Compared effects of selected colloids on extravascular lung water in dogs after oleic acid-induced lung injury and severe hemorrhage

1983 ◽  
Vol 11 (4) ◽  
pp. 267-270 ◽  
Author(s):  
JAY S. FINCH ◽  
CARL REID ◽  
KENNETH BANDY ◽  
DAVID FICKLE
Keyword(s):  
Oleic Acid ◽  
Lung Injury ◽  
Extravascular Lung Water ◽  
Lung Water ◽  
Severe Hemorrhage

Bronchial vascular occlusion does not attenuate or accentuate oleic acid lung injury in anesthetized sheep

1993 ◽  
Vol 75 (6) ◽  
pp. 2671-2676 ◽  
Author(s):  
P. M. Dodek ◽  
A. Valenzuela ◽  
D. K. Minshall ◽  
E. M. Baile ◽  
P. D. Pare
Keyword(s):  
Blood Flow ◽  
Oleic Acid ◽  
Lung Injury ◽  
Arterial Pressure ◽  
Extravascular Lung Water ◽  
Arterial Oxygen Tension ◽  
Lung Mechanics ◽  
Arterial Oxygen ◽  
Lung Water ◽  
Group 1

To determine if bronchial blood flow affects the consequences of acute pulmonary vascular injury, we studied oleic acid lung injury in 12 anesthetized sheep. In six sheep (group 1), we injected 2 ml of ethanol directly into the bronchoesophageal artery to decrease bronchial blood flow. In the control sheep (group 2), we injected 2 ml of normal saline. One hour later, oleic acid (0.1 ml/kg) was injected into the right ventricle in both groups. We measured hemodynamics and lung mechanics at baseline, 1 h after injection into the bronchoesophageal artery but just before the injection of oleic acid, and 3 h after injection of oleic acid. We measured bronchial blood flow at baseline and 3 h after injection of oleic acid and extravascular lung water at 3 h after injection of oleic acid. One hour after injection of ethanol or saline into the bronchoesophageal artery, hemodynamics and lung mechanics did not change. Three hours after injection of oleic acid, systemic arterial pressure decreased, pulmonary arterial pressure increased, cardiac output decreased, dynamic compliance decreased, pulmonary resistance increased, arterial oxygen tension decreased, and extravascular lung water was greater than normal. There were no differences in these measurements between the two groups. However, bronchial blood flow decreased only in group 1. We conclude that decreasing bronchial blood flow does not attenuate or accentuate the consequences of oleic acid lung injury.

Regional measurements of pulmonary edema by using magnetic resonance imaging

1998 ◽  
Vol 84 (6) ◽  
pp. 2143-2153 ◽  
Author(s):  
S. D. Caruthers ◽  
C. B. Paschal ◽  
N. A. Pou ◽  
R. J. Roselli ◽  
T. R. Harris
Keyword(s):  
Magnetic Resonance Imaging ◽  
Oleic Acid ◽  
Magnetic Resonance ◽  
Pulmonary Edema ◽  
Surface Area ◽  
Extravascular Lung Water ◽  
Three Dimensional ◽  
Indicator Dilution ◽  
Resonance Imaging ◽  
Lung Water

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.

A positron emission tomographic comparison of diffuse and lobar oleic acid lung injury

1988 ◽  
Vol 64 (6) ◽  
pp. 2357-2365 ◽  
Author(s):  
D. P. Schuster ◽  
J. W. Haller ◽  
M. Velazquez
Keyword(s):  
Oleic Acid ◽  
Lung Injury ◽  
Dorsal Region ◽  
Lung Water ◽  
Positron Emission ◽  
Transcapillary Escape Rate ◽  
Severity Of Injury ◽  
Water Accumulation ◽  
The Right ◽  
Lung Lobes

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.

Eicosanoid balance and perfusion redistribution of oleic acid-induced acute lung injury

1992 ◽  
Vol 73 (5) ◽  
pp. 2126-2134 ◽  
Author(s):  
A. H. Stephenson ◽  
A. J. Lonigro ◽  
S. W. Holmberg ◽  
D. P. Schuster
Keyword(s):  
Acute Lung Injury ◽  
Oleic Acid ◽  
Lung Injury ◽  
Water Concentration ◽  
Dependent Lung ◽  
Lung Water ◽  
Tissue Concentrations ◽  
Tissue Samples ◽  
Positron Emission ◽  
Regional Lung

We have proposed that endogenous prostacyclin opposes the vasoconstriction responsible for redistribution of regional pulmonary blood flow (rPBF) away from areas of increased regional lung water concentration (rLWC) in canine oleic acid- (OA) induced acute lung injury (D. P. Schuster and J. Haller. J. Appl. Physiol. 69: 353–361, 1990). To test this hypothesis, we related regional lung tissue concentrations of 6-ketoprostaglandin (PG) F1 alpha and thromboxane (Tx) B2 in tissue samples obtained 2.5 h after administration of OA (0.08 ml/kg iv) to rPBF and rLWC measured by positron emission tomography. After OA only (n = 16), rLWC increased in dependent lung regions. Some animals responded to increased rLWC by redistribution of rPBF away from the most edematous regions (OA-R, n = 6), whereas others did not (OA-NR, n = 10). In another six animals, meclofenamate was administered after OA (OA-meclo). After OA, tissue concentrations of 6-keto-PGF1 alpha were greater than TxB2 in all groups, but concentrations of 6-keto-PGF1 alpha were not different between OA-R and OA-NR animals. TxB2 was increased in the dependent regions of animals in both OA-R and OA-NR groups compared with controls (no OA, n = 4, P < 0.05). The tissue TxB2/6-keto-PGF1 alpha ratio was smaller in controls and OA-NR in which no perfusion redistribution occurred than in OA-R and OA-meclo in which it did occur. This TxB2/6-keto-PGF1 alpha ratio correlated significantly with the magnitude of perfusion redistribution.(ABSTRACT TRUNCATED AT 250 WORDS)

Type of lung injury influences the thermal-dye estimation of extravascular lung water

1984 ◽  
Vol 57 (3) ◽  
pp. 680-685 ◽  
Author(s):  
P. V. Carlile ◽  
B. A. Gray
Keyword(s):  
Lung Injury ◽  
Extravascular Lung Water ◽  
Base Line ◽  
Shunt Fraction ◽  
Lung Water ◽  
Animal Group ◽  
Group I ◽  
Injury Group ◽  
Anesthetized Dogs ◽  
Group Ii

To determine the effect of the type of lung injury on the thermodilution estimation of extravascular lung water, we produced pulmonary edema in 25 anesthetized dogs by injection of alloxan or alpha-naphthylthiourea (ANTU) into the pulmonary circulation or by instillation of hydrochloric acid (HCI) into the airway. HCl injury was bilateral, unilateral with tidal volume equal in each lung, or unilateral with equal airway pressure. Extravascular thermal volume (ETV) was measured at base line and 4 h after lung injury, and the final measurement was compared with the postmortem determination of extravascular lung mass (ELM). In 11 of 15 animals with HCl injury final ETV was less than the base-line measurement. The ratio of final ETV to ELM for all HCl animal (group I) averaged 0.31 +/- 0.14, which was different from the value for animals with alloxan or ANTU injury (group II), 1.04 +/- 0.14 (P less than 0.01). Extravascular lung water per gram of blood-free dry tissue was not different for the two groups (8.1 +/- 1.2 and 8.7 +/- 2.6 for I and II, respectively), indicating equally severe lung injury; however, shunt fraction was less in group I (P less than 0.01). ETV/ELM correlated with the shunt fraction for group I (r = 0.70) but not for group II (r = 0.32). These findings indicate that ETV underestimates lung water after HCl injury due to the redistribution of pulmonary blood flow away from edematous areas.

Effect of eicosanoid inhibition on the development of pulmonary edema after acute lung injury

1996 ◽  
Vol 80 (3) ◽  
pp. 915-923 ◽  
Author(s):  
D. P. Schuster ◽  
A. H. Stephenson ◽  
S. Holmberg ◽  
P. Sandiford
Keyword(s):  
Acute Lung Injury ◽  
Oleic Acid ◽  
Lung Injury ◽  
Pulmonary Edema ◽  
Experimental Models ◽  
Nuclear Medicine Imaging ◽  
Lung Water ◽  
Edema Formation ◽  
Cyclooxygenase Inhibition ◽  
Positron Emission

In experimental models of acute lung injury, cyclooxygenase inhibition improves oxygenation, presumably by causing a redistribution of blood flow away from edematous lung regions. This effect on perfusion pattern could also reduce alveolar edema formation. On the other hand, pulmonary pressures usually increase after cyclooxygenase inhibition, an effect that could exacerbate edema accumulation. Therefore we tested the following hypothesis: the total accumulation of pulmonary edema in dogs during a 24- to 28-h period of observation after acute lung injury caused by oleic acid will be less in a group of animals treated with meclofenamate (n = 6) or with the thromboxane-receptor blocker ONO-3708 (n = 5) than in a group of animals treated with oleic acid alone (placebo, n = 6). Lung water concentrations (LWC), the regional pattern of pulmonary perfusion, and protein permeability were measured with the nuclear medicine imaging technique of positron emission tomography. After 24-28 h, LWC was significantly less (P < 0.05) in the ONO-3708 group than in the meclofenamate group (a similar trend was seen compared with the placebo group, P = 0.12). After 24-28 h, pulmonary arterial pressures were highest in the meclofenamate group. Regardless of group, the only significant correlation with the change in LWC was with the integral of pulmonary pressures over the 24- to 28-h period. The data suggest that thromboxane inhibition will reduce edema accumulation in acute lung injury but that this effect depends on reducing as much as possible the simultaneous development of pulmonary hypertension from other causes.

Simultaneous measurement of lung clearance rates for Tc- and In-DTPA in normal and damaged lungs

1989 ◽  
Vol 66 (5) ◽  
pp. 2293-2297 ◽  
Author(s):  
H. O'Brodovich ◽  
G. Coates ◽  
J. Kay ◽  
D. Muysson
Keyword(s):  
Oleic Acid ◽  
Lung Injury ◽  
Computer Assisted ◽  
Clearance Rates ◽  
Lung Water ◽  
Imaging Characteristics ◽  
Widespread Availability ◽  
Lung Water Content ◽  
Arterial Po2

We investigated the relative clearance rates for 99mTc-labeled diethylenetriamine-pentaacetate (Tc-DTPA) and 113mIn-labeled DTPA (In-DTPA) when they were inhaled and deposited together within the lungs of same animal. Submicronic aerosols containing Tc-DTPA and In-DTPA were simultaneously generated by different nebulizers and collected within the same anesthetic bag. The combined aerosols were insufflated into piglets. Clearances for both compounds were measured simultaneously in normal lungs and when the lungs were damaged by intravenous oleic acid or by a presumed oxidant agent, intravenous or intratracheal phorbol myristate acetate (PMA). A medium-energy collimator and a computer-assisted gamma camera were used to calculate clearances. Correction was made for downscatter from the In photopeak into the Tc window. Marked lung injury occurred as evidenced by increases in lung water content and decreases in arterial PO2. The clearance of In-DTPA was slightly but significantly slower than for Tc-DTPA in each group of animals. The correlation (r = 0.93) between clearances for Tc-DTPA and In-DTPA was good, even though in vitro studies demonstrated that Tc-DTPA, but not In-DTPA, slowly dissociated at room and body temperatures. Oleic acid increased, but surprisingly, PMA had no effect on clearance rates for both In-DTPA and Tc-DTPA. We recommend continued use of Tc-DTPA for these measurements in view of its lower cost, requirement for only low-energy collimation, better imaging characteristics, and widespread availability. The overlap between control and injured lungs and the lack of increased clearance rates after PMA suggest this technique does not always detect acute lung injury.

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