Unilateral acute lung injury induced by ethchlorvynol in anesthetized dogs

1984 ◽  
Vol 56 (5) ◽  
pp. 1252-1259 ◽  
Author(s):  
A. H. Stephenson ◽  
R. S. Sprague ◽  
T. E. Dahms ◽  
A. J. Lonigro
Keyword(s):  
Blood Flow ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Airway Pressure ◽  
Left Lung ◽  
Arterial Occlusion ◽  
Peak Airway Pressure ◽  
Lung Water ◽  
Injured Lung ◽  
Anesthetized Dogs

Ethchlorvynol (ECV) was used to induce unilateral acute lung injury in anesthetized dogs. Measurements of extravascular thermal volume by double-indicator (thermal-dye) dilution with and without left main pulmonary arterial occlusion permitted sequential estimates of extravascular lung water (EVLW) for each lung. Determinations of EVLW by thermal-dye and gravimetric methods were highly correlated (r = 0.80). ECV (9–15 mg/kg) administered into the right pulmonary circulation produced progressive increases in right lung EVLW, which by 120 min post-ECV was increased 152 +/- 22% (SE) over control (P less than 0.001). Left lung EVLW remained unchanged. Similarly, right, but not left, peak airway pressure was increased. Thermal dilution, coupled with electromagnetic methods, permitted estimates of blood flow to each lung. Despite redistribution of flow to the uninjured lung, systemic PO2 decreased (P less than 0.001) and venous admixture increased (P less than 0.05), suggesting impaired matching of ventilation and perfusion. In summary, introduction of ECV into one lung produced unilateral acute lung injury. EVLW increased solely in the injured lung as did peak airway pressure. Although there was a partial redistribution of blood flow away from the injured lung to the uninjured one, it was apparently inadequate to prevent impaired oxygenation of the blood.

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

1987 ◽  
Vol 62 (2) ◽  
pp. 732-738 ◽  
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.

Distribution of pulmonary blood flow and total lung water during partial liquid ventilation in acute lung injury

Surgery ◽  
1997 ◽  
Vol 122 (2) ◽  
pp. 313-323 ◽  
Author(s):  
Paul G Gauger ◽  
Michael C Overbeck ◽  
Robert A Koeppe ◽  
Barry L Shulkin ◽  
Julia N Hrycko ◽  
...  
Keyword(s):  
Blood Flow ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Pulmonary Blood Flow ◽  
Partial Liquid Ventilation ◽  
Lung Water ◽  
Liquid Ventilation

Hypoxia enhances unilateral lung injury by increasing blood flow to the injured lung

1987 ◽  
Vol 63 (6) ◽  
pp. 2516-2523 ◽  
Author(s):  
K. Takeda ◽  
M. J. Knapp ◽  
W. G. Wolfe ◽  
J. D. Crapo
Keyword(s):  
Blood Flow ◽  
Lung Injury ◽  
Left Lung ◽  
Weight Ratio ◽  
Normal Lung ◽  
Lung Edema ◽  
Lung Weight ◽  
Edema Formation ◽  
Concomitant Decrease ◽  
Injured Lung

We hypothesized that in unilateral lung injury, bilateral hypoxic ventilation would induce vasoconstriction in the normal lung, redirect blood flow to the injured lung, and cause enhanced edema formation. Unilateral left lung injury was induced by intrabronchial instillation of 1.5 ml/kg of 0.1 N HCl. After HCl injury, blood flow to the injured left lung decreased progressively from 0.70 +/- 0.04 to 0.37 +/- 0.05 l/min and percent of flow to the injured left lung (QL/QT) decreased from 37.7 +/- 2.2 to 23.6 +/- 2.2% at 240 min. Exposure to hypoxia (12% O2) for three 10-min episodes did not affect QL/QT in normal animals, but after unilateral HCl injury, it caused blood flow to the injured left lung to increase significantly. A concomitant decrease in blood flow occurred to the noninjured right lung, resulting in a significant increase in QL/QT. The enhanced blood flow to the injured lung was associated with a significant increase in the wet-to-dry lung weight ratio in the dependent regions of the injured lung. These findings demonstrate that in unilateral HCl-induced lung injury, transient hypoxia can enhance blood flow to the areas of injury and increase lung edema formation.

scholarly journals Effects of Different Levels of Pressure Support Variability in Experimental Lung Injury

2009 ◽  
Vol 110 (2) ◽  
pp. 342-350 ◽  
Author(s):  
Peter M. Spieth ◽  
Alysson R. Carvalho ◽  
Andreas Güldner ◽  
Paolo Pelosi ◽  
Oleg Kirichuk ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Pressure Support Ventilation ◽  
Airway Pressure ◽  
Pressure Support ◽  
Inspiratory Effort ◽  
Peak Airway Pressure ◽  
Support Ventilation ◽  
Different Levels ◽  
Surfactant Depletion

Background Noisy pressure support ventilation has been reported to improve respiratory function compared to conventional assisted mechanical ventilation. We aimed at determining the optimal level of pressure support variability during noisy pressure support ventilation. Methods Twelve pigs were anesthetized and mechanically ventilated. Acute lung injury was induced by surfactant depletion. At four levels of pressure support variability (coefficients of variation of pressure support equal to 7.5, 15, 30, and 45%, 30 min each, crossover design, special Latin squares sequence), we measured respiratory variables, gas exchange, hemodynamics, inspiratory effort, and comfort of breathing. The mean level of tidal volume was constant among variability levels. Results Compared to conventional pressure support ventilation, different levels of variability in pressure support improved the elastance of the respiratory system, peak airway pressure, oxygenation, and intrapulmonary shunt. Oxygenation and venous admixture benefited more from intermediate (30%) levels of variability, whereas elastance and peak airway pressure improved linearly with increasing variability. Heart rate as well as mean arterial and pulmonary arterial pressures decreased slightly at intermediate to high (30-45%) levels of variability in pressure support. Inspiratory effort and comfort of breathing were not importantly influenced by increased variability in pressure support. Conclusion In a surfactant depletion model of acute lung injury, variability of pressure support improves lung function. The variability level of 30% seems to represent a reasonable compromise to improve lung functional variables during noisy pressure support ventilation.

scholarly journals Redistribution of Pulmonary Blood Flow Impacts Thermodilution-based Extravascular Lung Water Measurements in a Model of Acute Lung Injury

2009 ◽  
Vol 111 (5) ◽  
pp. 1065-1074 ◽  
Author(s):  
R Blaine Easley ◽  
Daniel G. Mulreany ◽  
Christopher T. Lancaster ◽  
Jason W. Custer ◽  
Ana Fernandez-Bustamante ◽  
...  
Keyword(s):  
Blood Flow ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Pulmonary Blood Flow ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Shunt Fraction ◽  
Lung Water ◽  
Computed Tomographic ◽  
Pulmonary Vasoconstriction

Background Studies using transthoracic thermodilution have demonstrated increased extravascular lung water (EVLW) measurements attributed to progression of edema and flooding during sepsis and acute lung injury. The authors hypothesized that redistribution of pulmonary blood flow can cause increased apparent EVLW secondary to increased perfusion of thermally silent tissue, not increased lung edema. Methods Anesthetized, mechanically ventilated canines were instrumented with PiCCO (Pulsion Medical, Munich, Germany) catheters and underwent lung injury by repetitive saline lavage. Hemodynamic and respiratory physiologic data were recorded. After stabilized lung injury, endotoxin was administered to inactivate hypoxic pulmonary vasoconstriction. Computed tomographic imaging was performed to quantify in vivo lung volume, total tissue (fluid) and air content, and regional distribution of blood flow. Results Lavage injury caused an increase in airway pressures and decreased arterial oxygen content with minimal hemodynamic effects. EVLW and shunt fraction increased after injury and then markedly after endotoxin administration. Computed tomographic measurements quantified an endotoxin-induced increase in pulmonary blood flow to poorly aerated regions with no change in total lung tissue volume. Conclusions The abrupt increase in EVLW and shunt fraction after endotoxin administration is consistent with inactivation of hypoxic pulmonary vasoconstriction and increased perfusion to already flooded lung regions that were previously thermally silent. Computed tomographic studies further demonstrate in vivo alterations in regional blood flow (but not lung water) and account for these alterations in shunt fraction and EVLW.

scholarly journals Effects of Antibiotic Therapy on Pseudomonas aeruginosa-Induced Lung Injury in a Rat Model

1999 ◽  
Vol 43 (10) ◽  
pp. 2389-2394 ◽  
Author(s):  
Erika J. Ernst ◽  
Satoru Hashimoto ◽  
Joseph Guglielmo ◽  
Teiji Sawa ◽  
Jean-Francois Pittet ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Rat Model ◽  
In Vivo Model ◽  
Antibiotic Administration ◽  
Lung Water ◽  
Alveolar Epithelial ◽  
The Right

ABSTRACT The effect of antibiotics on the acute lung injury induced by virulent Pseudomonas aeruginosa PA103 was quantitatively analyzed in a rat model. Lung injury was induced by the instillation of PA103 directly into the right lower lobes of the lungs of anesthetized rats. The alveolar epithelial injury, extravascular lung water, and total plasma equivalents were measured as separate, independent parameters of acute lung injury. Four hours after the instillation of PA103, all the parameters were increased linearly depending on the dose of P. aeruginosa. Next, we examined the effects of intravenously administered antibiotics on the parameters of acute lung injury in d-galactosamine-sensitized rats. One hour after the rats received 107 CFU of PA103, an intravenous bolus injection of aztreonam (60 mg/kg) or imipenem-cilastatin (30 mg/kg) was administered. Despite an MIC indicating resistance, imipenem-cilastatin improved all the measurements of lung injury; in contrast, aztreonam, which had an MIC indicating sensitivity, did not improve any of the lung injury parameters. The antibiotics did not generate different quantities of plasma endotoxin; therefore, endotoxin did not appear to explain the differences in lung injury. This in vivo model is useful to quantitatively compare the efficacies of parenteral antibiotic administration on Pseudomonas airspace infections.

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