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.

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

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.

Effects of pulmonary edema on regional pulmonary perfusion in the intact dog lung

1980 ◽  
Vol 49 (5) ◽  
pp. 834-840 ◽  
Author(s):  
A. B. Malik ◽  
H. van der Zee ◽  
P. H. Neumann ◽  
N. B. Gertzberg
Keyword(s):  
Blood Flow ◽  
Pulmonary Edema ◽  
Pulmonary Blood Flow ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Weight Ratio ◽  
Flow Distribution ◽  
Base Line ◽  
Dependent Lung ◽  
Lung Water ◽  
Pulmonary Hemodynamics

Regional pulmonary blood flow was determined in dogs during varying degrees of pulmonary edema induced by infusing 179.2-659.4 ml/kg normal saline over 2-3 h. Pulmonary hemodynamics and regional blood flows were measured during the base-line period and at 30 min postinfusion. The degree of pulmonary edema was determined by the final extravascular lung water-to-bloodless dry lung weight ratio (W/D). In dogs developing gross alveolar edema (W/D of 10.70 +/- 0.88 vs. 3.10 +/- 0.30 in controls), the blood flow was shifted to either upper or dependent lung regions. The shift to the upper regions was associated with an increased (P < 0.05) pulmonary arterial pressure (Ppa), whereas the shift to the dependent lung was not associated with a significant change in Ppa. Breathing 100% O2 did not prevent these shifts, suggesting that they were not due to localized hypoxic pulmonary vasoconstriction. The flow distribution patterns were also not related to regional differences in edema. In contrast to the changes during fulminant edema, blood flow distribution did not change after moderate levels of pulmonary edema (W/D of 6.03 0.69), suggesting that gross alveolar flooding is required for a redistribution of pulmonary blood flow. Flow redistribution to the upper lung during airway flooding may be due to increase in Ppa, whereas the increased flow in the dependent lung during the same degree of edema may be due to "bulging" of alveolar vessels into the air spaces, secondary to a decrease in surface activity.

Response to Inhaled Nitric Oxide in Acute Lung Injury Depends on Distribution of Pulmonary Blood Flow Prior to Its Administration

1999 ◽  
Vol 159 (2) ◽  
pp. 563-570 ◽  
Author(s):  
RENÉ GUST ◽  
TIMOTHY J. McCARTHY ◽  
JAMES KOZLOWSKI ◽  
ALAN H. STEPHENSON ◽  
DANIEL P. SCHUSTER
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Pulmonary Blood Flow ◽  
Inhaled Nitric Oxide

Predicting The Influence Of Hypoxic Pulmonary Vasoconstriction On The Distribution Of Pulmonary Blood Flow

2011 ◽  
Author(s):  
Kelly S. Burrowes ◽  
Annalisa J. Swan ◽  
Alys R. Clark ◽  
Quentin P.P. Croft ◽  
Keith L. Dorrington ◽  
...  
Keyword(s):  
Blood Flow ◽  
Pulmonary Blood Flow ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Pulmonary Vasoconstriction

Effect of activated protein C on pulmonary blood flow and cytokine production in experimental acute lung injury

2007 ◽  
Vol 33 (12) ◽  
pp. 2199-2206 ◽  
Author(s):  
Jean-Christophe Richard ◽  
Fabienne Bregeon ◽  
Véronique Leray ◽  
Didier Le Bars ◽  
Nicolas Costes ◽  
...  
Keyword(s):  
Blood Flow ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Pulmonary Blood Flow ◽  
Protein C ◽  
Cytokine Production ◽  
Activated Protein C

Leukotriene inhibitors do not block hypoxic pulmonary vasoconstriction in dogs

1987 ◽  
Vol 62 (5) ◽  
pp. 1808-1813 ◽  
Author(s):  
D. P. Schuster ◽  
D. R. Dennis
Keyword(s):  
Blood Flow ◽  
Pulmonary Blood Flow ◽  
Pressor Response ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Lower Lobe ◽  
Left Lower Lobe ◽  
The Other ◽  
Pulmonary Vasoconstriction ◽  
Other Hand ◽  
Alveolar Hypoxia

We studied whether intravenously administered inhibitors of leukotriene synthesis (diethylcarbamazine, DEC) or end-organ effect (FPL-55712) would change the distribution of regional pulmonary blood flow (rPBF) caused by left lower lobe (LLL) alveolar hypoxia in dogs. Both drugs failed to alter rPBF. In addition, the pressor response to whole-lung hypoxia was not blocked by an FPL-55712 infusion. On the other hand, nitroprusside, as a nonspecific vasodilator also administered intravenously, was able to partially reverse the effects of LLL hypoxia on rPBF. Thus our data do not support a role for leukotriene mediation of hypoxic pulmonary vasoconstriction in dogs.

Mechanism by Which a Sustained Inflation Can Worsen Oxygenation in Acute Lung Injury

2004 ◽  
Vol 100 (2) ◽  
pp. 323-330 ◽  
Author(s):  
Guido Musch ◽  
R. Scott Harris ◽  
Marcos F. Vidal Melo ◽  
Kevin R. O’Neill ◽  
J. Dominick H. Layfield ◽  
...  
Keyword(s):  
Blood Flow ◽  
Acute Lung Injury ◽  
Gas Exchange ◽  
Lung Injury ◽  
Pulmonary Blood Flow ◽  
Lung Inflation ◽  
Positron Emission ◽  
Regional Lung Function ◽  
Sustained Inflation ◽  
Physiologic Data

Background Sustained lung inflations (recruitment maneuvers [RMs]) are occasionally used during mechanical ventilation of patients with acute lung injury to restore aeration to atelectatic alveoli. However, RMs do not improve, and may even worsen, gas exchange in a fraction of these patients. In this study, the authors sought to determine the mechanism by which an RM can impair gas exchange in acute lung injury. Methods The authors selected a model of acute lung injury that was unlikely to exhibit sustained recruitment in response to a lung inflation. In five sheep, lung injury was induced by lavage with 0.2% polysorbate 80 in saline. Positron emission tomography and [13N]nitrogen were used to assess regional lung function in dependent, middle, and nondependent lung regions. Physiologic data and positron emission scans were collected before and 5 min after a sustained inflation (continuous positive airway pressure of 50 cm H2O for 30 s). Results All animals showed greater loss of aeration and higher perfusion and shunting blood flow in the dependent region. After the RM, Pao2 decreased in all animals by 35 +/- 22 mmHg (P &lt; 0.05). This decrease in Pao2 was associated with redistribution of pulmonary blood flow from the middle, more aerated region to the dependent, less aerated region (P &lt; 0.05) and with an increase in the fraction of pulmonary blood flow that was shunted in the dependent region (P &lt; 0.05). Neither respiratory compliance nor aeration of the dependent region improved after the RM. Conclusions When a sustained inflation does not restore aeration to atelectatic regions, it can worsen oxygenation by increasing the fraction of pulmonary blood flow that is shunted in nonaerated regions.

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