Distribution of extravascular lung water after acute smoke inhalation

1990 ◽  
Vol 68 (6) ◽  
pp. 2394-2402 ◽  
Author(s):  
W. R. Clark ◽  
G. Nieman ◽  
T. S. Hakim

Anesthetized dogs with thoracotomy were injected with Evans blue dye and were exposed acutely (5 min) to wood smoke inhalation. Thin slices from freeze-dried samples were photographed and assessed for periarterial and perivenous cuff area and for blue coloration with a score of 0 to 5. Bloodless extravascular lung water (EVLW) was also measured. The smoke-exposed animals were compared with controls and with animals exposed to alloxan or to high-pressure-induced pulmonary edema. EVLW at 2 h after smoke (6.46 +/- 0.80) was above control value (4.30 +/- 0.63) but not different from the alloxan (6.13 +/- 0.70) or high-pressure (6.88 +/- 1.30) groups. Despite the similarity in EVLW in the edematous lungs, there were marked differences in the intensity of blue color and size of cuffing around arteries and veins: the smoke, alloxan, and high-pressure groups had blue color scores of 1.0 +/- 0.1, 2.9 +/- 0.3, and 0.3 +/- 0.1, respectively. These scores indicated a large increase in microvascular permeability to proteins in the alloxan group, a moderate increase in the smoke group, and minimal change in the high-pressure group. The perivascular cuff area was largest in the alloxan group and moderate in the smoke and high-pressure groups. The cuff area was higher for arteries than for veins in all groups except the 0.5-h smoke group. We conclude that smoke inhalation causes a moderate increase in permeability and EVLW compared with alloxan. The extravascular lung water accumulates preferentially around the arteries, but the size of the perivascular cuff is not similar for all causes of pulmonary edema.

1984 ◽  
Vol 56 (1) ◽  
pp. 248-253 ◽  
Author(s):  
M. Julien ◽  
M. R. Flick ◽  
J. M. Hoeffel ◽  
J. F. Murray

To test the hypothesis that dry blood-free lung weight is increased during pulmonary edema, thereby leading to an underestimation of the ratio of extravascular lung water-to-dry lung weight, we measured postmortem lung water, dry mass, and hydroxyproline content in 33 sheep with normal lungs (n = 10), high-pressure edema (n = 9), or increased permeability edema (n = 14). Residual blood in the lung, measured using hemoglobin as the intravascular marker in all sheep, and also using 51Cr-tagged red blood cells in 24 sheep, was not different between the two methods or among the three groups of sheep. Extravascular lung water increased 64% in sheep with high-pressure edema and 82% in those with increased permeability edema compared with control values. Dry blood-free lung weight was significantly greater (33% more than control values) in sheep with increased permeability edema, causing the ratio of extravascular lung water-to-dry blood-free lung weight to underestimate accumulated lung water by about 50%. Because hydroxyproline content of the lung was not affected by edema, the ratio of extravascular lung water-to-lung hydroxyproline content was more accurate than the ratio of extravascular lung water-to-dry blood-free lung weight in the quantification of pulmonary edema.


1998 ◽  
Vol 84 (6) ◽  
pp. 2143-2153 ◽  
Author(s):  
S. D. Caruthers ◽  
C. B. Paschal ◽  
N. A. Pou ◽  
R. J. Roselli ◽  
T. R. Harris

A three-dimensional magnetic resonance imaging (MRI) method to measure pulmonary edema and lung microvascular barrier permeability was developed and compared with conventional methods in nine mongrel dogs. MRIs were obtained covering the entire lungs. Injury was induced by injection of oleic acid (0.021–0.048 ml/kg) into a jugular catheter. Imaging followed for 0.75–2 h. Extravascular lung water and permeability-related parameters were measured from multiple-indicator dilution curves. Edema was measured as magnetic resonance signal-to-noise ratio (SNR). Postinjury wet-to-dry lung weight ratio was 5.30 ± 0.38 ( n = 9). Extravascular lung water increased from 2.03 ± 1.11 to 3.00 ± 1.45 ml/g ( n = 9, P < 0.01). Indicator dilution studies yielded parameters characterizing capillary exchange of urea and butanediol: the product of the square root of equivalent diffusivity of escape from the capillary and capillary surface area ( D 1/2 S) and the capillary permeability-surface area product ( PS). The ratio of D 1/2 Sfor urea to D 1/2 Sfor butanediol increased from 0.583 ± 0.027 to 0.852 ± 0.154 ( n = 9, P < 0.05). Whole lung SNR at baseline, before injury, correlated with D 1/2 Sand PS ratios (both P < 0.02). By using rate of SNR change, the mismatch of transcapillary filtration flow and lymph clearance was estimated to be 0.2–1.8 ml/min. The filtration coefficient was estimated from these values. Results indicate that pulmonary edema formation during oleic acid injury can be imaged regionally and quantified globally, and the results suggest possible regional quantification by using three-dimensional MRI.


1982 ◽  
Vol 10 (3) ◽  
pp. 209
Author(s):  
Duncan McCallum ◽  
Michael Lefcoe ◽  
Ronald Holliday ◽  
Joanne Harris ◽  
Richard Finley ◽  
...  

1986 ◽  
Vol 61 (3) ◽  
pp. 1132-1138 ◽  
Author(s):  
G. J. Huchon ◽  
A. Lipavsky ◽  
J. M. Hoeffel ◽  
J. F. Murray

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.


1986 ◽  
Vol 14 (1) ◽  
pp. 48-51 ◽  
Author(s):  
EDWARD D. SIVAK ◽  
JAMES TITA ◽  
GLENN MEDEN ◽  
MASAAKI ISHIGAMI ◽  
JOHN GRAVES ◽  
...  

1983 ◽  
Vol 11 (7) ◽  
pp. 498-501 ◽  
Author(s):  
EDWARD D. SIVAK ◽  
BRADFORD J. RICHMOND ◽  
PETER B. OʼDONAVAN ◽  
GREGORY P. BORKOWSKI

1980 ◽  
Vol 49 (5) ◽  
pp. 841-845 ◽  
Author(s):  
A. Johnson ◽  
A. B. Malik

We determined the effects of chronic fibrinogen depletion on the development of pulmonary edema after pulmonary microembolization. Dogs were defibrinogenated with a purified fraction of Malayan pitviper venom (ancrod). Studies were made in four groups: control untreated (group I); emboli untreated (group II); control defibrinogenated (group III); and emboli defibrinogenated (group IV). Fibrinogen decreased (P < 0.05) from 570.6 +/- 100.9 to 5.3 +/- 3.1 mg/100 ml in the ancrod-treated groups. Pulmonary arterial pressure was increased to similar levels in both embolized groups after infusion of 100-mug-diam nonsiliconized glass beads into the right atrium. Pulmonary vascular resistance and pulmonary perfusion pressure were initially increased to similar levels in both embolized groups, but by 75 min postembolization (PE) both parameters were higher (P < 0.05) in the defibrinogenated group. The extravascular lung water-to-bloodless dry lung ratio at 75 min PE of 4.53 +/- 0.24 in group II was greater than the control value of 2.84 +/- 0.22 in group I (P < 0.05). In contrast, the extravascular lung water-to-bloodless dry lung ratio of 3.64 +/- 0.09 in group IV was not different from the control value of 3.38 +/- 0.04 in group III, but was less than 4.53 +/- 0.24 in group II (P < 0.05). Therefore, chronic defibrinogenation in dogs prevented the development of pulmonary edema after pulmonary microembolization. The protective effect may be due to inhibition of the increase in lung vascular permeability and to a time-dependent reduction in pulmonary microvascular pressure.


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