Mechanisms of pulmonary edema induced by an organophosphorus compound in anesthetized dogs

“Closing volume” (CV) was measured by the single-breath oxygen (SBO2) test in six dogs (alloxan group) before and after alloxan 100–200 mg/kg iv) was injected. CV increased significantly (P less than 0.05) from 32 +/- 3.2% (base line) to 45 +/- 3.5 % in period 1 (0–30 min after alloxan), but vital capacity (VC), respiratory system pressure volume (PV) curves, and alveolar plateau slopes did not change. No radiologic evidence of pulmonary edema was demonstrated in two dogs studied in period 1. CV decreased to 20 +/- 3.9% during period 2 (30–80 min after alloxan) and was associated with tracheal frothing, decreased VC, changes in the PV curve, and alveolar plateau slope, as well as histologic evidence of severe pulmonary edema. CV was 29 +/- 3.0%, and there were no changes in VC, PV curves, or alveolar plateau slopes in 6 other dogs studied for 2 h (control group). CV increased during period 1 before pulmonary edema could be demonstrated by changes in VC, PV curves, or radiography, but in period 2 lung function was so altered that CV by the SBO2 technique gave no useful information.

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Pulmonary mechanics during induced pulmonary edema in anesthetized dogs

Journal of Applied Physiology ◽

10.1152/jappl.1959.14.2.177 ◽

1959 ◽

Vol 14 (2) ◽

pp. 177-186 ◽

Cited By ~ 108

Author(s):

C. D. Cook ◽

J. Mead ◽

G. L. Schreiner ◽

N. R. Frank ◽

J. M. Craig

Keyword(s):

Pulmonary Edema ◽

Lung Compliance ◽

Tidal Range ◽

Pulmonary Mechanics ◽

Vascular Congestion ◽

Anesthetized Dogs ◽

Trapped Gas ◽

Aortic Obstruction ◽

Gas Volume ◽

Normal Lungs

In order to study the mechanisms underlying the changes in the mechanical properties of the lungs during pulmonary edema, pulmonary vascular congestion was produced in spontaneously breathing, anesthetized dogs by partial aortic obstruction and intravenous infusion. Brief periods of congestion were associated with small changes in the lung compliance compared with the progressive and striking compliance reduction (-78%) noted with more prolonged congestion. Lung volume at end-expiration showed little change if edema fluid and trapped gas as well as the ventilated gas volume were taken into account. When edematous lungs were forcibly inflated beyond the tidal range, it was found that the overall compliance at a distending pressure of 30 cm H2O was not much less (-6%) than that of normal lungs. Furthermore, edematous lungs manifested marked ‘static’ hysteresis during such maneuvers. These findings suggested that surface phenomena were responsible for the mechanical behavior of edematous lungs rather than vascular congestion, per se, or intrinsic tissue changes. This was borne out by experiments on excised lungs which showed that the elastic properties of edematous lungs were not significantly different from normal lungs when surface forces were minimized. Submitted on August 25, 1958

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Solute permeability of the alveolar epithelium in acute hemodynamic pulmonary edema in dogs

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1977.233.1.h80 ◽

1977 ◽

Vol 233 (1) ◽

pp. H80-H86 ◽

Cited By ~ 2

Author(s):

E. A. Egan ◽

R. M. Nelson ◽

I. H. Gessner

Keyword(s):

Pulmonary Edema ◽

Isotonic Saline ◽

Alveolar Epithelium ◽

Lung Epithelium ◽

Solute Permeability ◽

Blue Dextran ◽

Lung Segment ◽

Anesthetized Dogs ◽

The One ◽

Alveolar Edema

Ten anesthetized dogs, 48 h postintravenous 131I-albumin injection, had a segment of lung airspace isolated by a balloon-tipped catheter lodged in a bronchus. An isotonic saline solution containing trace amounts of Blue Dextran, 125I-albumin, and 57Co-cyanocobalamin was instilled into the lung segment. During control periods, lung saline was absorbed at a rate of 0.133% per minute as measured by indicator dilution of Blue Dextran. Only 57Co-cyanocobalamin crossed the epithelium. Acute hemodynamic pulmonary edema was produced by aortic constriction plus saline overload. In pulmonary edema the fluid volume in the airspace increased at the rate of 0.96% per minute, and there was a significant influx of 131I-albumin into the lung saline from the blood in all animals. However, neither 125I-albumin nor Blue Dextran diffused from the airspace into blood during edema; both were merely diluted by fluid influx. The rate of diffusion of 57Co-cyanocobalamin increased fivefold during edema. A small number of discrete breaks in the lung epithelium allowing bulk flow of interstitial fluid is proposed to account for the one-way movement of albumin in hemodynamic alveolar edema.

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Inspiratory muscle activity during pulmonary edema in anesthetized dogs

Respiration Physiology ◽

10.1016/0034-5687(92)90087-d ◽

1992 ◽

Vol 89 (3) ◽

pp. 287-298

Author(s):

Arie Oliven ◽

Steven G. Kelsen

Keyword(s):

Pulmonary Edema ◽

Muscle Activity ◽

Inspiratory Muscle ◽

Anesthetized Dogs

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Protein composition of lung fluids in acute alloxan edema in dogs

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1976.230.2.376 ◽

1976 ◽

Vol 230 (2) ◽

pp. 376-379 ◽

Cited By ~ 30

Author(s):

CE Vreim ◽

NC Staub

Keyword(s):

Pulmonary Edema ◽

Protein Concentration ◽

Interstitial Fluid ◽

Protein Composition ◽

Total Protein Concentration ◽

Alveolar Epithelial ◽

Anesthetized Dogs ◽

Free Interstitial ◽

High Concentrations ◽

Paired Analysis

In 11 anesthetized dogs with acute alloxan-induced pulmonary edema, we measured the protein composition of 1-mul samples of plasma, free interstitial fluid, alveolar fluid, and airway fluid. We obtained plasma and airway fluid at regular intervals as edema developed. We sampled alveolar fluid by pleural micropuncture in the unfrozen, excised lung and free interstitial fluid from perivascular cuffs in the frozen, excised lung. The average (+/- 1 SD) total protein concentration of plasma was 4.9 +/- 0.6, airway fluid 4.4 +/- 0.7, free interstitial fluid 4.9 +/- 0.7, and alveolar fluid 5.2 +/- 0.8 g/100 ml. The average fractions of albumin were 0.42 +/- 0.05, 0.50 +/- 0.05, 0.49 +/- 0.06, and 0.49 +/- 0.07, respectively. By paired analysis, the protein concentration of interstitial fluid was not significantly different from alveolar fluid. The protein concentration of airway fluid was significantly less than that in interstitial and alveolar fluid. The albumin fraction of the three lung fluids was identical but significantly different from plasma. We conclude that in alloxan-induced pulmonary edema the lung fluids contain high concentrations of protein and the alveolar epithelial membrane becomes freely permeable to protein molecules.

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Effect of regional alveolar hypoxia on permeability pulmonary edema formation in dogs

Journal of Applied Physiology ◽

10.1152/jappl.1987.62.4.1690 ◽

1987 ◽

Vol 62 (4) ◽

pp. 1690-1697 ◽

Cited By ~ 5

Author(s):

F. W. Cheney ◽

M. J. Bishop ◽

E. Y. Chi ◽

B. L. Eisenstein

Keyword(s):

Pulmonary Edema ◽

Lower Lobe ◽

Dry Weight ◽

Left Pulmonary Artery ◽

Edema Formation ◽

Pulmonary Capillary ◽

Anesthetized Dogs ◽

Alveolar Hypoxia ◽

Permeability Pulmonary Edema ◽

The Right

We studied the effects of regional alveolar hypoxia on permeability pulmonary edema formation. Anesthetized dogs had a bronchial divider placed so that the left lower lobe (LLL) could be ventilated with a hypoxic gas mixture (HGM) while the right lung was continuously ventilated with 100% O2. Bilateral permeability edema was induced with 0.05 ml/kg oleic acid and after 4 h of LLL ventilation with an HGM (n = 9) LLL gross weight was 161 +/- 13 (SE) g compared with 204 +/- 13 (SE) g (P less than 0.05) in the right lower lobe (RLL). Bloodless lobar water and dry weight were also significantly lower in the LLL as compared with the RLL of the study animals. In seven control animals in which the LLL fractional inspired concentration of O2 (FIO2) was 1.0 during permeability edema, there were no differences in gravimetric variables between LLL and RLL. In eight additional animals, pulmonary capillary pressure (Pc), measured by simultaneous occlusion of left pulmonary artery and vein, was not significantly different between LLL FIO2 of 1.0 and 0.05 either before or after pulmonary edema. We conclude that, in the presence of permeability pulmonary edema, regional alveolar hypoxia causes reduction in edema formation. The decreased edema formation during alveolar hypoxia is not due to a reduction in Pc.

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PULMONARY GAS EXCHANGE DURING INDUCTION OF PULMONARY EDEMA IN ANESTHETIZED DOGS

Survey of Anesthesiology ◽

10.1097/00132586-196512000-00006 ◽

1965 ◽

Vol 9 (6) ◽

pp. 544???545 ◽

Cited By ~ 1

Author(s):

S. I. SAID ◽

J. W. LONGACHER ◽

R. K. DAVIS ◽

C. M. BANERJEE ◽

W. M. DAVIS ◽

...

Keyword(s):

Gas Exchange ◽

Pulmonary Edema ◽

Pulmonary Gas Exchange ◽

Anesthetized Dogs

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Treatment of sea-water aspiration

Journal of Applied Physiology ◽

10.1152/jappl.1960.15.6.1113 ◽

1960 ◽

Vol 15 (6) ◽

pp. 1113-1116 ◽

Cited By ~ 9

Author(s):

Joseph S. Redding ◽

G. Carl Voigt ◽

Peter Safar

Keyword(s):

Body Weight ◽

Pulmonary Edema ◽

Intravenous Infusion ◽

Spontaneous Breathing ◽

Sea Water ◽

Artificial Respiration ◽

Positive Pressure ◽

Plasma Infusion ◽

Dog Plasma ◽

Anesthetized Dogs

Lightly anesthetized dogs were subjected to obstructive asphyxia (simulating laryngospasm). When spontaneous breathing efforts ceased, the lungs were flooded with sea water for 30 seconds, according to a standardized experiment described previously. Five dogs were treated with intermittent positive pressure artificial respiration with 100% oxygen (IPPB/O2) for 3 hours. Five additional dogs were treated identically except for the addition of an intravenous infusion of dog plasma 50 ml/kg body weight, 10 minutes after the start of artificial respiration. All the dogs treated only with IPPB/O2 for 3 hours were more completely reoxygenated than were those ventilated with IPPB/air for 10 minutes in the earlier experiment. However, death with pulmonary edema followed the cessation of IPPB/O2 as well as IPPB/air. When the hemoconcentration and hypovolemia, caused by flooding of the lungs with sea water, were corrected by plasma infusion in addition to IPPB/O2, four of the five dogs survived. Submitted on May 19, 1960

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Increased leukotriene C4 in ethchlorvynol-induced acute lung injury in dogs

Journal of Applied Physiology ◽

10.1152/jappl.1987.62.2.732 ◽

1987 ◽

Vol 62 (2) ◽

pp. 732-738 ◽

Cited By ~ 6

Author(s):

A. H. Stephenson ◽

R. S. Sprague ◽

T. E. Dahms ◽

A. J. Lonigro

Keyword(s):

Acute Lung Injury ◽

Lung Injury ◽

Pulmonary Edema ◽

Leukotriene C4 ◽

Lung Water ◽

Control Value ◽

Edema Fluid ◽

Injured Lung ◽

Anesthetized Dogs ◽

Arterial Plasma

We investigated whether ethchlorvynol (ECV)-induced acute lung injury (ALI) is associated with an increase in leukotriene C4 (LTC4) production. In six pentobarbital sodium-anesthetized dogs, ECV (15 mg/kg iv) introduced into the pulmonary circulation resulted in a 164 +/- 31% increase in extravascular lung water 120 min after ECV administration. Concomitantly, the mean (+/- SE) concentration of LTC4 in arterial plasma measured by radioimmunoassay following 80% EtOH precipitation, XAD-7 extraction and high-pressure liquid chromatography purification was 5.0 +/- 1.3 pg/ml, unchanged from control (pre-ECV) values. In contrast, in pulmonary edema fluid 120 min post-ECV, the LTC4 concentration was 35.2 +/- 10.8 pg/ml, sevenfold greater than those values found in the arterial plasma (P less than 0.01). In six additional dogs, 120 min after unilateral ALI had been induced with ECV (9 mg/kg iv), LTC4 in the bronchoalveolar lavage (BAL) of the uninjured lung was 12.1 +/- 1.5 pg/ml, unchanged from pre-ECV values, whereas, LTC4 in the BAL of the injured lung increased from a control value of 10.2 +/- 1.6 to 24.2 +/- 3.5 pg/ml (P less than 0.01) 120 min after ECV administration. These results demonstrate that, in ECV-induced acute lung injury, LTC4 concentrations in pulmonary edema fluid are considerably greater than those found in arterial plasma in the case of bilateral acute lung injury and significantly greater in the BAL of the injured lung compared with the uninjured lung in the case of unilateral acute lung injury. The results are a necessary first step in support of the hypothesis that leukotrienes participate in the altered permeability of ECV-induced acute lung injury.

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