). Pulmonary venous pressure was kept at 0 cmH2O, with zero reference being the bottom of the lung. At PA of 10 cmH2O, flow was 64 +/- 40 and 5 +/- 3 ml/min (P < 0.05) and the mean VA/Q for perfusion was 1.1 +/- 0.4 and > 5 (P < 0.05) in zones 2 and 1, respectively. At PA of 20 cmH2O, flow was 89 +/- 36 and 22 +/- 13 ml/min (P < 0.05) and the mean VA/Q for perfusion was 0.8 +/- 0.3 and 3.7 +/- 2.4 (P < 0.05) in zones 2 and 1, respectively. Shunt averaged < 5% of total flow in all conditions. Blood flowing through vessels remaining open under zone 1 conditions 1) exchanges gas, 2) does not occur through anatomic or physiological shunts, and 3) may explain the high VA/Q seen with positive end-expiratory pressure.

Peribronchial pressure in excised dog lungs

1978 ◽  
Vol 45 (6) ◽  
pp. 858-869 ◽  
Author(s):  
H. Sasaki ◽  
F. G. Hoppin ◽  
T. Takishima
Keyword(s):  
Smooth Muscle ◽  
Lung Volume ◽  
Radial Stress ◽  
Similar Magnitude ◽  
Alveolar Pressure ◽  
Lung Inflation ◽  
Bronchial Wall ◽  
Lobar Bronchus ◽  
Intrabronchial Pressure

To characterize the stresses which determine bronchial diameter in the lung, we estimated peribronchial pressure (Px) relative to intrabronchial pressure (Pbr) and to alveolar pressure (PA) for the main lobar bronchus of excised dog lobes using the technique of Takishima et al. (J. Appl. Physiol. 38: 875--881, 1975). The recoil of the bronchial wall, Pbr---Px, when smooth muscle was relaxed varied primarily with bronchial diameter. The recoil of the parenchyma around the bronchus, Px---Pa, varied with lung volume but was also diameter-dependent and served to double approximately the effective elastance of the bronchus in situ. We estimated recoils during slow deflations from TLC with the bronchus untreated, or pharmacologically contracted or relaxed. In untreated and relaxed states, local parenchymal and bronchial recoils were of similar magnitude to overall lung recoil (i.e., Px congruent to Ppl) except at high inflating pressure (PA -- Ppl = 30 cmH2O) where they were about half as great. With contraction, bronchial and local parenchymal recoils increased to as much as twice overall lung recoil. Contracted smooth muscle exerted a radial stress of 36+/-14 cmH2O at full lung inflation but much less during stepwise deflation.

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.

Zone 2 and zone 3 pulmonary blood flow

1987 ◽  
Vol 62 (5) ◽  
pp. 1982-1988 ◽  
Author(s):  
S. L. Soohoo ◽  
H. S. Goldberg ◽  
R. Graham ◽  
A. C. Jasper
Keyword(s):  
Blood Flow ◽  
Pulmonary Blood Flow ◽  
Venous Pressure ◽  
Alveolar Pressure ◽  
The West ◽  
Zonal Distribution ◽  
Zonal Model ◽  
Flow Channels ◽  
Flow Through ◽  
Pulmonary Arterial

In the West model of zonal distribution of pulmonary blood flow, increases in flow down zone 2 are attributed to an increase in driving pressure and a decrease in resistance resulting from recruitment and distension. The increase in flow down zone 3 is attributed to a decrease in resistance only. Recent studies indicate that, besides the pressure required to maintain flow through a vessel, there is an added pressure cost that must be overcome in order to initiate flow. These additional pressure costs are designated critical pressures (Pcrit). Because Pcrit exceed alveolar pressure, the distinction between zones in the West model becomes less secure, and the explanation for the increase in flow even in West zone 3 requires reexamination. We used two methods to test the hypothesis that the Pcrit is the pertinent backpressure to flow even in zone 3, when the pulmonary venous pressure (Ppv) exceeds alveolar pressure (PA) but is less than Pcrit in the isolated canine left caudal lobe. First, PA was maintained at 5 cmH2O, and pressure flow (P-Q) characteristics were obtained in zone 2 and zone 3. Next, with PA still at 5 cmH2O, we maintained a constant flow and measured the change in pulmonary arterial pressure as Ppv was varied. Both techniques indicated that the pertinent backpressure to flow was the greater of either Pcrit or Ppv and that PA was never the pertinent backpressure to flow. Also, our results indicate no significant change in the geometry of the flow channels between zone 2 and zone 3. These findings refine the zonal model of the pulmonary circulation.

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