Key result
Oleic acid rapidly induces acute permeability pulmonary edema, endothelial damage, and reduced cardiac output in dogs.
Why the study?
The mechanisms underlying the development of acute lung edema induced by oleic acid required investigation.
What are the mechanisms and hemodynamic effects of acute lung edema induced by oleic acid (0.04 ml/kg) and modulated by prostaglandin I2 in adult mongrel dogs?
What are the mechanisms and hemodynamic effects of acute lung edema induced by oleic acid (0.04 ml/kg) and modulated by prostaglandin I2 in adult mongrel dogs?
Oleic acid-induced acute lung edema in dogs is caused by direct toxic injury to the vascular endothelium increasing protein clearance rather than indirect platelet-mediated mechanisms, though associated hemodynamic and airway changes can be normalized by prostaglandin I2.
Answers are grounded in this paper and cite their sources.
Supports direct endothelial toxicity in oleic acid lung edema model; leaves open applicability to human ARDS.
We investigated mechanisms related to the development of acute lung edema, as induced by oleic acid in adult mongrel dogs. The intravenous injection of oleic acid (0.04 ml/kg) was considered to induce a permeability edema, as an enhancement of transvascular protein clearance was observed after the injection. The effects of oleic acid injection on systemic blood pressure (SBP), pulmonary arterial pressure (PAP), pulmonary arterial wedge pressure (PAWP), cardiac output (CO) and airway pressure (AWP) were measured. A significant decrease in CO and increase in AWP were evident after the injection, but there were no changes in SBP, PAP and PAWP. Treatment of the animals with prostaglandin I2 (PGI2) did not alter the induction of edema by oleic acid. However, the decrease in CO and increase in AWP were normalized by treatment with PGI2. Blood platelet count was not affected by oleic acid given in a dose of 0.04 ml/kg. To determine the direct effect of oleic acid on the vascular endothelium, the agent was injected through a catheter placed in the pulmonary artery. Electron microscopic examination revealed severe vacuolation on the endothelium of the pulmonary artery after only 1 min of exposure to oleic acid. Increased permeation of Evans blue into the subendothelial tissue was also observed with oleic acid treatment, compared with findings in the controls. These results indicate that the lung edema induced by oleic acid is due to an increased protein clearance, probably through a direct toxic effect on the vascular endothelium rather than an indirect toxic effect of chemical mediators released from the aggregated platelets.
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Motohiro et al. (2008) studied Acute lung edema induced by oleic acid. Oleic acid and Prostaglandin I2 (PGI2) vs. Controls was evaluated on Transvascular protein clearance, hemodynamic parameters (CO, AWP, SBP, PAP, PAWP), and endothelial morphology. Oleic acid (0.04 ml/kg) induced acute permeability lung edema, severe endothelial vacuolation within 1 minute, and decreased cardiac output in dogs.
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